start-ver=1.4
cd-journal=joma
no-vol=27
cd-vols=
no-issue=1
article-no=
start-page=219
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251121
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Does perioperative discontinuation of anti-rheumatic drugs increase postoperative complications in orthopedic surgery for rheumatoid arthritis?
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective This study aimed to investigate whether discontinuation of biological or targeted synthetic antirheumatic disease-modifying drugs (bDMARDs or tsDMARDs) influences the incidence of postoperative complications in patients with rheumatoid arthritis (RA) undergoing orthopedic surgery.<br>
Methods A retrospective multicenter cohort study including patients receiving bDMARDs or tsDMARDs who underwent orthopedic surgery was conducted. Data collected encompassed the duration of drug discontinuation and postoperative adverse events, such as delayed wound healing, surgical site infection (SSI), disease flare-ups, and mortality. The association between drug discontinuation and these outcomes was analyzed. Multivariate analyses were conducted to identify potential risk factors for these events.<br>
Results A total of 2,060 cases were initially enrolled. After applying inclusion and exclusion criteria, data from 1,953 patients were analyzed. No significant differences were observed between the groups regarding delayed wound healing, SSI, or mortality. However, the incidence of disease flare-ups was substantially higher in the drug discontinuation group and in the interleukin (IL)-6 inhibitor group. Multivariate analysis identified that tumor necrosis factor α and IL-6 inhibitor use was associated with a higher risk of delayed wound healing relative to T-cell function modifiers.<br>
Conclusion In orthopedic surgery for patients with RA, maintaining the standard or the half of administration interval of bDMARD appears safe in the preoperative period. However, the drug discontinuation may increase the risk of postoperative flare-ups, particularly with IL-6 inhibitors. In addition, T-cell function modifiers may be associated with a lower risk of delayed wound healing, suggesting their safety profile in this context.
en-copyright=
kn-copyright=

en-aut-name=ItoHiromu
en-aut-sei=Ito
en-aut-mei=Hiromu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IshikawaHajime
en-aut-sei=Ishikawa
en-aut-mei=Hajime
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TsujiShigeyoshi
en-aut-sei=Tsuji
en-aut-mei=Shigeyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakayamaMasanori
en-aut-sei=Nakayama
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NishidaKeiichiro
en-aut-sei=Nishida
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MochizukiTakeshi
en-aut-sei=Mochizuki
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=EbinaKosuke
en-aut-sei=Ebina
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KojimaToshihisa
en-aut-sei=Kojima
en-aut-mei=Toshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MatsumotoTakumi
en-aut-sei=Matsumoto
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KubotaAyako
en-aut-sei=Kubota
en-aut-mei=Ayako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NakajimaArata
en-aut-sei=Nakajima
en-aut-mei=Arata
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KanekoAtsushi
en-aut-sei=Kaneko
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MatsushitaIsao
en-aut-sei=Matsushita
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=HaraRyota
en-aut-sei=Hara
en-aut-mei=Ryota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=SakurabaKoji
en-aut-sei=Sakuraba
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=AkasakiYukio
en-aut-sei=Akasaki
en-aut-mei=Yukio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=MatsubaraTsukasa
en-aut-sei=Matsubara
en-aut-mei=Tsukasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=MochidaYuichi
en-aut-sei=Mochida
en-aut-mei=Yuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=KanbeKatsuaki
en-aut-sei=Kanbe
en-aut-mei=Katsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=NakagawaNatsuko
en-aut-sei=Nakagawa
en-aut-mei=Natsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=MurataKoichi
en-aut-sei=Murata
en-aut-mei=Koichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=MomoharaShigeki
en-aut-sei=Momohara
en-aut-mei=Shigeki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

affil-num=1
en-affil=Department of Orthopaedic Surgery, Kurashiki Central Hospital
kn-affil=

affil-num=2
en-affil=Department of Rheumatology, Niigata Rheumatic Center
kn-affil=

affil-num=3
en-affil=Department of Orthopaedic Surgery, Osaka Minami Medical Center
kn-affil=

affil-num=4
en-affil=Department of Orthopaedic Surgery, International University of Health and Welfare
kn-affil=

affil-num=5
en-affil=Locomotive Pain Center, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Department of Orthopaedic Surgery, Kamagaya General Hospital
kn-affil=

affil-num=7
en-affil=Department of Orthopaedic Surgery, Osaka University Faculty of Medicine Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Orthopaedic Surgery, Nagoya University Hospital
kn-affil=

affil-num=9
en-affil=Department of Orthopaedic Surgery, University of Tokyo
kn-affil=

affil-num=10
en-affil=Department of Orthopaedic Surgery, Toho University Omori Medical Center
kn-affil=

affil-num=11
en-affil=Department of Orthopaedic Surgery and Rehabilitation, Toho University Sakura Medical Center
kn-affil=

affil-num=12
en-affil=Department of Orthopaedic Surgery, Nagoya Medical Center
kn-affil=

affil-num=13
en-affil=Department of Rehabilitation Medicine, Kanazawa Medical University
kn-affil=

affil-num=14
en-affil=The Center for Rheumatic Diseases, Nara Medical University
kn-affil=

affil-num=15
en-affil=Department of Orthopaedic Surgery, Kyushu Medical Center
kn-affil=

affil-num=16
en-affil=Department of Orthopaedic Surgery, Kyushu University
kn-affil=

affil-num=17
en-affil=Department of Orthopaedic Surgery, Matsubara Mayflower Hospital
kn-affil=

affil-num=18
en-affil=Department of Orthopaedic Surgery, Yokohama City University Medical Center
kn-affil=

affil-num=19
en-affil=Department of Orthopaedic Surgery, Nippori Orthopaedics and Rheumatic Clinic
kn-affil=

affil-num=20
en-affil=Department of Orthopaedic Surgery, Kakogawa Medical Center
kn-affil=

affil-num=21
en-affil=Department of Orthopaedic Surgery, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=22
en-affil=Endowed Course for Advanced Therapy for Musculoskeletal Disorders, Keio University School of Medicine
kn-affil=
en-keyword=Rheumatoid arthritis
kn-keyword=Rheumatoid arthritis
en-keyword=Orthopaedic surgery
kn-keyword=Orthopaedic surgery
en-keyword=DMARD
kn-keyword=DMARD
en-keyword=Perioperative complications
kn-keyword=Perioperative complications
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=関連線維芽細胞が誘導するインターロイキン6を標的とした胃癌腹膜転移に対する新規治療戦略
kn-title=Novel treatment strategy targeting interleukin-6 induced by cancer associated fibroblasts for peritoneal metastasis of gastric cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MITSUIEma
en-aut-sei=MITSUI
en-aut-mei=Ema
kn-aut-name=光井恵麻
kn-aut-sei=光井
kn-aut-mei=恵麻
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Gemcitabine-induced neutrophil extracellular traps via interleukin-8-CXCR1/2 pathway promote chemoresistance in pancreatic cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive cancers, and chemoresistance poses a significant challenge in its treatment. Neutrophil extracellular traps (NETs) have emerged as key players in the tumour microenvironment, but their role in chemoresistance remains unclear.<br>
Methods: We investigated the involvement of NETs in PDAC chemoresistance using patient tumour samples, in vitro assays with gemcitabine (GEM)-treated PDAC cells, and in vivo mouse models. We evaluated cytokine production, NET formation and tumour response to GEM, with or without the CXCR1/2 inhibitor navarixin.<br>
Results: NETs are significantly accumulated in the tumours of PDAC patients exhibiting poor response to chemotherapy. GEM-treated PDAC cells secrete pro-inflammatory cytokines such as interleukin-8 (IL-8). IL-8 promote the formation of chemotherapy-induced NETs (chemoNETosis) through activation of CXCR 1/2 on neutrophils. Importantly, treatment with navarixin significantly suppressed chemoNETosis, restored sensitivity to GEM, and significantly reduced tumour growth in vivo.<br>
Conclusions: Our findings reveal that NETs contribute to chemoresistance in PDAC and that IL-8?mediated chemoNETosis plays a pivotal role in this process. Inhibition of CXCR1/2-mediated NET formation enhances the efficacy of GEM. This approach may represent a promising therapeutic strategy for overcoming chemoresistance in PDAC. These results support further clinical investigation of anti-NETs therapies.
en-copyright=
kn-copyright=

en-aut-name=NogiShohei
en-aut-sei=Nogi
en-aut-mei=Shohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KagawaShunsuke
en-aut-sei=Kagawa
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TaniguchiAtsuki
en-aut-sei=Taniguchi
en-aut-mei=Atsuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YagiTomohiko
en-aut-sei=Yagi
en-aut-mei=Tomohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KanayaNobuhiko
en-aut-sei=Kanaya
en-aut-mei=Nobuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KakiuchiYoshihiko
en-aut-sei=Kakiuchi
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YasuiKazuya
en-aut-sei=Yasui
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FujiTomokazu
en-aut-sei=Fuji
en-aut-mei=Tomokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KonoYoshiyasu
en-aut-sei=Kono
en-aut-mei=Yoshiyasu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KikuchiSatoru
en-aut-sei=Kikuchi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakagiKosei
en-aut-sei=Takagi
en-aut-mei=Kosei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KurodaShinji
en-aut-sei=Kuroda
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TeraishiFuminori
en-aut-sei=Teraishi
en-aut-mei=Fuminori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=TazawaHiroshi
en-aut-sei=Tazawa
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=FujiwaraToshiyoshi
en-aut-sei=Fujiwara
en-aut-mei=Toshiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

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

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

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

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

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

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

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

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

affil-num=9
en-affil=Department of Gastroenterology and Hepatology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

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

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

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

affil-num=13
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=142
cd-vols=
no-issue=
article-no=
start-page=104967
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cross-feeding between beneficial and pathogenic bacteria to utilize eukaryotic host cell-derived sialic acids and bacteriophages shape the pathogen-host interface milieu
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Under an inflamed-intestinal milieu, increased free sialic acids are associated with the overgrowth of some pathogenic bacterial strains. Recently, the protective immunomodulatory activity of gut bacteriophages (phages) has also been highlighted. However, the role of phages in triple reciprocal interactions between pathogenic bacteria, beneficial bacteria, and their host cell sialic acids has not been studied so far. We established a sialidase-explicit model in which beneficial and pathogenic bacteria interact through cross-feeding and competition for free sialic acid using a human triple co-culture cell model incorporating colonocytes (T84 cells), monocytes (THP-1 cells), and hepatocytes (Huh7 cells). Triple co-cultured cells were challenged with Gram-positive Bifidobacterium bifidum (B. bifidum) and Gram-negative Pseudomonas aeruginosa PAO1 (P. a PAO1) in the absence or presence of its KPP22 phage in two different cell culture mediums: 1) standard Dulbecco's Modified Eagle Medium (DMEM) and 2) DMEM with 2,3-dehydro-2-deoxy-N-acetylneuraminic acid (DANA). Changes in physiological, functional, and structural health markers of stimulated cocultured cells were evaluated. The concentrations of sialic acid and pro-inflammatory cytokines in the cell culture supernatants were quantified. P. a PAO1 triggered the release of interleukin 6 and 8 (IL-6 and IL-8), accompanied by increased levels of free sialic acid, reduced viability of co-cultured cells, and disrupted the integrity of the cellular monolayer. These disruptive effects were markedly attenuated by KPP22 phage and B. bifidum. In addition to well-documented differences in the structure and composition of the bacterial cell walls of Gram-negative pathogenic bacteria and bifidobacteria, two distinct factors seem to be pivotal in modulating the pathogen-host interface milieu: (i) the presence of phages and (ii) the utilization of free sialic acids secreted from host cells by bifidobacteria.
en-copyright=
kn-copyright=

en-aut-name=GhadimiDarab
en-aut-sei=Ghadimi
en-aut-mei=Darab
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=F?lster-HolstRegina
en-aut-sei=F?lster-Holst
en-aut-mei=Regina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Bl?merSophia
en-aut-sei=Bl?mer
en-aut-mei=Sophia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=EbsenMichael
en-aut-sei=Ebsen
en-aut-mei=Michael
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=R?ckenChristoph
en-aut-sei=R?cken
en-aut-mei=Christoph
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UchiyamaJumpei
en-aut-sei=Uchiyama
en-aut-mei=Jumpei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsuzakiShigenobu
en-aut-sei=Matsuzaki
en-aut-mei=Shigenobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=BockelmannWilhelm
en-aut-sei=Bockelmann
en-aut-mei=Wilhelm
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Microbiology and Biotechnology, Max Rubner-Institut
kn-affil=

affil-num=2
en-affil=Clinic of Dermatology, Venerology und Allergology, University Hospital Schleswig-Holstein
kn-affil=

affil-num=3
en-affil=Clinic of Dermatology, Venerology und Allergology, University Hospital Schleswig-Holstein
kn-affil=

affil-num=4
en-affil=St?dtisches MVZ Kiel GmbH (Kiel City Hospital), Department of Pathology
kn-affil=

affil-num=5
en-affil=Institute of Pathology, Kiel University, University Hospital, Schleswig-Holstein
kn-affil=

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

affil-num=7
en-affil=Department of Medical Laboratory Science, Faculty of Health Sciences, Kochi Gakuen University
kn-affil=

affil-num=8
en-affil=Department of Microbiology and Biotechnology, Max Rubner-Institut
kn-affil=
en-keyword=Bacterial sialidase
kn-keyword=Bacterial sialidase
en-keyword=Inflammation
kn-keyword=Inflammation
en-keyword=Cytokines
kn-keyword=Cytokines
en-keyword=Infection
kn-keyword=Infection
en-keyword=Bifidobacteria
kn-keyword=Bifidobacteria
en-keyword=Phages
kn-keyword=Phages
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=roaf042
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250603
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Recommendations for the treatment of juvenile idiopathic arthritis with oligoarthritis or polyarthritis from the 2024 update of the Japan College of Rheumatology Clinical Practice Guidelines for the management of rheumatoid arthritis including juvenile idiopathic arthritis with oligoarthritis or polyarthritis ? secondary publication
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objectives: To conduct systematic reviews (SRs) and develop clinical practice guidelines (CPGs) for managing juvenile idiopathic arthritis (JIA) with oligoarthritis or polyarthritis.<br>
Methods: The Grading of Recommendations, Assessment, Development, and Evaluation methodology was employed to carry out SRs and formulate the CPGs. An expert panel, including patients, paediatric and nonpaediatric rheumatologists, guideline specialists, and patient representatives, used the Delphi method to discuss and agree on the recommendations.<br>
Results: Six clinical questions (CQs) on the efficacy and safety of medical treatments were evaluated. These included CQ1 on methotrexate (MTX), CQ2 on non-MTX conventional synthetic disease-modifying antirheumatic drugs, CQ3 on glucocorticoids, CQ4 on tumour necrosis factor inhibitors, CQ5 on interleukin-6 inhibitors, and CQ6 on Janus kinase inhibitors. Two randomized controlled trials were identified for CQ1, three for CQ2, two for CQ3, eight for CQ4, two for CQ5, and two for CQ6. Based on these evaluations, three strong and three conditional recommendations were established. The CPGs have been endorsed by the Japan College of Rheumatology and the Pediatric Rheumatology Association of Japan.<br>
Conclusions: The SRs provided the necessary evidence to develop the CPGs, which are intended to guide not only paediatric but also nonpaediatric rheumatologists, caregivers, patients, and their families in treatment decision-making.
en-copyright=
kn-copyright=

en-aut-name=MiyamaeTakako
en-aut-sei=Miyamae
en-aut-mei=Takako
kn-aut-name=
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kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OkamotoNami
en-aut-sei=Okamoto
en-aut-mei=Nami
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aut-affil-num=2
ORCID=

en-aut-name=InoueYuzaburo
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aut-affil-num=3
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en-aut-name=KubotaTomohiro
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en-aut-name=EbatoTakasuke
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en-aut-name=IrabuHitoshi
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en-aut-name=KanekoYuko
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en-aut-name=KuboHiroshi
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en-aut-name=MitsunagaKanako
en-aut-sei=Mitsunaga
en-aut-mei=Kanako
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en-aut-name=MoriMasaaki
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aut-affil-num=11
ORCID=

en-aut-name=NakajimaAyako
en-aut-sei=Nakajima
en-aut-mei=Ayako
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kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=NishimuraKenichi
en-aut-sei=Nishimura
en-aut-mei=Kenichi
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aut-affil-num=13
ORCID=

en-aut-name=OhkuboNaoaki
en-aut-sei=Ohkubo
en-aut-mei=Naoaki
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kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=SatoTomomi
en-aut-sei=Sato
en-aut-mei=Tomomi
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kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=SugitaYuko
en-aut-sei=Sugita
en-aut-mei=Yuko
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kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=TakanashiSatoshi
en-aut-sei=Takanashi
en-aut-mei=Satoshi
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=TanakaTakayuki
en-aut-sei=Tanaka
en-aut-mei=Takayuki
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aut-affil-num=18
ORCID=

en-aut-name=UmebayashiHiroaki
en-aut-sei=Umebayashi
en-aut-mei=Hiroaki
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=YashiroMasato
en-aut-sei=Yashiro
en-aut-mei=Masato
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=YamanishiShingo
en-aut-sei=Yamanishi
en-aut-mei=Shingo
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=FusamaMie
en-aut-sei=Fusama
en-aut-mei=Mie
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=HirataShintaro
en-aut-sei=Hirata
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=KishimotoMitsumasa
en-aut-sei=Kishimoto
en-aut-mei=Mitsumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=KohnoMasataka
en-aut-sei=Kohno
en-aut-mei=Masataka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=KojimaMasayo
en-aut-sei=Kojima
en-aut-mei=Masayo
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

en-aut-name=KojimaToshihisa
en-aut-sei=Kojima
en-aut-mei=Toshihisa
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=MorinobuAkio
en-aut-sei=Morinobu
en-aut-mei=Akio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=SugiharaTakahiko
en-aut-sei=Sugihara
en-aut-mei=Takahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
ORCID=

en-aut-name=TanakaEiichi
en-aut-sei=Tanaka
en-aut-mei=Eiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

en-aut-name=YajimaNobuyuki
en-aut-sei=Yajima
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=31
ORCID=

en-aut-name=YanaiRyo
en-aut-sei=Yanai
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=32
ORCID=

en-aut-name=KawahitoYutaka
en-aut-sei=Kawahito
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=33
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=34
ORCID=

affil-num=1
en-affil=Department of Pediatric Rheumatology, Institute of Rheumatology, Tokyo Women’s Medical University Hospital
kn-affil=

affil-num=2
en-affil=Department of Pediatrics, Osaka Rosai Hospital, Japan Organization of Occupational Health and Safety
kn-affil=

affil-num=3
en-affil=Department of General Medical Science, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=4
en-affil=Department of Pediatrics, Kagoshima Prefectural Satsunan Hospital
kn-affil=

affil-num=5
en-affil=Department of Pediatrics, Kitasato University
kn-affil=

affil-num=6
en-affil=Department of Pediatrics and Development Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University
kn-affil=

affil-num=7
en-affil=Division of Rheumatology, Department of Internal Medicine, Toho University
kn-affil=

affil-num=8
en-affil=Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine
kn-affil=

affil-num=9
en-affil=Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=10
en-affil=Department of Allergy and Rheumatology, Chiba Children's Hospital
kn-affil=

affil-num=11
en-affil=Department of Lifetime Clinical Immunology, Tokyo Medical and Dental University
kn-affil=

affil-num=12
en-affil=Center for Rheumatic Diseases, Mie University Hospital
kn-affil=

affil-num=13
en-affil=Department of Pediatrics, Yokohama City University Graduate School of Medicine
kn-affil=

affil-num=14
en-affil=Iizuka Hospital
kn-affil=

affil-num=15
en-affil=Clinical Education Center For Physicians, Shiga University of Medical Science
kn-affil=

affil-num=16
en-affil=Department of Pediatrics, School of Medicine, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=17
en-affil=Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine
kn-affil=

affil-num=18
en-affil=Department of Pediatrics, Japanese Red Cross Otsu Hospital
kn-affil=

affil-num=19
en-affil=Department of Rheumatology and Infectious Diseases, Miyagi Children’s Hospital
kn-affil=

affil-num=20
en-affil=Department of Pediatrics, Okayama University Hospital
kn-affil=

affil-num=21
en-affil=Department of Pediatrics, Nippon Medical School
kn-affil=

affil-num=22
en-affil=Health Sciences Department of Nursing, Kansai University of International Studies
kn-affil=

affil-num=23
en-affil=Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital
kn-affil=

affil-num=24
en-affil=Department of Nephrology and Rheumatology, Kyorin University School of Medicine
kn-affil=

affil-num=25
en-affil=Inflammation and Immunology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=26
en-affil=Graduate School of Medical Sciences, Nagoya City University
kn-affil=

affil-num=27
en-affil=Department of Orthopedic Surgery, National Hospital Organization Nagoya Medical Center
kn-affil=

affil-num=28
en-affil=Department of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=29
en-affil=Division of Rheumatology, Department of Internal Medicine, Toho University School of Medicine
kn-affil=

affil-num=30
en-affil=Division of Rheumatology, Department of Internal Medicine, School of Medicine, Tokyo Women's Medical University
kn-affil=

affil-num=31
en-affil=Division of Rheumatology, Department of Medicine, Showa University School of Medicine
kn-affil=

affil-num=32
en-affil=Division of Rheumatology, Department of Medicine, Showa University School of Medicine
kn-affil=

affil-num=33
en-affil=Inflammation and Immunology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=34
en-affil=Division of Rheumatology, Department of Internal Medicine, School of Medicine, Tokyo Women's Medical University
kn-affil=
en-keyword=Clinical practice guidelines
kn-keyword=Clinical practice guidelines
en-keyword=baricitinib
kn-keyword=baricitinib
en-keyword=GRADE (Grading of Recommendations, Assessment, Development, and Evaluation)
kn-keyword=GRADE (Grading of Recommendations, Assessment, Development, and Evaluation)
en-keyword=juvenile idiopathic arthritis
kn-keyword=juvenile idiopathic arthritis
en-keyword=systematic review
kn-keyword=systematic review
END

start-ver=1.4
cd-journal=joma
no-vol=329
cd-vols=
no-issue=1
article-no=
start-page=L183
end-page=L196
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250701
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Activated factor X inhibition ameliorates NF-κB-IL-6-mediated perivascular inflammation and pulmonary hypertension
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Activated factor X (FXa) induces inflammatory response and cell proliferation in various cell types via activation of proteinase-activated receptor-1 (PAR1) and/or PAR2. We thus aimed to investigate the impact of FXa on the development of pulmonary arterial hypertension (PAH) and the mechanisms involved. The effects of edoxaban, a selective FXa inhibitor, on hemodynamic, right ventricular (RV) hypertrophy, and vascular remodeling were evaluated in a monocrotaline (MCT)-exposed pulmonary hypertension (PH) rat model. At 21 days after a single subcutaneous injection of MCT of 60 mg/kg, right ventricular systolic pressure (RVSP) and total pulmonary vascular resistance index (TPRI) were elevated concomitant with the increased plasma FXa and lung interleukin-6 (IL-6) mRNA. Daily administration of edoxaban (10 mg/kg/day, by gavage) starting from the day of MCT injection for 21 days ameliorated RVSP, TPRI, RV hypertrophy, pulmonary vascular remodeling, and macrophage accumulation. Edoxaban reduced nuclear factor-kappa B (NF-κB) activity and IL-6 mRNA level in the lungs of MCT-exposed rats. mRNA levels of FXa, PAR1, and PAR2 in cultured pulmonary arterial smooth muscle cells (PASMCs) isolated from patients with PAH were higher than those seen in normal PASMCs. FXa stimulation increased cell proliferation and mRNA level of IL-6 in normal PASMCs, both of which were blunted by edoxaban and PAR1 antagonist. Moreover, FXa stimulation activated extracellularly regulated kinases 1/2 in a PAR1-dependent manner. Inhibition of FXa ameliorates NF-κB-IL-6-mediated perivascular inflammation, pulmonary vascular remodeling, and the development of PH in MCT-exposed rats, suggesting that FXa may be a potential target for the treatment of PAH.<br>
NEW & NOTEWORTHY This study demonstrated that chronic treatment with activated factor X (FXa) inhibitor ameliorated NF-κB-IL-6-mediated perivascular inflammation in a rat model with pulmonary arterial hypertension, which is associated with elevated FXa activity. FXa may act on pulmonary arterial smooth muscle cells, inducing cell proliferation and inflammatory response via upregulated PAR1, thereby contributing to pulmonary vascular remodeling. Understanding the patient-specific pathophysiology is a prerequisite for applying FXa-targeted therapy to the treatment of pulmonary arterial hypertension.
en-copyright=
kn-copyright=

en-aut-name=ImakiireSatomi
en-aut-sei=Imakiire
en-aut-mei=Satomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KimuroKeiji
en-aut-sei=Kimuro
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YoshidaKeimei
en-aut-sei=Yoshida
en-aut-mei=Keimei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MasakiKohei
en-aut-sei=Masaki
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IzumiRyo
en-aut-sei=Izumi
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ImabayashiMisaki
en-aut-sei=Imabayashi
en-aut-mei=Misaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=WatanabeTakanori
en-aut-sei=Watanabe
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IshikawaTomohito
en-aut-sei=Ishikawa
en-aut-mei=Tomohito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HosokawaKazuya
en-aut-sei=Hosokawa
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MatsushimaShouji
en-aut-sei=Matsushima
en-aut-mei=Shouji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HashimotoToru
en-aut-sei=Hashimoto
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=ShinoharaKeisuke
en-aut-sei=Shinohara
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KatsukiShunsuke
en-aut-sei=Katsuki
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MatobaTetsuya
en-aut-sei=Matoba
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
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=15
ORCID=

en-aut-name=HiranoKatsuya
en-aut-sei=Hirano
en-aut-mei=Katsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=TsutsuiHiroyuki
en-aut-sei=Tsutsui
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=AbeKohtaro
en-aut-sei=Abe
en-aut-mei=Kohtaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=15
en-affil=Department of Cardiovascular Medicine, Okayama University
kn-affil=

affil-num=16
en-affil=Department of Cardiovascular Physiology, Faculty of Medicine, Kagawa University
kn-affil=

affil-num=17
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=

affil-num=18
en-affil=Department of Cardiovascular Medicine, Faculty of Medical Sciences, Kyushu University
kn-affil=
en-keyword=factor Xa
kn-keyword=factor Xa
en-keyword=IL-6
kn-keyword=IL-6
en-keyword=proteinase-activated receptor
kn-keyword=proteinase-activated receptor
en-keyword=pulmonary arterial hypertension
kn-keyword=pulmonary arterial hypertension
en-keyword=pulmonary hypertension
kn-keyword=pulmonary hypertension
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=2025
dt-pub=20250802
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Berberine Prevents NSAID-Induced Small Intestinal Injury by Protecting Intestinal Barrier and Inhibiting Inflammasome-Associated Activation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Nonsteroidal anti-inflammatory drugs (NSAID), which are commonly used to manage pain and inflammation, often cause gastrointestinal injuries, including small intestinal damage. Berberine (BBR) is a traditional Chinese medicine that protects against these injuries. However, the mechanism of action is not fully understood.<br>
Aims This study aimed to evaluate the protective effects of BBR against NSAID-induced intestinal injury and elucidate the underlying molecular mechanisms.<br>
Methods We evaluated the effects of BBR on NSAID-induced intestinal injury using a combination of mouse models and human gut organoids. Mice were treated with indomethacin with or without BBR to induce small intestinal injury. Human gut organoids were exposed to NSAID, with or without BBR, to assess their direct epithelial effects. Histological analyses, cytokine measurements, and Western blotting were performed to evaluate intestinal damage, tight junction integrity, and inflammasome-associated activation.<br>
Results In NSAID-treated mice, BBR markedly reduced ulcers and adhesions and preserved ileal Claudin-1, Occludin, and Zonula Occludens-1 (ZO-1) levels. BBR inhibited both NOD-like receptor family pyrin domain-containing 6 and NOD-like receptor family caspase recruitment domain?containing protein 4 inflammasome activation, reducing Caspase-1 maturation and downstream interleukin-1β and tumor necrosis factor-α release. In human gut organoids, BBR demonstrated comparable protective effects by directly mitigating NSAID-induced epithelial barrier disruption caused by Claudin-1 and Occludin downregulation, although it did not restore ZO-1 expression.<br>
Conclusions BBR effectively prevented NSAID-induced small intestinal injury by maintaining tight junction integrity and inhibiting inflammasome-associated activation, indicating its potential as a therapeutic agent against such damage.
en-copyright=
kn-copyright=

en-aut-name=IshiguroMikako
en-aut-sei=Ishiguro
en-aut-mei=Mikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakaharaMasahiro
en-aut-sei=Takahara
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakakiAkinobu
en-aut-sei=Takaki
en-aut-mei=Akinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HiraokaSakiko
en-aut-sei=Hiraoka
en-aut-mei=Sakiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ToyosawaJyunki
en-aut-sei=Toyosawa
en-aut-mei=Jyunki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AoyamaYuki
en-aut-sei=Aoyama
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IgawaShoko
en-aut-sei=Igawa
en-aut-mei=Shoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamasakiYasushi
en-aut-sei=Yamasaki
en-aut-mei=Yasushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=InokuchiToshihiro
en-aut-sei=Inokuchi
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KinugasaHideaki
en-aut-sei=Kinugasa
en-aut-mei=Hideaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OtsukaMotoyuki
en-aut-sei=Otsuka
en-aut-mei=Motoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

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

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

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

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

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

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

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

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

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

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

affil-num=11
en-affil=Department of Gastroenterology and Hepatology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=
en-keyword=Nonsteroidal anti-inflammatory drugs-induced small intestinal injury
kn-keyword=Nonsteroidal anti-inflammatory drugs-induced small intestinal injury
en-keyword=Berberine
kn-keyword=Berberine
en-keyword=Tight junction protein
kn-keyword=Tight junction protein
en-keyword=Inflammasomes
kn-keyword=Inflammasomes
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=6
article-no=
start-page=e00110-25
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250519
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mycobacterium tuberculosis bacillus induces pyroptosis in human lung fibroblasts
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We previously reported that live, but not dead, virulent Mycobacterium tuberculosis (Mtb) H37Rv bacilli induce cell death in human lung fibroblast cell lines, MRC-5, MRC-9, and TIG-1. Here, using two distinct Mtb strains from two different lineages (HN878 lineage 2 and H37Rv lineage 4), we confirmed cell death at day 2 after infection with a device that measures cell growth/cytotoxicity in real time (Maestro-Z [AXION]). Mtb bacilli uptake by the fibroblast was confirmed with a transmission electron microscope on day 2. Expressions of inflammatory cytokines and interleukin (IL)?1β, IL-6, and IL-8 were observed when exposed to live, but not dead bacteria. The cell death of fibroblasts induced by both Mtb strains tested was prevented by caspase-1/4 and NLRP3 inflammasome inhibitors, but not by caspase-3 and caspase-9 inhibitors. Therefore, we classified the fibroblast cell death by Mtb infection as pyroptosis. To investigate the biological and pathological relevance of fibroblast cell death by Mtb infection, we performed dual RNA-Seq analysis on Mtb within fibroblasts and Mtb-infected fibroblasts at day 2. In Mtb bacilli tcrR, secE2, ahpD, and mazF8 genes were highly induced during infection. These genes play roles in survival in a hypoxic environment, production of a calcium-binding protein-inducing cytokine, and regulation of transcription in a toxin-antitoxin system. The gene expressions of IL-1β, IL-6, and IL-8, caspase-4, and NLRP3, but not of caspase-3 and caspase-9, were augmented in Mtb bacilli-infected fibroblasts. Taken together, our study suggests that Mtb bacilli attempt to survive in lung fibroblasts and that pyroptosis of the host fibroblasts activates the immune system against the infection.
en-copyright=
kn-copyright=

en-aut-name=TakiiTakemasa
en-aut-sei=Takii
en-aut-mei=Takemasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamadaHiroyuki
en-aut-sei=Yamada
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MotozonoChihiro
en-aut-sei=Motozono
en-aut-mei=Chihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamasakiSho
en-aut-sei=Yamasaki
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TorrellesJordi B.
en-aut-sei=Torrelles
en-aut-mei=Jordi B.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TurnerJoanne
en-aut-sei=Turner
en-aut-mei=Joanne
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KimishimaAoi
en-aut-sei=Kimishima
en-aut-mei=Aoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AsamiYukihiro
en-aut-sei=Asami
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OharaNaoya
en-aut-sei=Ohara
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HidaShigeaki
en-aut-sei=Hida
en-aut-mei=Shigeaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HayashiHidetoshi
en-aut-sei=Hayashi
en-aut-mei=Hidetoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OnozakiKikuo
en-aut-sei=Onozaki
en-aut-mei=Kikuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Mycobacterium Reference and Research, the Research Institute of Tuberculosis, Japan Anti-Tuberculosis Association
kn-affil=

affil-num=2
en-affil=Department of Mycobacterium Reference and Research, the Research Institute of Tuberculosis, Japan Anti-Tuberculosis Association
kn-affil=

affil-num=3
en-affil=Department of Molecular Immunology, Research Institute for Microbial Diseases, The University of Osaka
kn-affil=

affil-num=4
en-affil=Department of Molecular Immunology, Research Institute for Microbial Diseases, The University of Osaka
kn-affil=

affil-num=5
en-affil=Texas Biomedical Research Institute and International Center for the Advancement of Research & Education (I?CARE)
kn-affil=

affil-num=6
en-affil=Texas Biomedical Research Institute and International Center for the Advancement of Research & Education (I?CARE)
kn-affil=

affil-num=7
en-affil=Laboratory of Applied Microbial Chemistry, ?mura Satoshi Memorial Institute, Kitasato University
kn-affil=

affil-num=8
en-affil=Laboratory of Applied Microbial Chemistry, ?mura Satoshi Memorial Institute, Kitasato University
kn-affil=

affil-num=9
en-affil=Department of Oral Microbiology, Graduate School of Medicine, Density and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Hygienic Chemistry, Graduate School of Pharmaceutical Sciences, Nagoya City University
kn-affil=

affil-num=11
en-affil=Department of Cell Signaling, Graduate School of Pharmaceutical Sciences, Nagoya City University
kn-affil=

affil-num=12
en-affil=Department of Hygienic Chemistry, Graduate School of Pharmaceutical Sciences, Nagoya City University
kn-affil=
en-keyword=Mycobacterium tuberculosis
kn-keyword=Mycobacterium tuberculosis
en-keyword=pyroptosis
kn-keyword=pyroptosis
en-keyword=caspase
kn-keyword=caspase
en-keyword=RNA-Seq
kn-keyword=RNA-Seq
en-keyword=cytokine
kn-keyword=cytokine
en-keyword=fibroblasts
kn-keyword=fibroblasts
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=1
article-no=
start-page=158
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250719
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Oncolytic virus-mediated p53 activation boosts the antitumor immunity of a p53-transduced dendritic cell vaccine
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Dendritic cells (DCs) transduced with replication-deficient, wild-type human p53-expressing adenovirus Ad-p53 (Ad-p53 DCs) induce p53-targeting cytotoxic T lymphocytes (CTLs). However, the antitumor efficacy of Ad-p53 DCs is diminished by weak p53 immunogenicity in tumor cells and poor immune responses. We developed a p53-armed oncolytic adenovirus, OBP-702, to induce tumor-specific p53 expression and antitumor immune response, suggesting a role for OBP-702 in enhancing the antitumor efficacy of Ad-p53 DCs. The combined effect of Ad-p53 DCs and OBP-702 was investigated using murine colon cancer (CC) tumor models. Ad-p53 DCs were obtained by stimulating bone marrow-derived cells with granulocyte-macrophage colony-stimulating factor, interleukin-4, and Ad-p53. Subcutaneous tumor models of CT26 (p53 wild-type) and MC38 (p53 mutant-type) murine CC cell lines were used to evaluate the therapeutic potential of combination therapy in the terms of tumor growth, abscopal effect, antitumor immune response, and presentation of p53 peptides in tumor cells. Combination therapy with Ad-p53 DCs and OBP-702 significantly suppressed the growth of p53-intact CT26 tumors at treated and untreated sites by inducing tumor-infiltration of CD8+ CTLs and CD11c+ DCs. OBP-702-infected tumor cells presented human p53 epitopes in the context of major histocompatibility complex molecules, which were recognized by CTLs induced by Ad-p53 DCs. Combination therapy significantly suppressed the growth of p53-mutant MC38 tumors by activating the antitumor immune response. Our results suggest that OBP-702-mediated presentation of p53 epitopes on tumor cells enhances the antitumor efficacy of Ad-p53 DCs against murine CC tumors by attracting p53-targeting CTLs.
en-copyright=
kn-copyright=

en-aut-name=YamadaMotohiko
en-aut-sei=Yamada
en-aut-mei=Motohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TazawaHiroshi
en-aut-sei=Tazawa
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SuemoriKanto
en-aut-sei=Suemori
en-aut-mei=Kanto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OkadaNaohiro
en-aut-sei=Okada
en-aut-mei=Naohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KajiwaraYoshinori
en-aut-sei=Kajiwara
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShojiRyohei
en-aut-sei=Shoji
en-aut-mei=Ryohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NagaiYasuo
en-aut-sei=Nagai
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=InoueHiroaki
en-aut-sei=Inoue
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HashimotoNaoyuki
en-aut-sei=Hashimoto
en-aut-mei=Naoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KanayaNobuhiko
en-aut-sei=Kanaya
en-aut-mei=Nobuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KikuchiSatoru
en-aut-sei=Kikuchi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KurodaShinji
en-aut-sei=Kuroda
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MichiueHiroyuki
en-aut-sei=Michiue
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=UrataYasuo
en-aut-sei=Urata
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=KagawaShunsuke
en-aut-sei=Kagawa
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=FujiwaraToshiyoshi
en-aut-sei=Fujiwara
en-aut-mei=Toshiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

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

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

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

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

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

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

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

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

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

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

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

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

affil-num=13
en-affil=Neutron Therapy Research Center, Okayama University Hospital
kn-affil=

affil-num=14
en-affil=Oncolys BioPharma, Inc
kn-affil=

affil-num=15
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=7
article-no=
start-page=808
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Carnosol, a Rosemary Ingredient Discovered in a Screen for Inhibitors of SARM1-NAD+ Cleavage Activity, Ameliorates Symptoms of Peripheral Neuropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sterile alpha and Toll/interleukin receptor motif-containing protein 1 (SARM1) is a nicotinamide adenine dinucleotide (NAD+) hydrolase involved in axonal degeneration and neuronal cell death. SARM1 plays a pivotal role in triggering the neurodegenerative processes that underlie peripheral neuropathies, traumatic brain injury, and neurodegenerative diseases. Importantly, SARM1 knockdown or knockout prevents the degeneration; as a result, SARM1 has been attracting attention as a potent therapeutic target. In recent years, the development of several SARM1 inhibitors derived from synthetic chemical compounds has been reported; however, no dietary ingredients with SARM1 inhibitory activity have been identified. Therefore, we here focused on dietary ingredients and found that carnosol, an antioxidant contained in rosemary, inhibits the NAD+-cleavage activity of SARM1. Purified carnosol inhibited the enzymatic activity of SARM1 and suppressed neurite degeneration and cell death induced by the anti-cancer medicine vincristine (VCR). Carnosol also inhibited VCR-induced hyperalgesia symptoms, suppressed the loss of intra-epidermal nerve fibers in vivo, and reduced the blood fluid level of phosphorylated neurofilament-H caused by an axonal degeneration event. These results indicate that carnosol has a neuroprotective effect via SARM1 inhibition in addition to its previously known antioxidant effect via NF-E2-related factor 2 and thus suppresses neurotoxin-induced peripheral neuropathy.
en-copyright=
kn-copyright=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OgawaKazuki
en-aut-sei=Ogawa
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YasuiYu
en-aut-sei=Yasui
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OchiToshiki
en-aut-sei=Ochi
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamamotoKen-Ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WadaYoji
en-aut-sei=Wada
en-aut-mei=Yoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakamuraHiromichi
en-aut-sei=Nakamura
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NishiboriMasahiro
en-aut-sei=Nishibori
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

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

affil-num=2
en-affil=Tama Biochemical Co., Ltd.
kn-affil=

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

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

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

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

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

affil-num=8
en-affil=Tama Biochemical Co., Ltd.
kn-affil=

affil-num=9
en-affil=Tama Biochemical Co., Ltd.
kn-affil=

affil-num=10
en-affil=Department of Translational Research and Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=SARM1
kn-keyword=SARM1
en-keyword=carnosol
kn-keyword=carnosol
en-keyword=NAD+
kn-keyword=NAD+
en-keyword=axon degeneration
kn-keyword=axon degeneration
en-keyword=peripheral neuropathy
kn-keyword=peripheral neuropathy
END

start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=1
article-no=
start-page=e000923
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250427
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Reversible cerebral vasoconstriction syndrome in idiopathic multicentric Castleman disease under treatment with tocilizumab
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Idiopathic multicentric Castleman disease (iMCD) is a rare polyclonal lymphoproliferative disorder characterised by systemic inflammation resulting from overproduction of interleukin 6 (IL-6). While iMCD primarily affects the lymph nodes and related tissues, it can also rarely involve the central nervous system.<br>
Case presentation We report the case of a 58-year-old female patient with at least a 3-year history of iMCD, who experienced acute thunderclap headaches due to reversible cerebral vasoconstriction syndrome (RCVS). RCVS occurred 3?months after initiating treatment with tocilizumab, a humanised anti-IL-6 receptor monoclonal antibody, and was accompanied by focal cortical subarachnoid haemorrhage (SAH). Elevated IL-6 levels were found in both serum and cerebrospinal fluid. MR angiography revealed multiple diffuse stenotic lesions in the bilateral middle and posterior cerebral arteries, which, along with bilateral cerebral oedema, resolved within 3?months. The diffuse nature of the cerebral vasospasm and the presence of bilateral brain oedema suggested that cerebral vasospasm was due to RCVS rather than SAH.<br>
Conclusions In patients with Castleman disease, RCVS may occur due to IL-6-dependent chronic cerebral vascular inflammation, either as a primary condition or as a complication of tocilizumab treatment.
en-copyright=
kn-copyright=

en-aut-name=KamimuraNaoya
en-aut-sei=Kamimura
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UedaNaohisa
en-aut-sei=Ueda
en-aut-mei=Naohisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KimuraKatsuo
en-aut-sei=Kimura
en-aut-mei=Katsuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NishikoriAsami
en-aut-sei=Nishikori
en-aut-mei=Asami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SatoYasuharu
en-aut-sei=Sato
en-aut-mei=Yasuharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KishidaHitaru
en-aut-sei=Kishida
en-aut-mei=Hitaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TanakaFumiaki
en-aut-sei=Tanaka
en-aut-mei=Fumiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Neurology, Yokohama City University Medical Center
kn-affil=

affil-num=2
en-affil=Department of Neurology, Yokohama City University Medical Center
kn-affil=

affil-num=3
en-affil=Department of Neurology, Yokohama City University Medical Center
kn-affil=

affil-num=4
en-affil=
kn-affil=

affil-num=5
en-affil=
kn-affil=

affil-num=6
en-affil=Department of Neurology, Yokohama City University Medical Center
kn-affil=

affil-num=7
en-affil=Department of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine
kn-affil=
END

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

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

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

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

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

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

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

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

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

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

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

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

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

affil-num=3
en-affil=Department of Internal Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-N?rnberg (FAU) and Universit?tsklinikum Erlangen
kn-affil=

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

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

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

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

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

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

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

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=
article-no=
start-page=1547222
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250311
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Interleukin-6/soluble IL-6 receptor-induced secretion of cathepsin B and L from human gingival fibroblasts is regulated by caveolin-1 and ERK1/2 pathways
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aims: Cathepsins are essential lysosomal enzymes that maintain organismal homeostasis by degrading extracellular substrates. The inflammatory cytokine interleukin-6 (IL-6) increases the production of cathepsins through the caveolin-1 (Cav-1) and c-Jun N-terminal kinase (JNK) signaling pathways, which have been implicated in the destruction of periodontal tissue. This study investigated the effect of the IL-6/soluble IL-6 receptor (sIL-6R) complex on the extracellular secretion of cathepsins in human gingival fibroblasts (HGFs) and examined the function of extracellularly secreted cathepsins B and L under acidic culture conditions in vitro.<br>
Methods: HGFs were isolated from healthy volunteer donors. The expression of Cav-1 was suppressed via transfection with small interfering RNA (siRNA) targeting Cav-1. The expression levels of cathepsins B and L induced by extracellular IL-6/sIL-6R were measured using western blotting and enzyme-linked immunosorbent assay. Extracellular cathepsin activity following IL-6/sIL-6R stimulation was assessed using a methylcoumarylamide substrate in a fluorescence-based assay. IL-6/sIL-6R-induced expression of cathepsins B and L in HGFs was quantified under inhibitory conditions for extracellular signal-regulated kinase (ERK) 1/2 and/or JNK signaling, both of which are transduction pathways activated by IL-6/sIL-6R. This quantification was also performed in HGFs with suppressed Cav-1 expression using western blotting.<br>
Results: Cathepsins B and L were secreted in their precursor forms from HGFs, with significantly elevated protein levels observed at 24, 48, and 72 h post-IL-6/sIL-6R stimulation. Under acidic culture conditions, cathepsin B activity increased at 48 and 72 h. Cav-1 suppression inhibited the secretion of cathepsin B regardless of IL-6/sIL-6R stimulation, whereas the secretion of cathepsin L was reduced only after 48 h of IL-6/sIL-6R stimulation. Inhibition of ERK1/2 and JNK pathways decreased the secretion of cathepsin B after 48 h of IL-6/sIL-6R stimulation, and JNK inhibition reduced the secretion of cathepsin L under similar conditions.<br>
Conclusion: IL-6/sIL-6R stimulation increased the extracellular secretion of cathepsin B and L precursors in HGFs, and these precursors became activated under acidic conditions. Cav-1 and ERK1/2 are involved in regulating the secretion of cathepsin B precursors.
en-copyright=
kn-copyright=

en-aut-name=GotoAyaka
en-aut-sei=Goto
en-aut-mei=Ayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OmoriKazuhiro
en-aut-sei=Omori
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Yamaguchi-TomikawaTomoko
en-aut-sei=Yamaguchi-Tomikawa
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KobayashiHiroya
en-aut-sei=Kobayashi
en-aut-mei=Hiroya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=Shinoda-ItoYuki
en-aut-sei=Shinoda-Ito
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HiraiKimito
en-aut-sei=Hirai
en-aut-mei=Kimito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IkedaAtsushi
en-aut-sei=Ikeda
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakashibaShogo
en-aut-sei=Takashiba
en-aut-mei=Shogo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

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

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

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

affil-num=7
en-affil=Department of Periodontics & Endodontics, Division of Dentistry, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=cathepsin B
kn-keyword=cathepsin B
en-keyword=cathepsin L
kn-keyword=cathepsin L
en-keyword=human gingival fibroblast
kn-keyword=human gingival fibroblast
en-keyword=interleukin-6
kn-keyword=interleukin-6
en-keyword=caveolin
kn-keyword=caveolin
END

start-ver=1.4
cd-journal=joma
no-vol=17
cd-vols=
no-issue=3
article-no=
start-page=e81476
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250330
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Natural Course From Primary Intraocular Lymphoma to Brain Lymphoma in Four Years According to Patient's Choice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Primary intraocular lymphoma or vitreoretinal lymphoma is a rare entity of diffuse large B-cell lymphoma that presents vitreous opacity and retinal and choroidal infiltration. Primary central nervous system lymphoma would occur previously, later, or concurrently with respect to primary intraocular lymphoma. This study reported a 72-year-old patient with a pathological diagnosis of primary intraocular lymphoma who developed central nervous system lymphoma four years later in the course of no treatment. She presented with a four-year history of blurred vision in both eyes after cataract surgeries. Three weeks previously, she underwent a vitrectomy in the left eye at a clinic, and measurements of the vitreous fluid showed a high level of interleukin-10 at 5739 pg/mL, in contrast with interleukin-6 at 142 pg/mL. Cytology of the vitreous fluid was class III on the Papanicolaou classification. Head magnetic resonance imaging detected nothing abnormal. She underwent vitrectomy in the right eye as a diagnostic procedure to show large cells in the vitreous which were positive for CD20 and Ki-67 and negative for CD3, leading to a pathological diagnosis of large B-cell lymphoma. Prophylactic chemotherapy with high-dose methotrexate was recommended as a therapeutic option, but she chose observation since she did not have any eye or systemic symptoms. In the follow-up every three months by an oncologist and an ophthalmologist, she did not have any symptoms, and serum levels of soluble interleukin-2 receptor were in the normal range at each visit. She was well for four years until the age of 76 years when she fell and hit her head, and an emergency head computed tomography scan showed a mass in the left occipital lobe. Magnetic resonance imaging demonstrated a well-defined circular mass in the left occipital lobe with a hyperintense signal in the T2-weighted fluid-attenuated inversion recovery (FLAIR) image and diffusion-weighted image. Fluorodeoxyglucose positron emission tomography showed no abnormal uptake systemically, except for the left occipital lesion. She underwent a brain biopsy by craniotomy to pathologically prove diffuse large B-cell lymphoma. She was recommended to receive first-line chemotherapy as the standard treatment but chose observation with no treatment and died of brain lymphoma nine months later. This case happened to illustrate a natural course of primary intraocular lymphoma which proceeded to central nervous system lymphoma four years later.
en-copyright=
kn-copyright=

en-aut-name=MatsuoToshihiko
en-aut-sei=Matsuo
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanakaTakehiro
en-aut-sei=Tanaka
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IshidaJoji
en-aut-sei=Ishida
en-aut-mei=Joji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoShotaro
en-aut-sei=Kondo
en-aut-mei=Shotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MatsuokaKen-ichi
en-aut-sei=Matsuoka
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Ophthalmology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

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

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

affil-num=4
en-affil=Department of Internal Medicine, Kurashiki Municipal Hospital
kn-affil=

affil-num=5
en-affil=Department of Hematology and Oncology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=brain biopsy
kn-keyword=brain biopsy
en-keyword=cell block pathology
kn-keyword=cell block pathology
en-keyword=diffuse large b-cell lymphoma
kn-keyword=diffuse large b-cell lymphoma
en-keyword=natural course
kn-keyword=natural course
en-keyword=primary central nervous system lymphoma
kn-keyword=primary central nervous system lymphoma
en-keyword=primary intraocular (vitreoretinal) lymphoma
kn-keyword=primary intraocular (vitreoretinal) lymphoma
en-keyword=vitrectomy
kn-keyword=vitrectomy
en-keyword=vitreous opacity
kn-keyword=vitreous opacity
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=5
article-no=
start-page=577
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250306
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Efficacy of Oral Intake of Hydrogen-Rich Jelly Intake on Gingival Inflammation: A Double-Blind, Placebo-Controlled and Exploratory Randomized Clinical Trial
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/Objectives: Initiation and progression of periodontal disease include oxidative stress. Systemic application of antioxidants may provide clinical benefits against periodontal disease including gingivitis. Recently, a jelly containing a high concentration of hydrogen (40 ppm) was developed. We hypothesized that oral intake of this hydrogen-rich jelly may be safe and effective on gingivitis. This clinical trial was designed to investigate the safety and efficacy of oral intake of hydrogen-rich jelly against gingival inflammation. Methods: Participants with gingivitis were instructed to orally ingest 30 g of hydrogen-rich jelly (experimental group) or placebo jelly (control group) three times a day for 14 consecutive days. The primary outcome of this trial was the percentage of bleeding on probing (BOP) sites. Secondary outcomes were oral parameters, serum reactive oxygen metabolites, antioxidant capacity, oxidative index, concentrations of cytokine (interleukin [IL]-1β, IL-6, IL-10, IL-17, and tumor necrosis factor-alpha) in gingival crevicular fluid, and adverse events. For all parameters, Mann?Whitney U test was used for comparison between experimental and control groups. Analysis of covariance, controlling for baseline periodontal inflamed surface area, was performed to evaluate the association between the effect of the hydrogen-rich jelly and gingival inflammation. Results: In the experiment and control groups, the percentage of sites with BOP and PISA significantly decreased at the end of the experiment compared to the baseline. However, no significant differences were found between groups (p > 0.05). Conclusions: Administration of hydrogen-rich jelly for 14 days decreased gingival inflammation. However, no significant differences were identified compared to the control group.
en-copyright=
kn-copyright=

en-aut-name=MaruyamaTakayuki
en-aut-sei=Maruyama
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakayamaEiji
en-aut-sei=Takayama
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TokunoShinichi
en-aut-sei=Tokuno
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MoritaManabu
en-aut-sei=Morita
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=EkuniDaisuke
en-aut-sei=Ekuni
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Preventive Dentistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Oral Biochemistry, Asahi University School of Dentistry
kn-affil=

affil-num=3
en-affil=Graduate School of Health Innovation, Kanagawa University of Human Services
kn-affil=

affil-num=4
en-affil=Department of Oral Health, Takarazuka University of Medical and Health Care
kn-affil=

affil-num=5
en-affil=Department of Preventive Dentistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=periodontal disease
kn-keyword=periodontal disease
en-keyword=oxidative stress
kn-keyword=oxidative stress
en-keyword=hydrogen
kn-keyword=hydrogen
en-keyword=randomized controlled trial
kn-keyword=randomized controlled trial
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=2025
dt-pub=20250224
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A randomized controlled trial of conventional GVHD prophylaxis with or without teprenone for the prevention of severe acute GVHD
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Therapies that effectively suppress graft-versus-host disease (GVHD) without compromising graft-versus-leukemia/lymphoma (GVL) effects is important in allogeneic hematopoietic stem cell transplantation (allo-HSCT) for hematopoietic malignancies. Geranylgeranylacetone (GGA) is a main component of teprenone, a gastric mucosal protectant commonly used in clinical practice. In preclinical models, GGA suppresses proinflammatory cytokines, including interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α), which are associated with GVHD as well as induces thioredoxin-1 (Trx-1), which suppresses GVHD while maintaining GVL effects. Here, we investigated whether the addition of teprenone to standard GVHD prophylaxis could reduce the cumulative incidence of severe acute GVHD (aGVHD) without attenuating GVL effects. This open-label, randomized clinical trial enrolled 40 patients (21 control and 19 teprenone group) who received allo-HSCT between May 2022 and February 2023 in our institution. Patients in the teprenone group received 50 mg of teprenone orally thrice daily for 21 days from the initiation of the conditioning regimen. The cumulative incidence of severe aGVHD by day 100 after allo-HSCT was not significantly different in the two groups (27.9 vs. 16.1%, p?=?0.25). The exploratory studies revealed no obvious changes in Trx-1 levels, but the alternations from baseline in IL-1β and TNF-α levels at day 28 after allo-HSCT tended to be lower in the teprenone group. In conclusion, we could not demonstrate that teprenone significantly prevented the development of severe aGVHD. Discrepancy with preclinical model suggests that appropriate dose of teprenone may be necessary to induce the expression of antioxidant enzymes that suppress severe aGVHD. Clinical Trial Registration number:jRCTs 061210072.
en-copyright=
kn-copyright=

en-aut-name=KitamuraWataru
en-aut-sei=Kitamura
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujiiKeiko
en-aut-sei=Fujii
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TsugeMitsuru
en-aut-sei=Tsuge
en-aut-mei=Mitsuru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MitsuhashiToshiharu
en-aut-sei=Mitsuhashi
en-aut-mei=Toshiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KobayashiHiroki
en-aut-sei=Kobayashi
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KamoiChihiro
en-aut-sei=Kamoi
en-aut-mei=Chihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamamotoAkira
en-aut-sei=Yamamoto
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KondoTakumi
en-aut-sei=Kondo
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SeikeKeisuke
en-aut-sei=Seike
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=FujiwaraHideaki
en-aut-sei=Fujiwara
en-aut-mei=Hideaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=AsadaNoboru
en-aut-sei=Asada
en-aut-mei=Noboru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=EnnishiDaisuke
en-aut-sei=Ennishi
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MatsuokaKen-ichi
en-aut-sei=Matsuoka
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=FujiiNobuharu
en-aut-sei=Fujii
en-aut-mei=Nobuharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Pediatric Acute Diseases, Okayama University Academic Field of Medicine Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=12
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=13
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=14
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=15
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=
en-keyword=Allogeneic hematopoietic stem cell transplantation
kn-keyword=Allogeneic hematopoietic stem cell transplantation
en-keyword=Graft-versus-host disease
kn-keyword=Graft-versus-host disease
en-keyword=Teprenone
kn-keyword=Teprenone
en-keyword=Oxidative stress
kn-keyword=Oxidative stress
en-keyword=Interleukin-33
kn-keyword=Interleukin-33
END

start-ver=1.4
cd-journal=joma
no-vol=79
cd-vols=
no-issue=1
article-no=
start-page=51
end-page=58
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202502
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Photoinitiators Induce Histamine Production in Human Mast Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Photoinitiators are used in the manufacture of many daily products, and may produce harmful effects due to their cytotoxicity. They have also been detected in human serum. Here, we investigated the histamine-producing effects in HMC-1 cells and the inflammatory cytokine release effects in RAW264 cells for four photoinitiators: 1-hydroxycyclohexyl phenyl ketone; 2-isopropylthioxanthone; methyl 2-benzoylbenzoate; and 2-methyl-4´-(methylthio)-2-morpholinopropiophenone. All four promoted histamine production in HMC-1 cells; however, they did not significantly affect the release of inflammatory cytokines in RAW264 cells. These findings suggest that these four photoinitiators induce inflammatory cytokine-independent histamine production, potentially contributing to histamine-mediated chronic inflammation in vitro.
en-copyright=
kn-copyright=

en-aut-name=MiuraTaro
en-aut-sei=Miura
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawasakiYoichi
en-aut-sei=Kawasaki
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HamanoHirofumi
en-aut-sei=Hamano
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ZamamiYoshito
en-aut-sei=Zamami
en-aut-mei=Yoshito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SendoToshiaki
en-aut-sei=Sendo
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

affil-num=2
en-affil=Laboratory of Clinical Pharmacology and Therapeutics, Kagawa School of Pharmaceutical Sciences, Tokushima Bunri University
kn-affil=

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

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

affil-num=5
en-affil=Department of Clinical Pharmacy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=photoinitiator
kn-keyword=photoinitiator
en-keyword=ink
kn-keyword=ink
en-keyword=injection
kn-keyword=injection
en-keyword=histamine
kn-keyword=histamine
en-keyword=inflammation
kn-keyword=inflammation
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=3267
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250125
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Novel treatment strategy targeting interleukin-6 induced by cancer associated fibroblasts for peritoneal metastasis of gastric cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cancer-associated fibroblasts (CAFs) are a crucial component in the tumor microenvironment (TME) of peritoneal metastasis (PM), where they contribute to tumor progression and metastasis via secretion of interleukin-6 (IL-6). Here, we investigated the role of IL-6 in PM of gastric cancer (GC) and assessed whether anti-IL-6 receptor antibody (anti-IL-6R Ab) could inhibit PM of GC. We conducted immunohistochemical analysis of IL-6 and alpha-smooth muscle (alpha-SMA) expressions in clinical samples of GC and PM, and investigated the interactions between CAFs and GC cells in vitro. Anti-tumor effects of anti-IL-6R Ab on PM of GC were investigated in an orthotopic murine PM model. IL-6 expression was significantly correlated with alpha-SMA expression in clinical samples of GC, and higher IL-6 expression in the primary tumor was associated with poor prognosis of GC. Higher IL-6 and alpha-SMA expressions were also observed in PM of GC. In vitro, differentiation of fibroblasts into CAFs and chemoresistance were observed in GC cells cocultured with fibroblasts. Anti-IL-6R Ab inhibited the progression of PM in GC cells cocultured with fibroblasts in the orthotopic mouse model but could not inhibit the progression of PM consisting of GC cells alone. IL-6 expression in the TME was associated with poor prognosis of GC, and CAFs were associated with establishment and progression of PM via IL-6. Anti-IL-6R Ab could inhibit PM of GC by the blockade of IL-6 secreted by CAFs, which suggests its therapeutic potential for PM of GC.
en-copyright=
kn-copyright=

en-aut-name=MitsuiEma
en-aut-sei=Mitsui
en-aut-mei=Ema
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KikuchiSatoru
en-aut-sei=Kikuchi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OkuraTomohiro
en-aut-sei=Okura
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TazawaHiroshi
en-aut-sei=Tazawa
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UneYuta
en-aut-sei=Une
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NishiwakiNoriyuki
en-aut-sei=Nishiwaki
en-aut-mei=Noriyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KurodaShinji
en-aut-sei=Kuroda
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NomaKazuhiro
en-aut-sei=Noma
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KagawaShunsuke
en-aut-sei=Kagawa
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OharaToshiaki
en-aut-sei=Ohara
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OhtsukaJunko
en-aut-sei=Ohtsuka
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OhkiRieko
en-aut-sei=Ohki
en-aut-mei=Rieko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=FujiwaraToshiyoshi
en-aut-sei=Fujiwara
en-aut-mei=Toshiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

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

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

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

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

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

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

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

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

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

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

affil-num=11
en-affil=Laboratory of Fundamental Oncology, National Cancer Center Research Institute
kn-affil=

affil-num=12
en-affil=Laboratory of Fundamental Oncology, National Cancer Center Research Institute
kn-affil=

affil-num=13
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Peritoneal metastasis
kn-keyword=Peritoneal metastasis
en-keyword=Gastric cancer
kn-keyword=Gastric cancer
en-keyword=Interleukin-6
kn-keyword=Interleukin-6
en-keyword=Cancer-associated fibroblasts
kn-keyword=Cancer-associated fibroblasts
en-keyword=Interleukin-6 receptor antibody
kn-keyword=Interleukin-6 receptor antibody
END

start-ver=1.4
cd-journal=joma
no-vol=31
cd-vols=
no-issue=1
article-no=
start-page=102494
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202501
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cryptococcal prostatitis in an immunocompromised patient with tocilizumab and glucocorticoid therapy: A case report
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cryptococcus prostatitis is an uncommon manifestation of cryptococcal infection that occurs mostly in immunocompromised patients. Tocilizumab, an anti-interleukin-6 receptor monoclonal antibody, has been associated with an increased risk of cryptococcal infections. However, there have been no documented cases of cryptococcal prostatitis in patients receiving tocilizumab therapy. We report a case of cryptococcal prostatitis in a 72-year-old man treated with glucocorticoids and tocilizumab for giant cell arteritis and granulomatosis with polyangiitis. The patient presented dysuria and his serum level of prostate-specific antigen was elevated. Magnetic resonance imaging revealed a prostate mass, and a prostate biopsy was performed, leading to a pathologic diagnosis of cryptococcal prostatitis. Fungal cultures for blood and urine were negative, while the cryptococcal antigen for both serum and urine showed positive results. There were no particular findings in the pulmonary and central nervous systems. The patient was successfully treated with oral fluconazole (400 mg/day) and was discharged. Although cryptococcal prostatitis is a rare entity, clinicians should note that an immunosuppressed patient may develop such a difficult-to-diagnose disease.

en-copyright=
kn-copyright=

en-aut-name=OguniKohei
en-aut-sei=Oguni
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FukushimaShinnosuke
en-aut-sei=Fukushima
en-aut-mei=Shinnosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HagiyaHideharu
en-aut-sei=Hagiya
en-aut-mei=Hideharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KatoAtsushi
en-aut-sei=Kato
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SuyamaAtsuhito
en-aut-sei=Suyama
en-aut-mei=Atsuhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IwataTakehiro
en-aut-sei=Iwata
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MiyawakiYoshia
en-aut-sei=Miyawaki
en-aut-mei=Yoshia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OnoSawako
en-aut-sei=Ono
en-aut-mei=Sawako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IioKoji
en-aut-sei=Iio
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
ORCID=

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

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

affil-num=3
en-affil=Department of Infectious Diseases, Okayama University Hospital
kn-affil=

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

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

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

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

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

affil-num=9
en-affil=Microbiology Division, Clinical Laboratory, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Cryptococcosis
kn-keyword=Cryptococcosis
en-keyword=Fluconazole
kn-keyword=Fluconazole
en-keyword=Glucocorticoids
kn-keyword=Glucocorticoids
en-keyword=Prostatitis
kn-keyword=Prostatitis
en-keyword=Tocilizumab
kn-keyword=Tocilizumab
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=22
article-no=
start-page=11942
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241106
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Distribution and Incorporation of Extracellular Vesicles into Chondrocytes and Synoviocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Osteoarthritis (OA) is a chronic disease affecting over 500 million people worldwide. As the population ages and obesity rates rise, the societal burden of OA is increasing. Pro-inflammatory cytokines, particularly interleukin-1β, are implicated in the pathogenesis of OA. Recent studies suggest that crosstalk between cartilage and synovium contributes to OA development, but the mechanisms remain unclear. Extracellular vesicles (EVs) were purified from cell culture-conditioned medium via ultracentrifugation and confirmed using transmission electron microscopy, nanoparticle tracking analysis, and western blotting. We demonstrated that EVs were taken up by human synoviocytes and chondrocytes in vitro, while in vivo experiments revealed that fluorescent-labelled EVs injected into mouse joints were incorporated into chondrocytes and synoviocytes. EV uptake was significantly inhibited by dynamin-mediated endocytosis inhibitors, indicating that endocytosis plays a major role in this process. Additionally, co-culture experiments with HEK-293 cells expressing red fluorescent protein (RFP)-tagged CD9 and the chondrocytic cell line OUMS-27 confirmed the transfer of RFP-positive EVs across a 600-nm but not a 30-nm filter. These findings suggest that EVs from chondrocytes are released into joint fluid and taken up by cells within the cartilage, potentially facilitating communication between cartilage and synovium. The results underscore the importance of EVs in OA pathophysiology.
en-copyright=
kn-copyright=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SatoIkumi
en-aut-sei=Sato
en-aut-mei=Ikumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakashitaRen
en-aut-sei=Takashita
en-aut-mei=Ren
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KodamaShintaro
en-aut-sei=Kodama
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IkemuraKentaro
en-aut-sei=Ikemura
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OpokuGabriel
en-aut-sei=Opoku
en-aut-mei=Gabriel
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=WatanabeShogo
en-aut-sei=Watanabe
en-aut-mei=Shogo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FurumatsuTakayuki
en-aut-sei=Furumatsu
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YamadaHiroshi
en-aut-sei=Yamada
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AndoMitsuru
en-aut-sei=Ando
en-aut-mei=Mitsuru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=AkiyoshiKazunari
en-aut-sei=Akiyoshi
en-aut-mei=Kazunari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NishidaKeiichiro
en-aut-sei=Nishida
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=HirohataSatoshi
en-aut-sei=Hirohata
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

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

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

affil-num=3
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

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

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

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

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

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

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

affil-num=10
en-affil=Laboratory of Biomaterials, Institute for Life and Medical Sciences, Kyoto University
kn-affil=

affil-num=11
en-affil=Department of Immunology, Graduate School of Medicine, Kyoto University
kn-affil=

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

affil-num=13
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=
en-keyword=extracellular vesicles (EVs)
kn-keyword=extracellular vesicles (EVs)
en-keyword=chondrocytes
kn-keyword=chondrocytes
en-keyword=synoviocytes
kn-keyword=synoviocytes
en-keyword=osteoarthritis (OA)
kn-keyword=osteoarthritis (OA)
END

start-ver=1.4
cd-journal=joma
no-vol=44
cd-vols=
no-issue=6
article-no=
start-page=2497
end-page=2509
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240531
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Senescent Fibroblasts Potentiate Peritoneal Metastasis of Diffuse-type Gastric Cancer Cells via IL-8?mediated Crosstalk
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/Aim: Diffuse-type gastric cancer (DGC) often forms peritoneal metastases, leading to poor prognosis. However, the underlying mechanism of DGC-mediated peritoneal metastasis is poorly understood. DGC is characterized by desmoplastic stroma, in which heterogeneous cancer-associated fibroblasts (CAFs), including myofibroblastic CAFs (myCAFs) and senescent CAFs (sCAFs), play a crucial role during tumor progression. This study investigated the CAF subtypes induced by GC cells and the role of sCAFs in peritoneal metastasis of DGC cells. Materials and Methods: Conditioned medium of human DGC cells (KATOIII, NUGC-4) and human intestinal-type GC (IGC) cells (MKN-7, N87) was used to induce CAFs. CAF subtypes were evaluated by analyzing the expression of α?smooth muscle actin (α-SMA), senescence-associated β-galactosidase (SA-β-gal), and p16 in human normal fibroblasts (GF, FEF-3). A cytokine array was used to explore the underlying mechanism of GC-induced CAF subtype development. The role of sCAFs in peritoneal metastasis of DGC cells was analyzed using a peritoneally metastatic DGC tumor model. The relationships between GC subtypes and CAF-related markers were evaluated using publicly available datasets. Results: IGC cells significantly induced α-SMA+ myCAFs by secreting transforming growth factor?β, whereas DGC cells induced SA-β-gal+/p16+ sCAFs by secreting interleukin (IL)-8. sCAFs further secreted IL-8 to promote DGC cell migration. In vivo experiments demonstrated that co-inoculation of sCAFs significantly enhanced peritoneal metastasis of NUGC-4 cells, which was attenuated by administration of the IL-8 receptor antagonist navarixin. p16 and IL-8 expression was significantly associated with poor prognosis of DGC patients. Conclusion: sCAFs promote peritoneal metastasis of DGC via IL-8?mediated crosstalk.
en-copyright=
kn-copyright=

en-aut-name=LIYUNCHENG
en-aut-sei=LI
en-aut-mei=YUNCHENG
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TAZAWAHIROSHI
en-aut-sei=TAZAWA
en-aut-mei=HIROSHI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NAGAIYASUO
en-aut-sei=NAGAI
en-aut-mei=YASUO
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FUJITASHUTO
en-aut-sei=FUJITA
en-aut-mei=SHUTO
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OKURATOMOHIRO
en-aut-sei=OKURA
en-aut-mei=TOMOHIRO
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SHOJIRYOHEI
en-aut-sei=SHOJI
en-aut-mei=RYOHEI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YAMADAMOTOHIKO
en-aut-sei=YAMADA
en-aut-mei=MOTOHIKO
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KIKUCHISATORU
en-aut-sei=KIKUCHI
en-aut-mei=SATORU
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KURODASHINJI
en-aut-sei=KURODA
en-aut-mei=SHINJI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OHARATOSHIAKI
en-aut-sei=OHARA
en-aut-mei=TOSHIAKI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NOMAKAZUHIRO
en-aut-sei=NOMA
en-aut-mei=KAZUHIRO
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NISHIZAKIMASAHIKO
en-aut-sei=NISHIZAKI
en-aut-mei=MASAHIKO
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KAGAWASHUNSUKE
en-aut-sei=KAGAWA
en-aut-mei=SHUNSUKE
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=FUJIWARATOSHIYOSHI
en-aut-sei=FUJIWARA
en-aut-mei=TOSHIYOSHI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

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

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

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

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

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

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

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

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

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

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

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

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

affil-num=13
en-affil=Departments of Gastroenterological Surgery and Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Departments of Gastroenterological Surgery and Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Gastric cancer
kn-keyword=Gastric cancer
en-keyword=peritoneal metastasis
kn-keyword=peritoneal metastasis
en-keyword=senescent fibroblast
kn-keyword=senescent fibroblast
en-keyword=IL-8
kn-keyword=IL-8
en-keyword=CXCR1/2
kn-keyword=CXCR1/2
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=11
article-no=
start-page=5889
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240528
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Anti-HMGB1 mAb Therapy Reduces Epidural Hematoma Injury
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Epidural and subdural hematomas are commonly associated with traumatic brain injury. While surgical removal is the primary intervention for these hematomas, it is also critical to prevent and reduce complications such as post-traumatic epilepsy, which may result from inflammatory responses in the injured brain areas. In the present study, we observed that high mobility group box-1 (HMGB1) decreased in the injured brain area beneath the epidural hematoma (EDH) in rats, concurrent with elevated plasma levels of HMGB1. Anti-HMGB1 monoclonal antibody therapy strongly inhibited both HMGB1 release and the subsequent increase in plasma levels. Moreover, this treatment suppressed the up-regulation of inflammatory cytokines and related molecules such as interleukin-1-beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and inducible nitric oxide synthase (iNOS) in the injured areas. Our in vitro experiments using SH-SY5Y demonstrated that hematoma components?thrombin, heme, and ferrous ion? prompted HMGB1 translocation from the nuclei to the cytoplasm, a process inhibited by the addition of the anti-HMGB1 mAb. These findings suggest that anti-HMGB1 mAb treatment not only inhibits HMGB1 translocation but also curtails inflammation in injured areas, thereby protecting the neural tissue. Thus, anti-HMGB1 mAb therapy could serve as a complementary therapy for an EDH before/after surgery.
en-copyright=
kn-copyright=

en-aut-name=GaoShangze
en-aut-sei=Gao
en-aut-mei=Shangze
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WangDengli
en-aut-sei=Wang
en-aut-mei=Dengli
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LiuKeyue
en-aut-sei=Liu
en-aut-mei=Keyue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TomonoYasuko
en-aut-sei=Tomono
en-aut-mei=Yasuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FuLi
en-aut-sei=Fu
en-aut-mei=Li
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=GaoYuan
en-aut-sei=Gao
en-aut-mei=Yuan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakahashiYohei
en-aut-sei=Takahashi
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YataMariko
en-aut-sei=Yata
en-aut-mei=Mariko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

affil-num=1
en-affil=Department of Translational Research & Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

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

affil-num=4
en-affil=Department of Translational Research & Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Translational Research & Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Translational Research & Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

affil-num=8
en-affil=Department of Translational Research & Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Translational Research & Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=epidural hematoma
kn-keyword=epidural hematoma
en-keyword=HMGB1
kn-keyword=HMGB1
en-keyword=inflammatory response
kn-keyword=inflammatory response
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=3
article-no=
start-page=271
end-page=279
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202406
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of Humidified High-Flow Nasal Cannula Oxygen Therapy with a Pulmonary Infection Control Window as a Ventilation Switching Indication in Combination with Atomizing Inhalation of Terbutaline on the Lung Function of Patients with Acute Exacerbation of COPD
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We investigated how humidified high-flow nasal cannula oxygen therapy (HFNC) with a pulmonary infection control (PIC) window as a ventilation switching indication in combination with atomizing inhalation of terbutaline affects the lung function of patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). We examined 140 hospitalized AECOPD patients randomized to control and observation groups. Conventional supportive therapy and invasive mechanical ventilation with tracheal intubation were conducted in both groups, with a PIC window as the indication for ventilation switching. Noninvasive positive pressure ventilation (NIPPV) plus atomizing inhalation of terbutaline was used in the control group. In the observation group, HFNC combined with atomizing inhalation of terbutaline was used. Compared to the control group, after 48-hr treatment and treatment completion, the observation group had significantly increased levels of lung function indicators (maximal voluntary ventilation [MVV] plus forced vital capacity [FVC], p<0.05) and oxygen metabolism indicators (arterial oxygen partial pressure [PaO2], arterial oxygen content [CaO2], and oxygenation index, p<0.05). The comparison of the groups revealed that the levels of airway remodeling indicators (matrix metalloproteinase-2 [MMP-2], tissue inhibitor of metalloproteinase 2 [TIMP-2] plus MMP-9) and inflammatory indicators (interferon gamma [IFN-γ] together with interleukin-17 [IL-17], IL-10 and IL-4) were significantly lower after 48 h of treatment as well as after treatment completion (both p<0.05). These results demonstrate that HFNC with a PIC window as the indication for ventilation switching combined with atomizing inhalation of terbutaline can relieve the disorder of oxygen metabolism and correct airway hyper-reactivity.
en-copyright=
kn-copyright=

en-aut-name=YeMengjiao
en-aut-sei=Ye
en-aut-mei=Mengjiao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ZhangRenwei
en-aut-sei=Zhang
en-aut-mei=Renwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Respiratory and Critical Care Medicine, Tiantai Hospital of Traditional Chinese Medicine
kn-affil=

affil-num=2
en-affil=Department of Respiratory and Critical Care Medicine, Tiantai Hospital of Traditional Chinese Medicine
kn-affil=
en-keyword=chronic obstructive pulmonary disease
kn-keyword=chronic obstructive pulmonary disease
en-keyword=inhalation
kn-keyword=inhalation
en-keyword=oxygen therapy
kn-keyword=oxygen therapy
en-keyword=pulmonary function
kn-keyword=pulmonary function
en-keyword=ventilation
kn-keyword=ventilation
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=3
article-no=
start-page=227
end-page=235
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202406
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of Lipopolysaccharide on the Duration of Zolpidem-Induced Loss of Righting Reflex in Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Zolpidem, a non-benzodiazepine hypnotic, is primarily used to treat insomnia. In a previous study, pior treatment with non-benzodiazepine receptor agonists was associated with inflammation. The present study aimed to clarify the association between the effects of zolpidem and inflammation in mice treated with lipopolysaccharide (LPS), a known model of inflammation. We assessed the zolpidem-induced loss of righting reflex (LORR) duration 24 h after LPS treatment in mice. Additionally, the expressions of γ-aminobutyric acid (GABA)A receptor subunit and K+-Cl? cotransporter isoform 2 (KCC2) mRNA in the hippocampus and frontal cortex were examined in LPS-treated mice. Pretreatment with LPS was associated with significantly prolonged duration of zolpidem-induced LORR compared to control mice. This effect was significantly attenuated by administering bicuculline, a GABAA receptor antagonist, or flumazenil, a benzodiazepine receptor antagonist, in LPS-treated mice. Compared to controls, LPS-treated mice showed no significant change in the expression of GABAA receptor subunits in the hippocampus or frontal cortex. Bumetanide, an Na+-K+-2Cl? cotransporter isoform 1 blocker, attenuated the extended duration of zolpidem-induced LORR observed in LPS-treated mice. LPS significantly decreased Kcc2 mRNA expression in the hippocampus and the frontal cortex. These findings suggest that inflammation increases zolpidem-induced LORR, possibly through a reduction in KCC2 expression.
en-copyright=
kn-copyright=

en-aut-name=WadaYudai
en-aut-sei=Wada
en-aut-mei=Yudai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UshioSoichiro
en-aut-sei=Ushio
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KitamuraYoshihisa
en-aut-sei=Kitamura
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ZamamiYoshito
en-aut-sei=Zamami
en-aut-mei=Yoshito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SendoToshiaki
en-aut-sei=Sendo
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

affil-num=2
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=

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

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

affil-num=5
en-affil=Department of Clinical Pharmacy, Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=lipopolysaccharide
kn-keyword=lipopolysaccharide
en-keyword=zolpidem
kn-keyword=zolpidem
en-keyword=GABAA receptor
kn-keyword=GABAA receptor
en-keyword=K+-Cl? cotransporters
kn-keyword=K+-Cl? cotransporters
END

start-ver=1.4
cd-journal=joma
no-vol=136
cd-vols=
no-issue=1
article-no=
start-page=4
end-page=6
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The 2022 Incentive Award of the Okayama Medical Association in General Medical Science (2022 Yuuki Prize)
kn-title=令和４年度岡山医学会賞　総合研究奨励賞（結城賞）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MeguriYusuke
en-aut-sei=Meguri
en-aut-mei=Yusuke
kn-aut-name=廻勇輔
kn-aut-sei=廻
kn-aut-mei=勇輔
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Hematology, Oncology and Respitatory Medicine, 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　血液・腫瘍・呼吸器内科学
END

start-ver=1.4
cd-journal=joma
no-vol=174
cd-vols=
no-issue=6
article-no=
start-page=533
end-page=548
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230919
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Phosphorylated SARM1 is involved in the pathological process of rotenone-induced neurodegeneration
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sterile alpha and Toll/interleukin receptor motif-containing protein 1 (SARM1) is a NAD+ hydrolase that plays a key role in axonal degeneration and neuronal cell death. We reported that c-Jun N-terminal kinase (JNK) activates SARM1 through phosphorylation at Ser-548. The importance of SARM1 phosphorylation in the pathological process of Parkinson’s disease (PD) has not been determined. We thus conducted the present study by using rotenone (an inducer of PD-like pathology) and neurons derived from induced pluripotent stem cells (iPSCs) from healthy donors and a patient with familial PD PARK2 (FPD2). The results showed that compared to the healthy neurons, FPD2 neurons were more vulnerable to rotenone-induced stress and had higher levels of SARM1 phosphorylation. Similar cellular events were obtained when we used PARK2-knockdown neurons derived from healthy donor iPSCs. These events in both types of PD-model neurons were suppressed in neurons treated with JNK inhibitors, Ca2+-signal inhibitors, or by a SARM1-knockdown procedure. The degenerative events were enhanced in neurons overexpressing wild-type SARM1 and conversely suppressed in neurons overexpressing the SARM1-S548A mutant. We also detected elevated SARM1 phosphorylation in the midbrain of PD-model mice. The results indicate that phosphorylated SARM1 plays an important role in the pathological process of rotenone-induced neurodegeneration.
en-copyright=
kn-copyright=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=PhooMay Tha Zin
en-aut-sei=Phoo
en-aut-mei=May Tha Zin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OchiToshiki
en-aut-sei=Ochi
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamamotoKen-ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NishiboriMasahiro
en-aut-sei=Nishibori
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

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

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

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

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

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

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

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

affil-num=8
en-affil=Department of Translational Research and Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

affil-num=10
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=JNK
kn-keyword=JNK
en-keyword=PARK2
kn-keyword=PARK2
en-keyword=Parkinson’sdisease
kn-keyword=Parkinson’sdisease
en-keyword=Phosphorylation
kn-keyword=Phosphorylation
en-keyword=SARM1
kn-keyword=SARM1
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=2
article-no=
start-page=123
end-page=134
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202404
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Sigle Agent of Posttransplant Cyclophosphamide Without Calcineurin Inhibitor Controls Severity of Experimental Chronic GVHD
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Chronic graft-versus-host disease (GVHD) is a major cause of late death and morbidity following allogeneic hematopoietic cell transplantation (HCT), but its pathogenesis remains unclear. Recently, haplo-identical HCT with post-transplant cyclophosphamide (Haplo-HCT with PTCY) was found to achieve a low incidence rate of acute GVHD and chronic GVHD. However, while the pathogenesis of acute GVHD following Haplo-HCT with PTCY has been well investigated, that of chronic GVHD remains to be elucidated, especially in HLA-matched HCT with PTCY. Based on its safety profile, PTCY is currently applied for the human leucocyte antigen (HLA)-matched HCT setting. Here, we investigated the mechanisms of chronic GVHD following HLA-matched HCT with PTCY using a well-defined mouse chronic GVHD model. PTCY attenuated clinical and pathological chronic GVHD by suppressing effector T-cells and preserving regulatory T-cells compared with a control group. Additionally, we demonstrated that cyclosporine A (CsA) did not show any additional positive effects on attenuation of GVHD in PTCY-treated recipients. These results suggest that monotherapy with PTCY without CsA could be a promising strategy for the prevention of chronic GVHD following HLA-matched HCT.
en-copyright=
kn-copyright=

en-aut-name=SaekiKyosuke
en-aut-sei=Saeki
en-aut-mei=Kyosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujiwaraHideaki
en-aut-sei=Fujiwara
en-aut-mei=Hideaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SeikeKeisuke
en-aut-sei=Seike
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KuroiTaiga
en-aut-sei=Kuroi
en-aut-mei=Taiga
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NishimoriHisakazu
en-aut-sei=Nishimori
en-aut-mei=Hisakazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TanakaTakehiro
en-aut-sei=Tanaka
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsuokaKen-ichi
en-aut-sei=Matsuoka
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FujiiNobuharu
en-aut-sei=Fujii
en-aut-mei=Nobuharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

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

affil-num=2
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

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

affil-num=5
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

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

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

affil-num=8
en-affil=Division of Transfusion, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=GVHD
kn-keyword=GVHD
en-keyword=posttransplant cyclophosphamide
kn-keyword=posttransplant cyclophosphamide
en-keyword=hematopoietic cell transplantation
kn-keyword=hematopoietic cell transplantation
en-keyword=HLA-identical
kn-keyword=HLA-identical
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=2
article-no=
start-page=95
end-page=106
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202404
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Roles of Neuropeptide Y in Respiratory Disease Pathogenesis via the Airway Immune Response
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The lungs are very complex organs, and the respiratory system performs the dual roles of repairing tissue while protecting against infection from various environmental stimuli. Persistent external irritation disrupts the immune responses of tissues and cells in the respiratory system, ultimately leading to respiratory disease. Neuropeptide Y (NPY) is a 36-amino-acid polypeptide and a neurotransmitter that regulates homeostasis. The NPY receptor is a seven-transmembrane-domain G-protein-coupled receptor with six subtypes (Y1, Y2, Y3, Y4, Y5, and Y6). Of these receptors, Y1, Y2, Y4, and Y5 are functional in humans, and Y1 plays important roles in the immune responses of many organs, including the respiratory system. NPY and the Y1 receptor have critical roles in the pathogenesis of asthma, chronic obstructive pulmonary disease, and idiopathic pulmonary fibrosis. The effects of NPY on the airway immune response and pathogenesis differ among respiratory diseases. This review focuses on the involvement of NPY in the airway immune response and pathogenesis of various respiratory diseases.
en-copyright=
kn-copyright=

en-aut-name=ItanoJunko
en-aut-sei=Itano
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KiuraKatsuyuki
en-aut-sei=Kiura
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyaharaNobuaki
en-aut-sei=Miyahara
en-aut-mei=Nobuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

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

affil-num=2
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

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

affil-num=4
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=
en-keyword=neuropeptide y
kn-keyword=neuropeptide y
en-keyword=Y1 receptor
kn-keyword=Y1 receptor
en-keyword=airway immune response
kn-keyword=airway immune response
en-keyword=bronchial epithelial cells
kn-keyword=bronchial epithelial cells
en-keyword=respiratory disease
kn-keyword=respiratory disease
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=6
article-no=
start-page=3252
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240313
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Age-Related Effects on MSC Immunomodulation, Macrophage Polarization, Apoptosis, and Bone Regeneration Correlate with IL-38 Expression
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Mesenchymal stem cells (MSCs) are known to promote tissue regeneration and suppress excessive inflammation caused by infection or trauma. Reported evidence indicates that various factors influence the expression of MSCs' endogenous immunomodulatory properties. However, the detailed interactions of MSCs with macrophages, which are key cells involved in tissue repair, and their regulatory mechanisms are not completely understood. We herein investigated how age-related immunomodulatory impairment of MSCs alters the interaction of MSCs with macrophages during bone healing using young (5-week old) and aged (50-week old) mice. To clarify the relationship between inflammatory macrophages (M1) and MSCs, their spatiotemporal localization at the bone healing site was investigated by immunostaining, and possible regulatory mechanisms were analyzed in vitro co-cultures. Histomorphometric analysis revealed an accumulation of M1 and a decrease in MSC number at the healing site in aged mice, which showed a delayed bone healing. In in vitro co-cultures, MSCs induced M1 apoptosis through cell-to-cell contact but suppressed the gene expression of pro-inflammatory cytokines by soluble factors secreted in the culture supernatant. Interestingly, interleukin 38 (Il-38) expression was up-regulated in M1 after co-culture with MSCs. IL-38 suppressed the gene expression of inflammatory cytokines in M1 and promoted the expression of genes associated with M1 polarization to anti-inflammatory macrophages (M2). IL-38 also had an inhibitory effect on M1 apoptosis. These results suggest that MSCs may induce M1 apoptosis, suppress inflammatory cytokine production by M1, and induce their polarization toward M2. Nevertheless, in aged conditions, the decreased number and immunomodulatory function of MSCs could be associated with a delayed M1 clearance (i.e., apoptosis and/or polarization) and consequent delayed resolution of the inflammatory phase. Furthermore, M1-derived IL-38 may be associated with immunoregulation in the tissue regeneration site.
en-copyright=
kn-copyright=

en-aut-name=ZhangJiewen
en-aut-sei=Zhang
en-aut-mei=Jiewen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AkiyamaKentaro
en-aut-sei=Akiyama
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MunAung Ye
en-aut-sei=Mun
en-aut-mei=Aung Ye
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TagashiraRyuji
en-aut-sei=Tagashira
en-aut-mei=Ryuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ZouTingling
en-aut-sei=Zou
en-aut-mei=Tingling
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsunagaNaoya
en-aut-sei=Matsunaga
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KohnoTeisaku
en-aut-sei=Kohno
en-aut-mei=Teisaku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KubokiTakuo
en-aut-sei=Kuboki
en-aut-mei=Takuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

affil-num=4
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

affil-num=7
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=mesenchymal stem cell
kn-keyword=mesenchymal stem cell
en-keyword=aging
kn-keyword=aging
en-keyword=apoptosis
kn-keyword=apoptosis
en-keyword=cytokines
kn-keyword=cytokines
en-keyword=monocytes and macrophages
kn-keyword=monocytes and macrophages
en-keyword=immunomodulation
kn-keyword=immunomodulation
END

start-ver=1.4
cd-journal=joma
no-vol=33
cd-vols=
no-issue=3
article-no=
start-page=e15040
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240301
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Elevated expression of interleukin-6 (IL-6) and serum amyloid A (SAA) in the skin and the serum of recessive dystrophic epidermolysis bullosa: Skin as a possible source of IL-6 through Toll-like receptor ligands and SAA
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The effect of persistent skin inflammation on extracutaneous organs and blood is not well studied. Patients with recessive dystrophic epidermolysis bullosa (RDEB), a severe form of the inherited blistering skin disorder, have widespread and persistent skin ulcers, and they develop various complications including anaemia, hyperglobulinaemia, hypoalbuminaemia and secondary amyloidosis. These complications are associated with the bioactivities of IL-6, and the development of secondary amyloidosis requires the persistent elevation of serum amyloid A (SAA) level. We found that patients with RDEB had significantly higher serum levels of IL-6 and SAA compared to healthy volunteers and patients with psoriasis or atopic dermatitis. Both IL-6 and SAA were highly expressed in epidermal keratinocytes and dermal fibroblasts of the skin ulcer lesions. Keratinocytes and fibroblasts surrounding the ulcer lesions are continuously exposed to Toll-like receptor (TLR) ligands, pathogen-associated and damage-associated molecular pattern molecules. In vitro, TLR ligands induced IL-6 expression via NF-κB in normal human epidermal keratinocytes (NHEKs) and dermal fibroblasts (NHDFs). SAA further induced the expression of IL-6 via TLR1/2 and NF-κB in NHEKs and NHDFs. The limitation of this study is that NHEKs and NHDFs were not derived from RDEB patients. These observations suggest that TLR-mediated persistent skin inflammation might increase the risk of IL-6-related systemic complications, including RDEB.
en-copyright=
kn-copyright=

en-aut-name=KawakamiYoshio
en-aut-sei=Kawakami
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KajitaAi
en-aut-sei=Kajita
en-aut-mei=Ai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HasuiKen‐Ichi
en-aut-sei=Hasui
en-aut-mei=Ken‐Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MatsudaYoshihiro
en-aut-sei=Matsuda
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IwatsukiKeiji
en-aut-sei=Iwatsuki
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MorizaneShin
en-aut-sei=Morizane
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

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

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

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

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

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

affil-num=6
en-affil=Department of Dermatology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=epidermolysis bullosa
kn-keyword=epidermolysis bullosa
en-keyword=fibroblasts
kn-keyword=fibroblasts
en-keyword=IL-6
kn-keyword=IL-6
en-keyword=keratinocytes
kn-keyword=keratinocytes
en-keyword=serum amyloid A
kn-keyword=serum amyloid A
END

start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=2023
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Safety and Clinical Effects of a Muse Cell-Based Product in Patients With Amyotrophic Lateral Sclerosis: Results of a Phase 2 Clinical Trial
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Amyotrophic lateral sclerosis (ALS) is characterized by progressive loss of motor neurons. Multilineage-differentiating stress-enduring (Muse) cells are unique endogenous stem cells that show therapeutic effects on motor function in ALS mouse models. We conducted a single-center open phase II clinical trial to evaluate the safety and clinical effects of repeated intravenous injections of an allogenic Muse cell-based product, CL2020, in patients with ALS. Five patients with ALS received CL2020 intravenously once a month for a total of six doses. The primary endpoints were safety and tolerability, and the secondary endpoint was the rate of change in the Revised Amyotrophic Lateral Sclerosis Functional Rating Scale (ALSFRS-R) score. In addition, serum tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), sphingosine-1-phosphate (S1P), cerebrospinal fluid chitotriosidase-1 (CHIT-1), and neurofilament light chain (NfL) levels were evaluated. The CL2020 treatment was highly tolerated without serious side effects. The ALSFRS-R score change trended upward at 12 months post-CL2020 treatment compared with that at 3 months pre-administration, but the difference was not statistically significant. Among five patients diagnosed with ALS, three exhibited a decrease in the rate of ALSFRS-R score change, one demonstrated an increase, and another showed no change. In addition, the patients’ serum IL-6 and TNF-α levels and cerebrospinal fluid CHIT-1 and NfL levels increased for up to 6 months post-treatment; however, their serum S1P levels continuously decreased over 12 months. These findings indicate a favorable safety profile of CL2020 therapy. In the near future, a double-blind study of a larger number of ALS patients should be conducted to confirm the efficacy of ALS treatment with CL2020.
en-copyright=
kn-copyright=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakanoYumiko
en-aut-sei=Nakano
en-aut-mei=Yumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SasakiRyo
en-aut-sei=Sasaki
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TadokoroKoh
en-aut-sei=Tadokoro
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OmoteYoshio
en-aut-sei=Omote
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YunokiTaijun
en-aut-sei=Yunoki
en-aut-mei=Taijun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KawaharaYuko
en-aut-sei=Kawahara
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MatsumotoNamiko
en-aut-sei=Matsumoto
en-aut-mei=Namiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TairaYuki
en-aut-sei=Taira
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MatsuokaChika
en-aut-sei=Matsuoka
en-aut-mei=Chika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

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

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

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

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

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

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

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

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

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

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

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

affil-num=12
en-affil=Department of Neurology, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=amyotrophic lateral sclerosis
kn-keyword=amyotrophic lateral sclerosis
en-keyword=clinical trial
kn-keyword=clinical trial
en-keyword=CL2020
kn-keyword=CL2020
en-keyword=multilineage-differentiating stress-enduring (Muse) cells
kn-keyword=multilineage-differentiating stress-enduring (Muse) cells
en-keyword=intravenous administration
kn-keyword=intravenous administration
END

start-ver=1.4
cd-journal=joma
no-vol=77
cd-vols=
no-issue=6
article-no=
start-page=671
end-page=674
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202312
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dramatic Response to Tezepelumab as an Initial Biologic Agent for Refractory Asthma Associated with Type 2 and Non-type 2 Traits
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A 74-year-old Japanese woman presented with a 45-year history of refractory asthma. She had been treated with inhaled corticosteroids, a long-acting β2-agonist, and a long-acting muscarinic antagonist for 6 months. She also had a repeated viral infection. Her condition had been characterized as a refractory asthma associated with type 2 and non-type 2 traits. We began treatment with tezepelumab. The control of the patient’s asthma symptoms and quality of life improved greatly within 1 month (changes in eosinophil count from 748 to 96 /μL, in FeNO from 32 to 17 ppb, in the Asthma Quality of Life Questionnaire score from 3.59 to 6.68, and in the Asthma Control Test score from 13 to 23). Tezepelumab was effective as an initial biologic agent for a patient with refractory asthma associated with type 2 and non-type 2 traits.
en-copyright=
kn-copyright=

en-aut-name=MinamiDaisuke
en-aut-sei=Minami
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HosoyaTakeshi
en-aut-sei=Hosoya
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HosoyaMasaharu
en-aut-sei=Hosoya
en-aut-mei=Masaharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NaganoAkichika
en-aut-sei=Nagano
en-aut-mei=Akichika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakajimaYasuhiro
en-aut-sei=Nakajima
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyaharaNobuaki
en-aut-sei=Miyahara
en-aut-mei=Nobuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KanehiroArihiko
en-aut-sei=Kanehiro
en-aut-mei=Arihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Internal Medicine, Hosoya Hospital
kn-affil=

affil-num=2
en-affil=Department of Internal Medicine, Hosoya Hospital
kn-affil=

affil-num=3
en-affil=Department of Internal Medicine, Hosoya Hospital
kn-affil=

affil-num=4
en-affil=Department of Respiratory Medicine, Himeji Saint Mary’s Hospital
kn-affil=

affil-num=5
en-affil=Department of Respiratory Medicine, Himeji Saint Mary’s Hospital
kn-affil=

affil-num=6
en-affil=Department of Internal Medicine, Himeji Saint Mary’s Hospital
kn-affil=

affil-num=7
en-affil=Department of Internal Medicine, Himeji Saint Mary’s Hospital
kn-affil=
en-keyword=tezepelumab
kn-keyword=tezepelumab
en-keyword=biologic agent
kn-keyword=biologic agent
en-keyword=eosinophilic
kn-keyword=eosinophilic
en-keyword=non-type 2
kn-keyword=non-type 2
en-keyword=severe asthma
kn-keyword=severe asthma
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=1
article-no=
start-page=103
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231205
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Successful use of dupilumab for egg-induced eosinophilic gastroenteritis with duodenal ulcer: a pediatric case report and review of literature
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Non-esophageal eosinophilic gastrointestinal disorder (non-EoE-EGID) is a rare disease in which eosinophils infiltrate parts of the gastrointestinal tract other than the esophagus; however, the number of patients with non-EoE-EGID has been increasing in recent years. Owing to its chronic course with repeated relapses, it can lead to developmental delays due to malnutrition, especially in pediatric patients. No established treatment exists for non-EoE-EGID, necessitating long-term systemic corticosteroid administration. Although the efficacy of dupilumab, an anti-IL-4/13 receptor monoclonal antibody, for eosinophilic esophagitis, has been reported, only few reports have demonstrated its efficacy in non-EoE EGIDs.<br>
Case presentation A 13-year-old boy developed non-EoE-EGID with duodenal ulcers, with chicken eggs as the trigger. He was successfully treated with an egg-free diet, proton pump inhibitors, and leukotriene receptor antagonists. However, at age 15, he developed worsening upper abdominal pain and difficulty eating. Blood analysis revealed eosinophilia; elevated erythrocyte sedimentation rate; and elevated levels of C-reactive protein, total immunoglobulin E, and thymic and activation-regulated chemokines. Upper gastrointestinal endoscopy revealed a duodenal ulcer with marked mucosal eosinophilic infiltration. Gastrointestinal symptoms persisted even after starting systemic steroids, making it difficult to reduce the steroid dose. Subcutaneous injection of dupilumab was initiated because of comorbid atopic dermatitis exacerbation. After 3 months, the gastrointestinal symptoms disappeared, and after 5 months, the duodenal ulcer disappeared and the eosinophil count decreased in the mucosa. Six months later, systemic steroids were discontinued, and the duodenal ulcer remained recurrence-free. The egg challenge test result was negative; therefore, the egg-free diet was discontinued. Blood eosinophil count and serum IL-5, IL-13, and eotaxin-3 levels decreased after dupilumab treatment. The serum levels of IL-5 and eotaxin-3 remained within normal ranges, although the blood eosinophil counts increased again after discontinuation of oral prednisolone.<br>
Conclusions Suppression of IL-4R/IL-13R-mediated signaling by dupilumab may improve abdominal symptoms and endoscopic and histologic findings in patients with non-EoE-EGID, leading to the discontinuation of systemic steroid administration and tolerance of causative foods.
en-copyright=
kn-copyright=

en-aut-name=TsugeMitsuru
en-aut-sei=Tsuge
en-aut-mei=Mitsuru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShigeharaKenji
en-aut-sei=Shigehara
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UdaKazuhiro
en-aut-sei=Uda
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawanoSeiji
en-aut-sei=Kawano
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IwamuroMasaya
en-aut-sei=Iwamuro
en-aut-mei=Masaya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SaitoYukie
en-aut-sei=Saito
en-aut-mei=Yukie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YashiroMasato
en-aut-sei=Yashiro
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TsukaharaHirokazu
en-aut-sei=Tsukahara
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Pediatric Acute Diseases, Okayama University Academic  Field of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Pediatrics, Okayama  University Hospital
kn-affil=

affil-num=3
en-affil=Department of Pediatrics, Okayama  University Hospital
kn-affil=

affil-num=4
en-affil=Department of Gastroenterology and Hepatology, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Gastroenterology and Hepatology, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Department of Pediatrics, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Pediatrics, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Pediatrics, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Department of Pediatrics, Okayama University Academic Field of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=Duodenal ulcer
kn-keyword=Duodenal ulcer
en-keyword=Dupilumab
kn-keyword=Dupilumab
en-keyword=Eosinophilic gastroenteritis
kn-keyword=Eosinophilic gastroenteritis
en-keyword=Eotaxin-3
kn-keyword=Eotaxin-3
en-keyword=Food allergy
kn-keyword=Food allergy
en-keyword=Interleukin-5
kn-keyword=Interleukin-5
en-keyword=Interleukin-13
kn-keyword=Interleukin-13
en-keyword=Non-esophageal eosinophilic gastrointestinal disorder
kn-keyword=Non-esophageal eosinophilic gastrointestinal disorder
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=2023
dt-pub=20230925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=がん関連線維芽細胞による腫瘍免疫抑制の抗インターロイキン6受容体抗体による克服
kn-title=Overcoming cancer?associated fibroblast?induced immunosuppression by anti?interleukin?6 receptor antibody
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NISHIWAKINoriyuki
en-aut-sei=NISHIWAKI
en-aut-mei=Noriyuki
kn-aut-name=西脇紀之
kn-aut-sei=西脇
kn-aut-mei=紀之
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=155
cd-vols=
no-issue=
article-no=
start-page=105797
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202311
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Ruxolitinib altered IFN-β induced necroptosis of human dental pulp stem cells during osteoblast differentiation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective: This study aimed to evaluate the role of ruxolitinib in the interferon beta (IFN-β) mediated osteoblast differentiation using human dental pulp stem cells (hDPSCs).<br>
Design: hDPSCs from five deciduous teeth of healthy patients were stimulated by adding human recombinant IFN-β protein (1 or 2 ng/ml) to the osteogenic differentiation induction medium. Substrate formation was determined using Alizarin Red staining, calcium concentration, and osteoblast marker expression levels. Ruxolitinib was used to inhibit the Janus kinase/signal transducers and activators of transcription (JAK-STAT) pathway. Apoptosis was detected using terminal deoxynucleotidyl nick-end labeling (TUNEL) staining, and necroptosis was detected using propidium iodide staining and phosphorylated mixed lineage kinase domain-like protein (pMLKL) expression.<br>
Results: In the IFN-β-treated group, substrate formation was inhibited by a reduction in alkaline phosphatase (ALP) expression in a concentration-dependent manner. Although the proliferation potency was unchanged between the IFN-β-treated and control groups, the cell number was significantly reduced in the experimental group. TUNEL-positive cell number was not significantly different; however, the protein level of necroptosis markers, interleukin-6 (IL-6) and pMLKL were significantly increased in the substrate formation. Cell number and ALP expression level were improved in the group administered ruxolitinib, a JAK-STAT inhibitor. Additionally, ruxolitinib significantly suppressed IL-6 and pMLKL levels.<br>
Conclusion: Ruxolitinib interfered with the IFN-β-mediated necroptosis and osteogenic differentiation via the JAK-STAT pathway.
en-copyright=
kn-copyright=

en-aut-name=TanakaAtsuko
en-aut-sei=Tanaka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HayanoSatoru
en-aut-sei=Hayano
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NagataMasayo
en-aut-sei=Nagata
en-aut-mei=Masayo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KosamiTakahiro
en-aut-sei=Kosami
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WangZiyi
en-aut-sei=Wang
en-aut-mei=Ziyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KamiokaHiroshi
en-aut-sei=Kamioka
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Orthodontics, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Orthodontics, Okayama University Hospital
kn-affil=

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

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

affil-num=5
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Type-I interferon
kn-keyword=Type-I interferon
en-keyword=Janus kinase/signal transducers and activators of transcription pathway
kn-keyword=Janus kinase/signal transducers and activators of transcription pathway
en-keyword=Osteoblast
kn-keyword=Osteoblast
en-keyword=Necroptosis
kn-keyword=Necroptosis
en-keyword=Singleton-Merten Syndrome
kn-keyword=Singleton-Merten Syndrome
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=6
article-no=
start-page=78
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Crosstalk between cancer and different cancer stroma subtypes promotes the infiltration of tumor?associated macrophages into the tumor microenvironment of oral squamous cell carcinoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Tumor?associated macrophages (TAMs) are linked to the progression of numerous types of cancer. However, the effects of the tumor microenvironment (TME) of oral squamous cell carcinoma (OSCC), particularly the cancer stroma on TAMs, remains to be elucidated. In the present study, the effects of verrucous SCC?associated stromal cells (VSCC?SCs), SCC?associated stromal cells (SCC?SCs) and human dermal fibroblasts (HDFs) on the differentiation, proliferation and migration of macrophages in vitro was assayed using Giemsa staining, and immunofluorescence, MTS and Transwell (migration) assays, respectively. The combined results suggested that both VSCC?SCs and SCC?SCs promoted the differentiation of macrophages into M2 type TAMs, as well as the proliferation and migration of macrophages following crosstalk with HSC?3 cells in vitro. Moreover, the SCC?SCs exerted a more prominent effect on TAMs than the VSCC?SCs. Immunohistochemical staining was used to examine the expression of CD34, CD45, CD11b and CD163 to assay the effects of VSCC?SCs, SCC?SCs and HDFs on microvessel density (MVD) and the infiltration of CD45(+) monocytes, CD11b(+) TAMs and CD163(+) M2 type macrophages. The results suggested that both VSCC?SCs and SCC?SCs promoted MVD and the infiltration of CD45(+) monocytes, CD11b(+) TAMs and CD163(+) M2 type TAMs into the TME of OSCC following crosstalk with HSC?3 cells in vivo. The SCC?SCs exerted a more prominent promoting effect than the VSCC?SCs. Finally, the potential genes underlying the differential effects of VSCC?SCs and SCC?SCs on the infiltration of TAMs were investigated using microarray analysis. The results revealed that interleukin 1β, bone morphogenetic protein 4, interleukin 6 and C?X?C motif chemokine ligand 12 had great potential to mediate the differential effects of VSCC?SCs and SCC?SCs on TAM infiltration. On the whole, the findings presented herein, demonstrate that both VSCC?SCs and SCC?SCs promote the infiltration of TAMs into the TME of OSCC following crosstalk with HSC?3 cells; the SCC?SCs were found to exert a more prominent promoting effect. This may represent a potential regulatory mechanism for the infiltration of TAMs into the TME of OSCC.
en-copyright=
kn-copyright=

en-aut-name=ShanQiusheng
en-aut-sei=Shan
en-aut-mei=Qiusheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakabatakeKiyofumi
en-aut-sei=Takabatake
en-aut-mei=Kiyofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KawaiHotaka
en-aut-sei=Kawai
en-aut-mei=Hotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OoMay Wathone
en-aut-sei=Oo
en-aut-mei=May Wathone
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SukegawaShintaro
en-aut-sei=Sukegawa
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FujiiMasae
en-aut-sei=Fujii
en-aut-mei=Masae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakanoKeisuke
en-aut-sei=Nakano
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NagatsukaHitoshi
en-aut-sei=Nagatsuka
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

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

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

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

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

affil-num=8
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
en-keyword=oral squamous cell carcinoma
kn-keyword=oral squamous cell carcinoma
en-keyword=tumor-associated macrophages
kn-keyword=tumor-associated macrophages
en-keyword=cancer stroma
kn-keyword=cancer stroma
en-keyword=tumor microenvironment
kn-keyword=tumor microenvironment
en-keyword=microvessel density
kn-keyword=microvessel density
en-keyword=microarray
kn-keyword=microarray
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=3
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211108
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Evaluation of skin sensitization based on interleukin?2 promoter activation in Jurkat cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Skin sensitization is an allergic reaction caused by certain chemical substances, and is an important factor to be taken into consideration when evaluating the safety of numerous types of products. Although animal testing has long been used to evaluate skin sensitization, the recent trend to regulate such testing has led to the development and use of alternative methods. Skin sensitization reactions are summarized in the form of an adverse outcome pathway consisting of four key events (KE), including covalent binding to skin proteins (KE1), keratinocyte activation (KE2), and dendritic cell activation (KE3). Equivalent alternative methods have been developed for KE1 to KE3, but no valid alternative has yet been developed for the evaluation of KE4 and T?cell activation. Current alternative methods rely on data from KE1 to KE3 to predict the effect of chemicals on skin sensitization. The addition of KE4 data is expected to improve the accuracy and reproducibility of such predictions. The aim of this study was to establish an assay to evaluate KE4 T?cell activation to supplement data on skin sensitization related to KE4. To evaluate T?cell activation, the Jurkat T?cell line stably expressing luciferase downstream of the pro?inflammatory cytokine interleukin?2 promoter was used. After exposure to known skin sensitizing agents and control substances, luciferase activity measurements revealed that this assay was valid for evaluating skin sensitization. However, two skin sensitizers known to have immunosuppressive effects on T?cells reacted negatively in this assay. The results revealed that this assay simultaneously allows for monitoring of the skin sensitization and immuno?suppressiveness of chemical substances and supplements KE4 T?cell activation data, and may thus contribute to reducing the use of animal experiments.
en-copyright=
kn-copyright=

en-aut-name=NagahataTaichi
en-aut-sei=Nagahata
en-aut-mei=Taichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TsujinoYoshio
en-aut-sei=Tsujino
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakayamaEiji
en-aut-sei=Takayama
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HikasaHaruka
en-aut-sei=Hikasa
en-aut-mei=Haruka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Science, Technology and Innovation, Kobe University
kn-affil=

affil-num=3
en-affil=Department of Oral Biochemistry, Asahi University School of Dentistry
kn-affil=

affil-num=4
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=skin sensitization
kn-keyword=skin sensitization
en-keyword=immunotoxicity
kn-keyword=immunotoxicity
en-keyword=interleukin-2 promoter
kn-keyword=interleukin-2 promoter
en-keyword=Jurkat
kn-keyword=Jurkat
en-keyword=T-cell activation
kn-keyword=T-cell activation
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=11
article-no=
start-page=4343
end-page=4354
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230915
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Efficacy of gilteritinib in comparison with alectinib for the treatment of ALK-rearranged non-small cell lung cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Gilteritinib is a multitarget tyrosine kinase inhibitor (TKI), approved for the treatment of FLT3-mutant acute myeloid leukemia, with a broad range of activity against several tyrosine kinases including anaplastic lymphoma kinase (ALK). This study investigated the efficacy of gilteritinib against ALK-rearranged non-small cell lung cancers (NSCLC). To this end, we assessed the effects of gilteritinib on cell proliferation, apoptosis, and acquired resistance responses in several ALK-rearranged NSCLC cell lines and mouse xenograft tumor models and compared its efficacy to alectinib, a standard ALK inhibitor. Gilteritinib was significantly more potent than alectinib, as it inhibited cell proliferation at a lower dose, with complete attenuation of growth observed in several ALK-rearranged NSCLC cell lines and no development of drug tolerance. Immunoblotting showed that gilteritinib strongly suppressed phosphorylated ALK and its downstream effectors, as well as mesenchymal-epithelial transition factor (MET) signaling. By comparison, MET signaling was enhanced in alectinib-treated cells. Furthermore, gilteritinib was found to more effectively abolish growth of ALK-rearranged NSCLC xenograft tumors, many of which completely receded. Interleukin-15 (IL-15) mRNA levels were elevated in gilteritinib-treated cells, together with a concomitant increase in the infiltration of tumors by natural killer (NK) cells, as assessed by immunohistochemistry. This suggests that IL-15 production along with NK cell infiltration may constitute components of the gilteritinib-mediated antitumor responses in ALK-rearranged NSCLCs. In conclusion, gilteritinib demonstrated significantly improved antitumor efficacy compared with alectinib against ALK-rearranged NSCLC cells, which can warrant its candidacy for use in anticancer regimens, after further examination in clinical trial settings.
en-copyright=
kn-copyright=

en-aut-name=AndoChihiro
en-aut-sei=Ando
en-aut-mei=Chihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IchiharaEiki
en-aut-sei=Ichihara
en-aut-mei=Eiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NishiTatsuya
en-aut-sei=Nishi
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MoritaAyako
en-aut-sei=Morita
en-aut-mei=Ayako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HaraNaofumi
en-aut-sei=Hara
en-aut-mei=Naofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakadaKenji
en-aut-sei=Takada
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakasukaTakamasa
en-aut-sei=Nakasuka
en-aut-mei=Takamasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WatanabeHiromi
en-aut-sei=Watanabe
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KanoHirohisa
en-aut-sei=Kano
en-aut-mei=Hirohisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NishiiKazuya
en-aut-sei=Nishii
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MakimotoGo
en-aut-sei=Makimoto
en-aut-mei=Go
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KondoTakumi
en-aut-sei=Kondo
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=NinomiyaKiichiro
en-aut-sei=Ninomiya
en-aut-mei=Kiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=FujiiMasanori
en-aut-sei=Fujii
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=KuboToshio
en-aut-sei=Kubo
en-aut-mei=Toshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=OhashiKadoaki
en-aut-sei=Ohashi
en-aut-mei=Kadoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=MatsuokaKen-Ichi
en-aut-sei=Matsuoka
en-aut-mei=Ken-Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=HottaKatsuyuki
en-aut-sei=Hotta
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=TabataMasahiro
en-aut-sei=Tabata
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=KiuraKatsuyuki
en-aut-sei=Kiura
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

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

affil-num=2
en-affil=Department of Allergy and Respiratory  Medicine, Okayama University Hospital
kn-affil=

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

affil-num=4
en-affil=Department of Hematology, Oncology  and Respiratory Medicine, Okayama  University Graduate School of Medicine,  Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Hematology, Oncology  and Respiratory Medicine, Okayama  University Graduate School of Medicine,  Dentistry, and Pharmaceutical Sciences
kn-affil=

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

affil-num=7
en-affil=Department of Hematology, Oncology  and Respiratory Medicine, Okayama  University Graduate School of Medicine,  Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Hematology, Oncology  and Respiratory Medicine, Okayama  University Graduate School of Medicine,  Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Hematology, Oncology  and Respiratory Medicine, Okayama  University Graduate School of Medicine,  Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Hematology, Oncology  and Respiratory Medicine, Okayama  University Graduate School of Medicine,  Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Center for Clinical Oncology, Okayama  University Hospital
kn-affil=

affil-num=12
en-affil=Department of Hematology and  Oncology, Okayama University Hospital
kn-affil=

affil-num=13
en-affil=Department of Allergy and Respiratory  Medicine, Okayama University Hospital
kn-affil=

affil-num=14
en-affil=Department of Allergy and Respiratory  Medicine, Okayama University Hospital
kn-affil=

affil-num=15
en-affil=Department of Allergy and Respiratory  Medicine, Okayama University Hospital
kn-affil=

affil-num=16
en-affil=Department of Allergy and Respiratory  Medicine, Okayama University Hospital
kn-affil=

affil-num=17
en-affil=Department of Hematology, Oncology  and Respiratory Medicine, Okayama  University Graduate School of Medicine,  Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=18
en-affil=Center for Innovative Clinical Medicine,  Okayama University Hospital
kn-affil=

affil-num=19
en-affil=Center for Clinical Oncology, Okayama  University Hospital
kn-affil=

affil-num=20
en-affil=Department of Hematology, Oncology  and Respiratory Medicine
kn-affil=

affil-num=21
en-affil=Department of Allergy and Respiratory  Medicine, Okayama University Hospital
kn-affil=
en-keyword=alectinib
kn-keyword=alectinib
en-keyword=ALK
kn-keyword=ALK
en-keyword=gilteritinib
kn-keyword=gilteritinib
en-keyword=non-small cell lung cancer
kn-keyword=non-small cell lung cancer
en-keyword=TKI
kn-keyword=TKI
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=16
article-no=
start-page=5174
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230809
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Switching to Dupilumab from Other Biologics without a Treatment Interval in Patients with Severe Asthma: A Multi-Center Retrospective Study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Dupilumab is a fully humanized monoclonal antibody that blocks interleukin4 and interleukin-13 signals. Several large clinical trials have demonstrated the efficacy of dupilumab in patients with severe asthma. However, few studies have examined a switch to dupilumab from other biologics. Methods: This retrospective, multi-center observational study was conducted by the Okayama Respiratory Disease Study Group. Consecutive patients with severe asthma who were switched to dupilumab from other biologics without a treatment interval between May 2019 and September 2021 were enrolled. Patients with a treatment interval of more than twice the standard dosing interval for the previous biologic prior to dupilumab administration were excluded. Results: The median patient age of the 27 patients enrolled in this study was 57 years (IQR, 45-68 years). Eosinophilic chronic rhinosinusitis (ECRS)/chronic rhinosinusitis with nasal polyp (CRSwNP) was confirmed in 23 patients. Previous biologics consisted of omalizumab (n = 3), mepolizumab (n = 3), and benralizumab (n = 21). Dupilumab significantly improved FEV1 (median improvement: +145 mL) and the asthma control test score (median improvement: +2). The overall response rate in patients receiving dupilumab for asthma as determined using the Global Evaluations of Treatment Effectiveness (GETE) was 77.8%. There were no significant differences in the baseline characteristics of the GETE-improved group vs. the non-GETE-improved group. ECRS/CRSwNP improved in 20 of the 23 patients (87.0%). Overall, 8 of the 27 patients (29.6%) developed transient hypereosinophilia (>1500/ mu L), but all were asymptomatic and able to continue dupilumab therapy. Conclusions: Dupilumab was highly effective for the treatment of severe asthma and ECRS/CRSwNP, even in patients switched from other biologics without a treatment interval.
en-copyright=
kn-copyright=

en-aut-name=HigoHisao
en-aut-sei=Higo
en-aut-mei=Hisao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IchikawaHirohisa
en-aut-sei=Ichikawa
en-aut-mei=Hirohisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ArakawaYukako
en-aut-sei=Arakawa
en-aut-mei=Yukako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MoriYoshihiro
en-aut-sei=Mori
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ItanoJunko
en-aut-sei=Itano
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TaniguchiAkihiko
en-aut-sei=Taniguchi
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SenooSatoru
en-aut-sei=Senoo
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KimuraGoro
en-aut-sei=Kimura
en-aut-mei=Goro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TanimotoYasushi
en-aut-sei=Tanimoto
en-aut-mei=Yasushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MiyakeKohei
en-aut-sei=Miyake
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KatsutaTomoya
en-aut-sei=Katsuta
en-aut-mei=Tomoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KataokaMikio
en-aut-sei=Kataoka
en-aut-mei=Mikio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KiuraKatsuyuki
en-aut-sei=Kiura
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=MiyaharaNobuaki
en-aut-sei=Miyahara
en-aut-mei=Nobuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=Okayama Respiratory Disease Study Group (ORDSG)
en-aut-sei=Okayama Respiratory Disease Study Group (ORDSG)
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

affil-num=1
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Respiratory Medicine, KKR Takamatsu Hospital
kn-affil=

affil-num=3
en-affil=Department of Respiratory Medicine, KKR Takamatsu Hospital
kn-affil=

affil-num=4
en-affil=Department of Respiratory Medicine, KKR Takamatsu Hospital
kn-affil=

affil-num=5
en-affil=Department of Allergy and Respiratory Medicine, National Hospital Organization Minami-Okayama Medical Center
kn-affil=

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

affil-num=7
en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Allergy and Respiratory Medicine, National Hospital Organization Minami-Okayama Medical Center
kn-affil=

affil-num=9
en-affil=Department of Allergy and Respiratory Medicine, National Hospital Organization Minami-Okayama Medical Center
kn-affil=

affil-num=10
en-affil=Department of Respiratory Medicine, National Hospital Organization Himeji Medical Center
kn-affil=

affil-num=11
en-affil=Department of Respiratory Medicine, Ehime Prefectural Central Hospital
kn-affil=

affil-num=12
en-affil=Department of Respiratory Medicine, Onomichi Municipal Hospital
kn-affil=

affil-num=13
en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=15
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=16
en-affil=
kn-affil=
en-keyword=dupilumab
kn-keyword=dupilumab
en-keyword=severe asthma
kn-keyword=severe asthma
en-keyword=treatment interval
kn-keyword=treatment interval
en-keyword=eosinophilic chronic rhinosinusitis
kn-keyword=eosinophilic chronic rhinosinusitis
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=2005
dt-pub=20050930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=マウスおよびラット子宮におけるインターロイキン-18の遺伝子発現とその生理作用の解析
kn-title=Analysis of gene expression and physiological roles of interleukin-18 in the mouse and rat uterus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MurakamiYousuke
en-aut-sei=Murakami
en-aut-mei=Yousuke
kn-aut-name=村上要介
kn-aut-sei=村上
kn-aut-mei=要介
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=62
cd-vols=
no-issue=16
article-no=
start-page=2433
end-page=2435
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230815
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cryptococcal Meningitis Developing in a Patient with Neurosarcoidosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cryptococcal meningitis is a critical disease that occasionally involves immunosuppressed patients. We herein report a 79-year-old Japanese man who received low-dose prednisolone therapy for neurosarcoidosis and panhypopituitarism. He presented a 10-day history of a fever and altered mental status. The FilmArray & REG; Meningitis/Encephalitis Panel and serum cryptococcal antigen tests were both negative, but the cerebrospinal fluid sample became positive for Cryptococcus neoformans after seven-day incubation. After the diagnosis of cryptococcal meningitis, we successfully treated the patient with a recommended treatment regimen. When an immunocompromised patient presents with a subacute fever accompanying any central nervous symptoms, cryptococcal meningitis should be screened for.
en-copyright=
kn-copyright=

en-aut-name=FukushimaShinnosuke
en-aut-sei=Fukushima
en-aut-mei=Shinnosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HagiyaHideharu
en-aut-sei=Hagiya
en-aut-mei=Hideharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamamotoYukichika
en-aut-sei=Yamamoto
en-aut-mei=Yukichika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OguniKohei
en-aut-sei=Oguni
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HasegawaKou
en-aut-sei=Hasegawa
en-aut-mei=Kou
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

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

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

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

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

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

affil-num=6
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=cryptococcal meningitis
kn-keyword=cryptococcal meningitis
en-keyword=Cryptococcus neoformans
kn-keyword=Cryptococcus neoformans
en-keyword=neurosarcoidosis
kn-keyword=neurosarcoidosis
en-keyword=interleukin-6
kn-keyword=interleukin-6
END

start-ver=1.4
cd-journal=joma
no-vol=77
cd-vols=
no-issue=4
article-no=
start-page=395
end-page=405
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Association of Tumor Necrosis Factor-Alpha with Psychopathology in Patients with Schizophrenia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We investigated the relationship between serum tumor necrosis factor-alpha (TNF-α) levels and psychopathological symptoms, clinical and socio-demographic characteristics and antipsychotic therapy in individuals with schizophrenia. TNF-α levels were measured in 90 patients with schizophrenia and 90 healthy controls matched by age, gender, smoking status, and body mass index. The Positive and Negative Syndrome Scale (PANSS) was used to assess the severity of psychopathology in patients. No significant differences in TNF-α levels were detected between the patients and controls (p=0.736). TNF-α levels were not correlated with total, positive, negative, general, or composite PANSS scores (all p>0.05). A significant negative correlation was observed between TNF-α levels and the PANSS cognitive factor (ρ=?0.222, p=0.035). A hierarchical regression analysis identified the cognitive factor as a significant predictor of the TNF-α level (beta=?0.258, t=?2.257, p=0.027). There were no significant differences in TNF-α levels among patients treated with different types of antipsychotics (p=0.596). TNF-α levels correlated positively with the age of onset (ρ=0.233, p=0.027) and negatively with illness duration (ρ=?0.247, p=0.019) and antipsychotic treatment duration (ρ=?0.256, p=0.015). These results indicate that TNF-α may be involved in cognitive impairment in schizophrenia, and would be a potential clinical-state marker in schizophrenia.
en-copyright=
kn-copyright=

en-aut-name=PavlovicMarko
en-aut-sei=Pavlovic
en-aut-mei=Marko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=BabicDragan
en-aut-sei=Babic
en-aut-mei=Dragan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=RastovicPejana
en-aut-sei=Rastovic
en-aut-mei=Pejana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ArapovicJurica
en-aut-sei=Arapovic
en-aut-mei=Jurica
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MartinacMarko
en-aut-sei=Martinac
en-aut-mei=Marko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=JakovacSanja
en-aut-sei=Jakovac
en-aut-mei=Sanja
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=BarbaricRomana
en-aut-sei=Barbaric
en-aut-mei=Romana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=University Hospital Center Mostar, University of Mostar
kn-affil=

affil-num=2
en-affil=University Hospital Center Mostar, University of Mostar
kn-affil=

affil-num=3
en-affil=University Hospital Center Mostar, University of Mostar
kn-affil=

affil-num=4
en-affil=University Hospital Center Mostar, University of Mostar
kn-affil=

affil-num=5
en-affil=Health Care Center Mostar, University of Mostar
kn-affil=

affil-num=6
en-affil=University Hospital Center Mostar, University of Mostar
kn-affil=

affil-num=7
en-affil=University Hospital Center Mostar, University of Mostar
kn-affil=
en-keyword=tumor necrosis factor-alpha
kn-keyword=tumor necrosis factor-alpha
en-keyword=schizophrenia
kn-keyword=schizophrenia
en-keyword=psychopathology
kn-keyword=psychopathology
en-keyword=immune system
kn-keyword=immune system
END

start-ver=1.4
cd-journal=joma
no-vol=77
cd-vols=
no-issue=4
article-no=
start-page=359
end-page=364
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Changes in TRPV1 Receptor, CGRP, and BDNF Expression in Rat Dorsal Root Ganglion with Resiniferatoxin-Induced Neuropathic Pain: Modulation by Pulsed Radiofrequency Applied to the Sciatic Nerve
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pulsed radiofrequency (PRF) is a safe method of treating neuropathic pain by generating intermittent electric fields at the needle tip. Resiniferatoxin (RTX) is an ultrapotent agonist of transient receptor potential vanilloid subtype-1 (TRPV1) receptors. We investigated the mechanism of PRF using a rat model of RTX-induced neuropathic pain. After administering RTX intraperitoneally, PRF was applied to the right sciatic nerve. We observed the changes in TRPV1, calcitonin gene-related peptide (CGRP), and brain-derived neurotrophic factor (BDNF) in the dorsal root ganglia by western blotting. Expressions of TRPV1 and CGRP were significantly lower in the contralateral (RTX-treated, PRF-untreated) tissue than in control rats (p<0.0001 and p<0.0001, respectively) and the ipsilateral tissues (p<0.0001 and p<0.0001, respectively). BDNF levels were significantly higher in the contralateral tissues than in the control rats (p<0.0001) and the ipsilateral tissues (p<0.0001). These results suggest that, while TRPV1 and CGRP are decreased by RTX-induced neuronal damage, increased BDNF levels result in pain development. PRF may promote recovery from neuronal damage with concomitant restoration of TRPV1 and CGRP, and exert its analgesic effect by reversing BDNF increase. Further research is required to understand the role of TRPV1 and CGRP restoration in improving mechanical allodynia.
en-copyright=
kn-copyright=

en-aut-name=KoshidaTomohiro
en-aut-sei=Koshida
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MarutaToyoaki
en-aut-sei=Maruta
en-aut-mei=Toyoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TanakaNobuhiko
en-aut-sei=Tanaka
en-aut-mei=Nobuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HidakaKotaro
en-aut-sei=Hidaka
en-aut-mei=Kotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KurogiMio
en-aut-sei=Kurogi
en-aut-mei=Mio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NemotoTakayuki
en-aut-sei=Nemoto
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YanagitaToshihiko
en-aut-sei=Yanagita
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakeyaRyu
en-aut-sei=Takeya
en-aut-mei=Ryu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TsuneyoshiIsao
en-aut-sei=Tsuneyoshi
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
kn-affil=

affil-num=2
en-affil=Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
kn-affil=

affil-num=3
en-affil=Tanaka homecare clinic
kn-affil=

affil-num=4
en-affil=Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
kn-affil=

affil-num=5
en-affil=Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
kn-affil=

affil-num=6
en-affil=Department of Pharmacology, Faculty of Medicine, Fukuoka University
kn-affil=

affil-num=7
en-affil=Department of Clinical Pharmacology, School of Nursing, Faculty of Medicine, University of Miyazaki
kn-affil=

affil-num=8
en-affil=Department of Pharmacology, Faculty of Medicine, University of Miyazaki
kn-affil=

affil-num=9
en-affil=Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
kn-affil=
en-keyword=pulsed radiofrequency
kn-keyword=pulsed radiofrequency
en-keyword=resiniferatoxin
kn-keyword=resiniferatoxin
en-keyword=transient receptor potential vanilloid subtype-1 (TRPV1)
kn-keyword=transient receptor potential vanilloid subtype-1 (TRPV1)
en-keyword=calcitonin gene-related peptide (CGRP)
kn-keyword=calcitonin gene-related peptide (CGRP)
en-keyword=brain-derived neurotrophic factor (BDNF)
kn-keyword=brain-derived neurotrophic factor (BDNF)
END

start-ver=1.4
cd-journal=joma
no-vol=45
cd-vols=
no-issue=7
article-no=
start-page=5263
end-page=5275
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230621
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Update in Molecular Aspects and Diagnosis of Autoimmune Gastritis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Recent studies have advanced our understanding of the pathophysiology of autoimmune gastritis, particularly its molecular aspects. The most noteworthy recent advancement lies in the identification of several candidate genes implicated in the pathogenesis of pernicious anemia through genome-wide association studies. These genes include PTPN22, PNPT1, HLA-DQB1, and IL2RA. Recent studies have also directed attention towards other genes such as ATP4A, ATP4B, AIRE, SLC26A7, SLC26A9, and BACH2 polymorphism. In-depth investigations have been conducted on lymphocytes and cytokines, including T helper 17 cells, interleukin (IL)-17A, IL-17E, IL-17F, IL-21, IL-19, tumor necrosis factor-α, IL-15, transforming growth factor-β1, IL-13, and diminished levels of IL-27. Animal studies have explored the involvement of roseolovirus and H. pylori in relation to the onset of the disease and the process of carcinogenesis, respectively. Recent studies have comprehensively examined the involvement of autoantibodies, serum pepsinogen, and esophagogastroduodenoscopy in the diagnosis of autoimmune gastritis. The current focus lies on individuals demonstrating atypical presentations of the disease, including those diagnosed in childhood, those yielding negative results for autoantibodies, and those lacking the typical endoscopic characteristics of mucosal atrophy. Here, we discuss the recent developments in this field, focusing on genetic predisposition, epigenetic modifications, lymphocytes, cytokines, oxidative stress, infectious agents, proteins, microRNAs, autoantibodies, serum pepsinogen, gastrin, esophagogastroduodenoscopy and microscopic findings, and the risk of gastric neoplasm.
en-copyright=
kn-copyright=

en-aut-name=IwamuroMasaya
en-aut-sei=Iwamuro
en-aut-mei=Masaya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanakaTakehiro
en-aut-sei=Tanaka
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OtsukaMotoyuki
en-aut-sei=Otsuka
en-aut-mei=Motoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

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

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

affil-num=3
en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=autoimmune gastritis
kn-keyword=autoimmune gastritis
en-keyword=esophagogastroduodenoscopy
kn-keyword=esophagogastroduodenoscopy
en-keyword=genetic predisposition
kn-keyword=genetic predisposition
en-keyword=lymphocyte
kn-keyword=lymphocyte
en-keyword=oxidative stress
kn-keyword=oxidative stress
END

start-ver=1.4
cd-journal=joma
no-vol=108
cd-vols=
no-issue=
article-no=
start-page=110717
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=STAT1/3 signaling suppresses axon degeneration and neuronal cell death through regulation of NAD+-biosynthetic and consuming enzymes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Nicotinamide adenine dinucleotide (NAD)+-biosynthetic and consuming enzymes are involved in various intracellular events through the regulation of NAD+ metabolism. Recently, it has become clear that alterations in the expression of NAD+-biosynthetic and consuming enzymes contribute to the axonal stability of neurons. We explored soluble bioactive factor(s) that alter the expression of NAD+-metabolizing enzymes and found that cytokine interferon (IFN)-γ increased the expression of nicotinamide nucleotide adenylyltransferase 2 (NMNAT2), an NAD+-biosynthetic enzyme. IFN-γ activated signal transducers and activators of transcription 1 and 3 (STAT1/3) followed by c-Jun N-terminal kinase (JNK) suppression. As a result, STAT1/3 increased the expression of NMNAT2 at both mRNA and protein levels in a dose- and time-dependent manner and, at the same time, suppressed activation of sterile alpha and Toll/interleukin receptor motif-containing 1 (SARM1), an NAD+-consuming enzyme, and increased intracellular NAD+ levels. We examined the protective effect of STAT1/3 signaling against vincristine-mediated cell injury as a model of chemotherapy-induced peripheral neuropathy (CIPN), in which axonal degeneration is involved in disease progression. We found that IFN-γ-mediated STAT1/3 activation inhibited vincristine-induced downregulation of NMNAT2 and upregulation of SARM1 phosphorylation, resulting in modest suppression of subsequent neurite degradation and cell death. These results indicate that STAT1/3 signaling induces NMNAT2 expression while simultaneously suppressing SARM1 phosphorylation, and that both these actions contribute to suppression of axonal degeneration and cell death.
en-copyright=
kn-copyright=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YasuiYu
en-aut-sei=Yasui
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OisoKazuma
en-aut-sei=Oiso
en-aut-mei=Kazuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OchiToshiki
en-aut-sei=Ochi
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamamotoKen-ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

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

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

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

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

affil-num=8
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=NMNAT2
kn-keyword=NMNAT2
en-keyword=SARM1
kn-keyword=SARM1
en-keyword=NAD+
kn-keyword=NAD+
en-keyword=STAT1/3
kn-keyword=STAT1/3
en-keyword=IFN-γ
kn-keyword=IFN-γ
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=2023
dt-pub=20230324
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=同種造血幹細胞移植後の低用量IL?２療法が制御性T細胞およびエフェクターT細胞に与える効果はホストの免疫状態に依存する
kn-title=Responses of regulatory and effector T-cells to low-dose interleukin-2 differ depending on the immune environment after allogeneic stem cell transplantation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MEGURIYusuke
en-aut-sei=MEGURI
en-aut-mei=Yusuke
kn-aut-name=?勇輔
kn-aut-sei=?
kn-aut-mei=勇輔
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=63
cd-vols=
no-issue=1
article-no=
start-page=25
end-page=31
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=2023
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Comparison of serum sIL-2R and LDH levels in patients with intravascular large B-cell lymphoma and patients with advanced stage diffuse large B-cell lymphoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Intravascular large B-cell lymphoma (IVL) is a rare type of lymphoma characterized by tumor growth selectively within the vessels. The 5th edition of the World Health Organization classification defines IVL as a large B-cell lymphoma, the same as diffuse large B-cell lymphoma, not otherwise specified (DLBCL, NOS). Since the clinical manifestations of IVL are nonspecific, the diagnosis is time-consuming, and the course is often fatal. Serum soluble interleukin-2 receptor (sIL-2R) and serum lactate dehydrogenase (LDH) levels are known to be elevated in a variety of lymphomas. However, the mechanism of sIL-2R elevation in B-cell lymphomas is not fully understood. In this study, we analyzed the serum level of laboratory findings, including sIL-2R and LDH, as well as the presence of B symptoms in 39 patients with IVL, and compared them with 56 patients with stage IV DLBCL. Both sIL-2R and LDH levels were significantly higher in IVL than in DLBCL (p = 0.035 andp = 0.002, respectively). In IVL, there were no significant differences in both sIL-2R and LDH levels between patients with and without B symptoms (p = 0.206 andp = 0.441, respectively). However, in DLBCL, both sIL-2R and LDH levels were significantly higher in the presence of B symptoms (p = 0.001 andp < 0.001, respectively). The high sIL-2R and LDH levels in IVL may be related to the peripheral blood microenvironment, but further studies are needed to verify this.
en-copyright=
kn-copyright=

en-aut-name=HiramiYuki
en-aut-sei=Hirami
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishimuraMidori Filiz
en-aut-sei=Nishimura
en-aut-mei=Midori Filiz
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UrataTomohiro
en-aut-sei=Urata
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MorimotoMichiko
en-aut-sei=Morimoto
en-aut-mei=Michiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MaekawaYukina
en-aut-sei=Maekawa
en-aut-mei=Yukina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YoshinoTadashi
en-aut-sei=Yoshino
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NishimuraYoshito
en-aut-sei=Nishimura
en-aut-mei=Yoshito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SatoYasuharu
en-aut-sei=Sato
en-aut-mei=Yasuharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

affil-num=3
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

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

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

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

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

affil-num=8
en-affil=Department of Molecular Hematopathology, Okayama University Graduate  School of Health Sciences
kn-affil=
en-keyword=intravascular large B-cell lymphoma
kn-keyword=intravascular large B-cell lymphoma
en-keyword=diffuse large B-cell lymphoma
kn-keyword=diffuse large B-cell lymphoma
en-keyword=soluble interleukin-2 receptor
kn-keyword=soluble interleukin-2 receptor
en-keyword=lactate dehy-drogenase
kn-keyword=lactate dehy-drogenase
en-keyword=B symptoms
kn-keyword=B symptoms
END

start-ver=1.4
cd-journal=joma
no-vol=77
cd-vols=
no-issue=1
article-no=
start-page=37
end-page=43
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202302
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Efficacy of Inflammatory and Immune Markers for Predicting the Prognosis of Patients with Stage IV Breast Cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Systemic therapy for stage IV breast cancer is usually an initial treatment and is based on findings regarding biomarkers (e.g., hormone receptors and human epidermal growth factor receptor-2 [HER2]). However, the response to therapy and outcomes sometime differ among patients with similar prognostic factors including grade, hormone receptor, HER2, and more. We conducted retrospective analyses to evaluate the correlations between the overall survival (OS) of 46 stage IV breast cancer patients and (i) the peripheral absolute lymphocyte count (ALC) and (ii) composite blood cell markers. The peripheral blood cell markers included the neutrophil- to-lymphocyte ratio (NLR), the monocyte-to-lymphocyte ratio (MLR), the systemic immune-inflammation index (SII), the systemic inflammation response index (SIRI), and the most recently introduced indicator, the pan-immune-inflammatory value (PIV). The SIRI and PIV showed prognostic impacts on the patients: those with a low SIRI or a low PIV showed significantly better OS than those with a high SIRI (5-year, 66.0% vs. 35.0%, p<0.05) or high PIV (5-year, 68.1% vs. 38.5%, p<0.05), respectively. This is the first report indicating the possible prognostic value of the PIV for OS in patients with stage IV breast cancer. Further studies with larger numbers of patients are necessary for further clarification.
en-copyright=
kn-copyright=

en-aut-name=YamanouchiKosho
en-aut-sei=Yamanouchi
en-aut-mei=Kosho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MaedaShigeto
en-aut-sei=Maeda
en-aut-mei=Shigeto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Surgery, National Hospital Organization, Nagasaki Medical Center
kn-affil=

affil-num=2
en-affil=Department of Surgery, National Hospital Organization, Nagasaki Medical Center
kn-affil=
en-keyword=breast cancer
kn-keyword=breast cancer
en-keyword=pan-immune-inflammatory value
kn-keyword=pan-immune-inflammatory value
en-keyword=prognosis
kn-keyword=prognosis
END

start-ver=1.4
cd-journal=joma
no-vol=172
cd-vols=
no-issue=5
article-no=
start-page=1522
end-page=1528
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202211
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Luminal administration of biliverdin ameliorates ischemia-reperfusion injury following intestinal transplant in rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Intestinal grafts are susceptible to ischemia-reperfusion injury, resulting in the loss of mucosal barrier function and graft failure. Biliverdin is known to exert a variety of cytoprotective functions against oxidative tissue injury. Because the mucosal layer is the primary site of ischemiareperfusion injury, mucosa-targeting strategies by luminal delivery of reagents might be beneficial. We tested whether intraluminal administration of biliverdin as an adjuvant to standard preservation solutions protected against ischemia-reperfusion injury. <br><br>
Methods: Orthotopic syngeneic intestinal transplants were performed on Lewis rats after 6 hours of cold preservation. Saline containing biliverdin (10 mM) or without biliverdin was introduced into the lumen of the intestinal grafts immediately before cold preservation. <br><br>
Results: Damage to the intestinal mucosa caused by ischemia-reperfusion injury resulted in severe morphological changes, including blunting of the villi and erosion, and led to significant loss of gut barrier function 3 hours after reperfusion. These changes to the mucosa were notably ameliorated by intraluminal administration of biliverdin. Biliverdin also effectively inhibited upregulation of messenger RNAs for interleukin-6, inducible nitric oxide synthase, and C-C motif chemokine 2. Additionally, biliverdin treatment prevented the loss of expression of claudin-1, a transmembrane, tight-junction barrier protein. The 14-day survival of recipients of biliverdin-treated grafts was significantly improved as compared with the recipients of saline-treated control grafts (83.3% vs 38.9%, P 1/4 .030). <br><br>
Conclusion: This study demonstrated that luminally delivered biliverdin provides beneficial effects during the transplant of rat small intestinal grafts and could be an attractive therapeutic option in organ transplantation.
en-copyright=
kn-copyright=

en-aut-name=NojimaTsuyoshi
en-aut-sei=Nojima
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ObaraTakafumi
en-aut-sei=Obara
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamamotoHirotsugu
en-aut-sei=Yamamoto
en-aut-mei=Hirotsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YumotoTetsuya
en-aut-sei=Yumoto
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IgawaTakuro
en-aut-sei=Igawa
en-aut-mei=Takuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AokageToshiyuki
en-aut-sei=Aokage
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SeyaMizuki
en-aut-sei=Seya
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakaoAtsunori
en-aut-sei=Nakao
en-aut-mei=Atsunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NaitoHiromichi
en-aut-sei=Naito
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

affil-num=6
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=6
article-no=
start-page=635
end-page=643
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=MiR-338-3p Is a Biomarker in Neonatal Acute Respiratory Distress Syndrome (ARDS) and Has Roles in the Inflammatory Response of ARDS Cell Models
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To investigate the association between serum miR-338-3p levels and neonatal acute respiratory distress syndrome (ARDS) and its mechanism. The relative miR-338-3p expression in serum was detected by quantitative real-time RT-PCR. Interleukin-1beta (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α) levels were detected by ELISAs. A receiver operating characteristic (ROC) curve analysis of serum miR-338-3p evaluated the diagnosis of miR-338-3p in neonatal ARDS. Pearson’s correlation analysis evaluated the correlation between serum miR-338-3p and neonatal ARDS clinical factors. Flow cytometry evaluated apoptosis, and a CCK-8 assay assessed cell viability. A luciferase assay evaluated the miR-338-3p/AKT3 relationship. The miR- 338-3p expression was decreased in neonatal ARDS patients and in lipopolysaccharide (LPS)-treated cells. The ROC curve showed the accuracy of miR-338-3p for evaluating neonatal ARDS patients. The correlation analysis demonstrated that miR-338-3p was related to PRISM-III, PaO2/FiO2, oxygenation index, IL-1β, IL-6, and TNF-α in neonatal ARDS patients. MiR-338-3p overexpression inhibited the secretion of inflammatory components, stifled cell apoptosis, and LPS-induced advanced cell viability. The double-luciferase reporter gene experiment confirmed that miR-338-3p negatively regulates AKT3 mRNA expression. Serum miR-338-3p levels were related to the diagnosis and severity of neonatal ARDS, which may be attributed to its regulatory effect on inflammatory response in ARDS.
en-copyright=
kn-copyright=

en-aut-name=ZhangCuicui
en-aut-sei=Zhang
en-aut-mei=Cuicui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=JiYanan
en-aut-sei=Ji
en-aut-mei=Yanan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WangQin
en-aut-sei=Wang
en-aut-mei=Qin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=RuanLianying
en-aut-sei=Ruan
en-aut-mei=Lianying
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Pediatric Intensive Care Unit, Xingtai People’s Hospital
kn-affil=

affil-num=2
en-affil=Pediatric Intensive Care Unit, Xingtai People’s Hospital
kn-affil=

affil-num=3
en-affil=Pediatric Intensive Care Unit, Xingtai People’s Hospital
kn-affil=

affil-num=4
en-affil=Pediatric Intensive Care Unit, Xingtai People’s Hospital
kn-affil=
en-keyword=miR-338-3p
kn-keyword=miR-338-3p
en-keyword=AKT3
kn-keyword=AKT3
en-keyword=neonatal ARDS
kn-keyword=neonatal ARDS
en-keyword=inflammation
kn-keyword=inflammation
en-keyword=diagnosis
kn-keyword=diagnosis
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=
article-no=
start-page=890048
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220812
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Anxiolytic-like effects of hochuekkito in lipopolysaccharide-treated mice involve interleukin-6 inhibition
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Hochuekkito (HET) is a Kampo medicine used to treat postoperative and post-illness general malaise and decreased motivation. HET is known to regulate immunity and modulate inflammation. However, the precise mechanism and effects of HET on inflammation-induced central nervous system disorders remain unclear. This study aimed to assess the effect of HET on inflammation-induced anxiety-like behavior and the mechanism underlying anxiety-like behavior induced by lipopolysaccharide (LPS). Institute of Cancer Research mice were treated with LPS (300 mu g/kg, intraperitoneally), a bacterial endotoxin, to induce systemic inflammation. The mice were administered HET (1.0 g/kg, orally) once a day for 2 weeks before LPS treatment. The light-dark box test and the hole-board test were performed 24 h after the LPS injection to evaluate the effects of HET on anxiety-like behaviors. Serum samples were obtained at 2, 5, and 24 h after LPS injection, and interleukin-6 (IL-6) levels in serum were measured. Human and mouse macrophage cells (THP-1 and RAW264.7 cells, respectively) were used to investigate the effect of HET on LPS-induced IL-6 secretion. The repeated administration of HET prevented anxiety-like behavior and decreased serum IL-6 levels in LPS-treated mice. HET significantly suppressed LPS-induced IL-6 secretion in RAW264.7 and THP-1 cells. Similarly, glycyrrhizin, one of the chemical constituents of HET, suppressed LPS-induced anxiety-like behaviors. Our study revealed that HET ameliorated LPS-induced anxiety-like behavior and inhibited IL-6 release in vivo and in vitro. Therefore, we postulate that HET may be useful against inflammation-induced anxiety-like behavior.
en-copyright=
kn-copyright=

en-aut-name=UshioSoichiro
en-aut-sei=Ushio
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WadaYudai
en-aut-sei=Wada
en-aut-mei=Yudai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraMizuki
en-aut-sei=Nakamura
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MatsumotoDaiki
en-aut-sei=Matsumoto
en-aut-mei=Daiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HoshikaKota
en-aut-sei=Hoshika
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShiromizuShoya
en-aut-sei=Shiromizu
en-aut-mei=Shoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IwataNaohiro
en-aut-sei=Iwata
en-aut-mei=Naohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=EsumiSatoru
en-aut-sei=Esumi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KajizonoMakoto
en-aut-sei=Kajizono
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KitamuraYoshihisa
en-aut-sei=Kitamura
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SendoToshiaki
en-aut-sei=Sendo
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=

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

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

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

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

affil-num=6
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=
en-keyword=anxiolytic
kn-keyword=anxiolytic
en-keyword=inflammation
kn-keyword=inflammation
en-keyword=immunomodulation
kn-keyword=immunomodulation
en-keyword=macrophages
kn-keyword=macrophages
en-keyword=Kampo medicine
kn-keyword=Kampo medicine
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=17
article-no=
start-page=10632
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220826
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Immunomodulatory Effects of Radon Inhalation on Lipopolysaccharide-Induced Inflammation in Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Typical indications for radon therapy include autoimmune diseases such as rheumatoid arthritis (RA). We had previously reported that radon inhalation inhibits Th17 immune responses in RA mice by activating Th1 and Th2 immune responses. However, there are no reports on how radon inhalation affects the activated Th1 and Th17 immune responses, and these findings may be useful for identifying new indications for radon therapy. Therefore, in this study, we investigated the effect of radon inhalation on the lipopolysaccharide (LPS)-induced inflammatory response, focusing on the expression of related cytokines and antioxidant function. Male BALB/c mice were exposed to 2000 Bq/m(3) radon for one day. Immediately after radon inhalation, LPS was administered intraperitoneally at 1.0 mg/kg body weight for 4 h. LPS administration increased the levels of Th1- and Th17-prone cytokines, such as interleukin-2, tumor necrosis factor-alpha, and granulocyte-macrophage colony-stimulating factor, compared to no treatment control (sham). However, these effects were suppressed by radon inhalation. IL-10 levels were significantly increased by LPS administration, with or without radon inhalation, compared to sham. However, radon inhalation did not inhibit oxidative stress induced by LPS administration. These findings suggest that radon inhalation has immunomodulatory but not antioxidative functions in LPS-induced injury.
en-copyright=
kn-copyright=

en-aut-name=KataokaTakahiro
en-aut-sei=Kataoka
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NaoeShota
en-aut-sei=Naoe
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MurakamiKaito
en-aut-sei=Murakami
en-aut-mei=Kaito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FujimotoYuki
en-aut-sei=Fujimoto
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YukimineRyohei
en-aut-sei=Yukimine
en-aut-mei=Ryohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TanakaAyumi
en-aut-sei=Tanaka
en-aut-mei=Ayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamaokaKiyonori
en-aut-sei=Yamaoka
en-aut-mei=Kiyonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

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

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

affil-num=3
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

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

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

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

affil-num=7
en-affil=Faculty of Health Sciences, Okayama University
kn-affil=
en-keyword=autoimmune diseases
kn-keyword=autoimmune diseases
en-keyword=cytokine
kn-keyword=cytokine
en-keyword=antioxidant function
kn-keyword=antioxidant function
en-keyword=lipopolysaccharide
kn-keyword=lipopolysaccharide
en-keyword=radon inhalation
kn-keyword=radon inhalation
END

start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=4
article-no=
start-page=359
end-page=371
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202208
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Therapeutic Approaches Targeting miRNA in Systemic Lupus Erythematosus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Systemic lupus erythematosus (SLE) is a potentially fatal systemic autoimmune disease, and its etiology involves both genetic and environmental factors such as sex hormone imbalance, genetic predisposition, epigenetic regulation, and immunological factors. Dysregulation of microRNA (miRNA) is suggested to be one of the epigenetic factors in SLE. miRNA is a 22-nucleotide single-stranded noncoding RNA that contributes to post-transcriptional modulation of gene expression. miRNA targeting therapy has been suggested to be useful for the treatment of cancers and other diseases. Gene knockout and miRNA targeting therapy have been demonstrated to improve SLE disease activity in mice. However, these approaches have not yet reached the level of clinical application. miRNA targeting therapy is limited by the fact that each miRNA has multiple targets. In addition, the expression of certain miRNAs may differ among cell tissues within a single SLE patient. This limitation can be overcome by targeted delivery and chemical modifications. In the future, further research into miRNA chemical modifications and delivery systems will help us develop novel therapeutic agents for SLE.
en-copyright=
kn-copyright=

en-aut-name=Hiramatsu-AsanoSumie
en-aut-sei=Hiramatsu-Asano
en-aut-mei=Sumie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

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

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=
en-keyword=systemic lupus erythematosus
kn-keyword=systemic lupus erythematosus
en-keyword=miRNA
kn-keyword=miRNA
en-keyword=miRNA targeting therapy
kn-keyword=miRNA targeting therapy
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=
article-no=
start-page=891925
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220802
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Responses of regulatory and effector T-cells to low-dose interleukin-2 differ depending on the immune environment after allogeneic stem cell transplantation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=CD4(+)Foxp3(+) regulatory T cells (Tregs) play a central role in the maintenance of immune tolerance after allogeneic hematopoietic stem cell transplantation (HSCT). Tregs promptly respond to low concentrations of IL-2 through the constitutive expression of high-affinity IL-2 receptors. It has been reported that low-dose IL-2 therapy increased circulating Tregs and improved clinical symptoms of chronic GVHD. Clinical studies of IL-2 therapy so far have mainly targeted patients in the chronic phase of transplantation when acute immune responses has subsided. However, the biological and clinical effects of exogenous IL-2 in an acute immune environment have not been well investigated. In the current study, we investigated the impact of exogenous IL-2 therapy on the post-transplant homeostasis of T cell subsets which influence the balance between GVHD and GVL in the acute phase, by setting the various immune environments early after HSCT in murine model. We initially found that 5,000 IU of IL-2 was enough to induce the active proliferation of Treg without influencing other conventional T cells (Tcons) when administered to normal mice. However, activated Tcons showed the response to the same dose of IL-2 in recipients after allogeneic HSCT. In a mild inflammatory environment within a threshold, exogenous IL-2 could effectively modulate Treg homeostasis with just limited influence to activated T cells, which resulted in an efficient GVHD suppression. In contrast, in a severely inflammatory environment, exogenous IL-2 enhanced activated T cells rather than Tregs, which resulted in the exacerbation of GVHD. Of interest, in an immune-tolerant state after transplant, exogenous IL-2 triggered effector T-cells to exert an anti-tumor effect with maintaining GVHD suppression. These data suggested that the responses of Tregs and effector T cells to exogenous IL-2 differ depending on the immune environment in the host, and the mutual balance of the response to IL-2 between T-cell subsets modulates GVHD and GVL after HSCT. Our findings may provide useful information in the optimization of IL-2 therapy, which may be personalized for each patient having different immune status.
en-copyright=
kn-copyright=

en-aut-name=MeguriYusuke
en-aut-sei=Meguri
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AsanoTakeru
en-aut-sei=Asano
en-aut-mei=Takeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YoshiokaTakanori
en-aut-sei=Yoshioka
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IwamotoMiki
en-aut-sei=Iwamoto
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IkegawaShuntaro
en-aut-sei=Ikegawa
en-aut-mei=Shuntaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SugiuraHiroyuki
en-aut-sei=Sugiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KishiYuriko
en-aut-sei=Kishi
en-aut-mei=Yuriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakamuraMakoto
en-aut-sei=Nakamura
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SandoYasuhisa
en-aut-sei=Sando
en-aut-mei=Yasuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KondoTakumi
en-aut-sei=Kondo
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SumiiYuichi
en-aut-sei=Sumii
en-aut-mei=Yuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MatsuokaKen-Ichi
en-aut-sei=Matsuoka
en-aut-mei=Ken-Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

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

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

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

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

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

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

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

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

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

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

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

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

affil-num=13
en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=regulatory T cell
kn-keyword=regulatory T cell
en-keyword=low-dose interleukin-2 therapy
kn-keyword=low-dose interleukin-2 therapy
en-keyword=graft-versus-host disease
kn-keyword=graft-versus-host disease
en-keyword=graft-versus-leukemia effect
kn-keyword=graft-versus-leukemia effect
en-keyword=transplantation tolerance
kn-keyword=transplantation tolerance
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=
article-no=
start-page=904215
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pemafibrate Prevents Rupture of Angiotensin II-Induced Abdominal Aortic Aneurysms
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Abdominal aortic aneurysm (AAA) is a life-threatening disease that lacks effective preventive therapies. This study aimed to evaluate the effect of pemafibrate, a selective peroxisome proliferator-activated receptor alpha (PPAR alpha) agonist, on AAA formation and rupture. <br>
Methods: Experimental AAA was induced by subcutaneous angiotensin II (AngII) infusion in ApoE(-)(/)(-) mice for 4 weeks. Pemafibrate (0.1 mg/kg/day) was administered orally. Dihydroethidium staining was used to evaluate the reactive oxygen species (ROS). <br>
Results: The size of the AngII-induced AAA did not differ between pemafibrate- and vehicle-treated groups. However, a decreased mortality rate due to AAA rupture was observed in pemafibrate-treated mice. Pemafibrate ameliorated AngII-induced ROS and reduced the mRNA expression of interleukin-6 and tumor necrosis factor-alpha in the aortic wall. Gelatin zymography analysis demonstrated significant inhibition of matrix metalloproteinase-2 activity by pemafibrate. AngII-induced ROS production in human vascular smooth muscle cells was inhibited by pre-treatment with pemafibrate and was accompanied by an increase in catalase activity. Small interfering RNA-mediated knockdown of catalase or PPAR alpha significantly attenuated the anti-oxidative effect of pemafibrate. <br>
Conclusion: Pemafibrate prevented AAA rupture in a murine model, concomitant with reduced ROS, inflammation, and extracellular matrix degradation in the aortic wall. The protective effect against AAA rupture was partly mediated by the anti-oxidative effect of catalase induced by pemafibrate in the smooth muscle cells.
en-copyright=
kn-copyright=

en-aut-name=AmiokaNaofumi
en-aut-sei=Amioka
en-aut-mei=Naofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YonezawaTomoko
en-aut-sei=Yonezawa
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoMegumi
en-aut-sei=Kondo
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
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=9
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Molecular Biology and Biochemistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=pemafibrate
kn-keyword=pemafibrate
en-keyword=angiotensin II
kn-keyword=angiotensin II
en-keyword=abdominal aortic aneurysm
kn-keyword=abdominal aortic aneurysm
en-keyword=oxidative stress
kn-keyword=oxidative stress
en-keyword=catalase
kn-keyword=catalase
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=2022
dt-pub=20220712
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Lung recruitment after cardiac arrest during procurement of atelectatic donor lungs is a protective measure in lung transplantation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Brain-dead donors are susceptible to pulmonary atelectasis (AT). In procurement surgery, lung recruitment under circulatory conditions and cold-flushing for atelectatic donor lungs often provoke graft injury due to the acute blood inflow. We hypothesized that lung recruitment without blood circulation can mitigate graft injury. This study aimed to examine the benefits of lung recruitment subsequent to cardiac arrest using a porcine lung-transplant model.<br>
<br>
Methods: Thirteen donor pigs were categorized into the non-atelectatic (No-AT) group (n=3) representing a healthy control group; AT-BCR group (n=5), in which AT was reverted by conventional blood-circulated recruitment (BCR); and AT-no-BCR group (n=5), in which AT was reverted by no-BCR following circulatory arrest. In the atelectatic donor models, the left main bronchus was ligated for 24 hours prior to lung procurement. Left lung transplantation (LTx) was subsequently performed in the thirteen recipient pigs. After 6 hours evaluation, the recipients were euthanized and the lung grafts were excised.<br>
<br>
Results: The post-transplant PaO2/FiO(2) ratio was significantly higher in the AT-no-BCR group than in the AT-BCR group (P=0.015). Wet/dry ratio, histological findings of graft injury and tissue interleukin-8 expression in the AT-no-BCR group were similar to those of the No-AlT group.<br>
<br>
Conclusions: Lung recruitment without circulation after circulatory arrest could be more protective for atelectatic donor lung than the conventional procedure.
en-copyright=
kn-copyright=

en-aut-name=NimanEito
en-aut-sei=Niman
en-aut-mei=Eito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiKentaroh
en-aut-sei=Miyoshi
en-aut-mei=Kentaroh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShiotaniToshio
en-aut-sei=Shiotani
en-aut-mei=Toshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TojiTomohiro
en-aut-sei=Toji
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IgawaTakuro
en-aut-sei=Igawa
en-aut-mei=Takuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OtaniShinji
en-aut-sei=Otani
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OkazakiMikio
en-aut-sei=Okazaki
en-aut-mei=Mikio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SugimotoSeiichiro
en-aut-sei=Sugimoto
en-aut-mei=Seiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YamaneMasaomi
en-aut-sei=Yamane
en-aut-mei=Masaomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

affil-num=4
en-affil=Department of Diagnostic Pathology, Okayama University Hospital
kn-affil=

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

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

affil-num=7
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Lung transplantation (LTx)
kn-keyword=Lung transplantation (LTx)
en-keyword=lung recruitment maneuver
kn-keyword=lung recruitment maneuver
en-keyword=atelectasis
kn-keyword=atelectasis
en-keyword=protective procurement
kn-keyword=protective procurement
END

start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=3
article-no=
start-page=281
end-page=290
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202206
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Histone Demethylase Jmjd3 Regulates the Osteogenic Differentiation and Cytokine Expressions of Periodontal Ligament Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Periodontal ligament (PDL) cells are critical for the bone remodeling process in periapical lesions since they can differentiate into osteoblasts and secrete osteoclastogenesis-promoting cytokines. Post-translational histone modifications including alterations of the methylation status of H3K27 are involved in cell differentiation and inflammatory reaction. The histone demethylase Jumonji domain-containing 3 (Jmjd3) specifically removes methylation of H3K27. We investigated whether Jmjd3 is involved in the osteogenic differentiation and secretion of PDL cells’ inflammatory factors. Jmjd3 expression in periapical lesions was examined by immunostaining. Using siRNA specific for Jmjd3 or the specific Jmjd3 inhibitor GSK-J4, we determined Jmjd3’s roles in osteogenic differentiation and cytokine production by real-time RT-PCR. The locations of Jmjd3 and NF-κB were analyzed by immunocytochemistry. Compared to healthy PDLs, the periapical lesion samples showed higher Jmjd3 expression. Treatment with GSK-J4 or Jmjd3 siRNA suppressed PDL cells’ osteogenic differentiation by suppressing the expressions of bone-related genes (Runx2, Osterix, and osteocalcin) and mineralization. Jmjd3 knockdown decreased the expressions of cytokines (TNF-α, IL-1β, and IL-6) induced by lipopolysaccharide extracted from Porphyromonas endodontalis (Pe-LPS). Pe-LPS induced the nuclear translocations of Jmjd3 and NF-κB; the latter was inhibited by GSK-J4 treatment. Jmjd3 appears to regulate PDL cells’ osteogenic differentiation and proinflammatory cytokine expressions.
en-copyright=
kn-copyright=

en-aut-name=YuBo
en-aut-sei=Yu
en-aut-mei=Bo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WangRui
en-aut-sei=Wang
en-aut-mei=Rui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LuoHuikun
en-aut-sei=Luo
en-aut-mei=Huikun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YangDi
en-aut-sei=Yang
en-aut-mei=Di
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WangSimo
en-aut-sei=Wang
en-aut-mei=Simo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YuYaqiong
en-aut-sei=Yu
en-aut-mei=Yaqiong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OkamuraHirohiko
en-aut-sei=Okamura
en-aut-mei=Hirohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=QiuLihong
en-aut-sei=Qiu
en-aut-mei=Lihong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Endodontics, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Disease
kn-affil=

affil-num=2
en-affil=Department of Endodontics, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Disease
kn-affil=

affil-num=3
en-affil=Department of Endodontics, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Disease
kn-affil=

affil-num=4
en-affil=Department of Endodontics, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Disease
kn-affil=

affil-num=5
en-affil=Department of Endodontics, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Disease
kn-affil=

affil-num=6
en-affil=Department of Endodontics, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Disease
kn-affil=

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

affil-num=8
en-affil=Department of Endodontics, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Disease
kn-affil=
en-keyword=periapical lesions
kn-keyword=periapical lesions
en-keyword=histone demethylase Jmjd3
kn-keyword=histone demethylase Jmjd3
en-keyword=periodontal ligament cell
kn-keyword=periodontal ligament cell
en-keyword=osteogenic differentiation
kn-keyword=osteogenic differentiation
en-keyword=proinflammatory cytokines
kn-keyword=proinflammatory cytokines
END

start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=3
article-no=
start-page=255
end-page=263
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202206
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Intrathecal Administration of the α1 Adrenergic Antagonist Phentolamine Upregulates Spinal GLT-1 and Improves Mirror Image Pain in SNI Model Rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Mirror image pain (MIP) is a type of extraterritorial pain that results in contralateral pain or allodynia. Glutamate transporter-1 (GLT-1) is expressed in astrocytes and plays a role in maintaining low glutamate levels in the synaptic cleft. Previous studies have shown that GLT-1 dysfunction induces neuropathic pain. Our previous study revealed bilateral GLT-1 downregulation in the spinal cord of a spared nerve injury (SNI) rat. We hypothesized that spinal GLT-1 is involved in the mechanism of MIP. We also previously demonstrated noradrenergic GLT-1 regulation. Therefore, this study aimed to investigate the effect of an α1 adrenergic antagonist on the development of MIP. Rats were subjected to SNI. Changes in pain behavior and GLT-1 protein levels in the SNI rat spinal cords were then examined by intrathecal administration of the α1 adrenergic antagonist phentolamine, followed by von Frey test and western blotting. SNI resulted in the development of MIP and bilateral downregulation of GLT-1 protein in the rat spinal cord. Intrathecal phentolamine increased contralateral GLT-1 protein levels and partially ameliorated the 50% paw withdrawal threshold in the contralateral hind paw. Spinal GLT-1 upregulation by intrathecal phentolamine ameliorates MIP. GLT-1 plays a role in the development of MIPs.
en-copyright=
kn-copyright=

en-aut-name=NakatsukaKosuke
en-aut-sei=Nakatsuka
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuokaYoshikazu
en-aut-sei=Matsuoka
en-aut-mei=Yoshikazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KuritaMasako
en-aut-sei=Kurita
en-aut-mei=Masako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WangRuilin
en-aut-sei=Wang
en-aut-mei=Ruilin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TsuboiChika
en-aut-sei=Tsuboi
en-aut-mei=Chika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SueNobutaka
en-aut-sei=Sue
en-aut-mei=Nobutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KakuRyuji
en-aut-sei=Kaku
en-aut-mei=Ryuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MorimatsuHiroshi
en-aut-sei=Morimatsu
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

affil-num=3
en-affil=Kinoshita Pain Clinic
kn-affil=

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

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

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

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

affil-num=8
en-affil=Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=alpha adrenergic receptor
kn-keyword=alpha adrenergic receptor
en-keyword=glutamate transporter-1
kn-keyword=glutamate transporter-1
en-keyword=mirror image pain
kn-keyword=mirror image pain
en-keyword=neuropathic pain
kn-keyword=neuropathic pain
en-keyword=spared nerve injury
kn-keyword=spared nerve injury
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=5
article-no=
start-page=1000
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220510
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Maternal Gut Microbiome Decelerates Fetal Endochondral Bone Formation by Inducing Inflammatory Reaction
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To investigate the effect of the maternal gut microbiome on fetal endochondral bone formation, fetuses at embryonic day 18 were obtained from germ-free (GF) and specific-pathogen-free (SPF) pregnant mothers. Skeletal preparation of the fetuses' whole bodies did not show significant morphological alterations; however, micro-CT analysis of the tibiae showed a lower bone volume fraction in the SPF tibia. Primary cultured chondrocytes from fetal SPF rib cages showed a lower cell proliferation and lower accumulation of the extracellular matrix. RNA-sequencing analysis showed the induction of inflammation-associated genes such as the interleukin (IL) 17 receptor, IL 6, and immune-response genes in SPF chondrocytes. These data indicate that the maternal gut microbiome in SPF mice affects fetal embryonic endochondral ossification, possibly by changing the expression of genes related to inflammation and the immune response in fetal cartilage. The gut microbiome may modify endochondral ossification in the fetal chondrocytes passing through the placenta.
en-copyright=
kn-copyright=

en-aut-name=Uchida-FukuharaYoko
en-aut-sei=Uchida-Fukuhara
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HattoriTakako
en-aut-sei=Hattori
en-aut-mei=Takako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FuShanqi
en-aut-sei=Fu
en-aut-mei=Shanqi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoSei
en-aut-sei=Kondo
en-aut-mei=Sei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KuwaharaMiho
en-aut-sei=Kuwahara
en-aut-mei=Miho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FukuharaDaiki
en-aut-sei=Fukuhara
en-aut-mei=Daiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IslamMd Monirul
en-aut-sei=Islam
en-aut-mei=Md Monirul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KataokaKota
en-aut-sei=Kataoka
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=EkuniDaisuke
en-aut-sei=Ekuni
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KubotaSatoshi
en-aut-sei=Kubota
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MoritaManabu
en-aut-sei=Morita
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=IikegameMika
en-aut-sei=Iikegame
en-aut-mei=Mika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OkamuraHirohiko
en-aut-sei=Okamura
en-aut-mei=Hirohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Department of Oral Morphology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biochemistry and Molecular Dentistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Biochemistry and Molecular Dentistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Biochemistry and Molecular Dentistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Biochemistry and Molecular Dentistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Preventive Dentistry, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Preventive Dentistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Preventive Dentistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Preventive Dentistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Biochemistry and Molecular Dentistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Preventive Dentistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Oral Morphology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University 
kn-affil=

affil-num=13
en-affil=Department of Oral Morphology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University 
kn-affil=
en-keyword=maternal microbiome
kn-keyword=maternal microbiome
en-keyword=endochondral ossification
kn-keyword=endochondral ossification
en-keyword=fetal chondrocytes
kn-keyword=fetal chondrocytes
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=
article-no=
start-page=249
end-page=261
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220616
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Modulation of p53 expression in cancer-associated fibroblasts prevents peritoneal metastasis of cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cancer-associated fibroblasts (CAFs) in the tumor microenvironment are associated with the establishment and progression of peritoneal metastasis. This study investigated the efficacy of replicative oncolytic adenovirus-mediated p53 gene therapy (OBP-702) against CAFs and peritoneal metastasis of gastric cancer (GC). Higher CAF expression in the primary tumor was associated with poor prognosis of GC, and higher CAF expression was also observed with peritoneal metastasis in immunohistochemical analysis of clinical samples. And, we found transcriptional alteration of p53 in CAFs relative to normal gastric fibroblasts (NGFs). CAFs increased the secretion of cancer-promoting cytokines, including interleukin-6, and gained resistance to chemotherapy relative to NGFs. OBP-702 showed cytotoxicity to both GC cells and CAFs but not to NGFs. Overexpression of wild-type p53 by OBP-702 infection caused apoptosis and autophagy of CAFs and decreased the secretion of cancer-promoting cytokines by CAFs. Combination therapy using intraperitoneal administration of OBP-702 and paclitaxel synergistically inhibited the tumor growth of peritoneal metastases and decreased CAFs in peritoneal metastases. OBP-702, a replicative oncolytic adenovirus-mediated p53 gene therapy, offers a promising biological therapeutic strategy for peritoneal metastasis, modulating CAFs in addition to achieving tumor lysis.
en-copyright=
kn-copyright=

en-aut-name=OgawaToshihiro
en-aut-sei=Ogawa
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KikuchiSatoru
en-aut-sei=Kikuchi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TabuchiMotoyasu
en-aut-sei=Tabuchi
en-aut-mei=Motoyasu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MitsuiEma
en-aut-sei=Mitsui
en-aut-mei=Ema
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UneYuta
en-aut-sei=Une
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TazawaHiroshi
en-aut-sei=Tazawa
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KurodaShinji
en-aut-sei=Kuroda
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NomaKazuhiro
en-aut-sei=Noma
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OharaToshiaki
en-aut-sei=Ohara
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KagawaShunsuke
en-aut-sei=Kagawa
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=UrataYasuo
en-aut-sei=Urata
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=FujiwaraToshiyoshi
en-aut-sei=Fujiwara
en-aut-mei=Toshiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

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

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

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

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

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

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

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

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

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

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

affil-num=11
en-affil=Oncolys BioPharma
kn-affil=

affil-num=12
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=45
cd-vols=
no-issue=
article-no=
start-page=1876
end-page=1890
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202247
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Three highly conserved hydrophobic residues in the predicted α2‐helix of rice NLR protein Pit contribute to its localization and immune induction
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Nucleotide-binding leucine-rich repeat (NLR) proteins work as crucial intracellular immune receptors. N-terminal domains of NLRs fall into two groups, coiled-coil (CC) and Toll-interleukin 1 receptor domains, which play critical roles in signal transduction and disease resistance. However, the activation mechanisms of NLRs, and how their N-termini function in immune induction, remain largely unknown. Here, we revealed that the CC domain of a rice NLR Pit contributes to self-association. The Pit CC domain possesses three conserved hydrophobic residues that are known to be involved in oligomer formation in two NLRs, barley MLA10 and Arabidopsis RPM1. Interestingly, the function of these residues in Pit differs from that in MLA10 and RPM1. Although three hydrophobic residues are important for Pit-induced disease resistance against rice blast fungus, they do not participate in self-association or binding to downstream signalling molecules. By homology modelling of Pit using the Arabidopsis ZAR1 structure, we tried to clarify the role of three conserved hydrophobic residues and found that they are located in the predicted α2-helix of the Pit CC domain and involved in the plasma membrane localization. Our findings provide novel insights for understanding the mechanisms of NLR activation as well as the relationship between subcellular localization and immune induction.
en-copyright=
kn-copyright=

en-aut-name=WangQiong
en-aut-sei=Wang
en-aut-mei=Qiong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=LiYuying
en-aut-sei=Li
en-aut-mei=Yuying
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KosamiKen‐ichi
en-aut-sei=Kosami
en-aut-mei=Ken‐ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=LiuChaochao
en-aut-sei=Liu
en-aut-mei=Chaochao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=LiJing
en-aut-sei=Li
en-aut-mei=Jing
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ZhangDan
en-aut-sei=Zhang
en-aut-mei=Dan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MikiDaisuke
en-aut-sei=Miki
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KawanoYoji
en-aut-sei=Kawano
en-aut-mei=Yoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=School of Horticulture and Plant Protection Yangzhou University Yangzhou China
kn-affil=

affil-num=2
en-affil=CAS Center for Excellence in Molecular Plant Sciences, Shanghai Center for Plant Stress Biology Chinese Academy of Sciences Shanghai China
kn-affil=

affil-num=3
en-affil=CAS Center for Excellence in Molecular Plant Sciences, Shanghai Center for Plant Stress Biology Chinese Academy of Sciences Shanghai China
kn-affil=

affil-num=4
en-affil=School of Biotechnology Jiangsu University of Science and Technology Zhenjiang China
kn-affil=

affil-num=5
en-affil=CAS Center for Excellence in Molecular Plant Sciences, Shanghai Center for Plant Stress Biology Chinese Academy of Sciences Shanghai China
kn-affil=

affil-num=6
en-affil=School of Horticulture and Plant Protection Yangzhou University Yangzhou China
kn-affil=

affil-num=7
en-affil=CAS Center for Excellence in Molecular Plant Sciences, Shanghai Center for Plant Stress Biology Chinese Academy of Sciences Shanghai China
kn-affil=

affil-num=8
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=NLR protein
kn-keyword=NLR protein
en-keyword=plasma membrane localization
kn-keyword=plasma membrane localization
en-keyword=self-association
kn-keyword=self-association
en-keyword=effector triggered immunity
kn-keyword=effector triggered immunity
en-keyword=rice
kn-keyword=rice
END

start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=2
article-no=
start-page=203
end-page=215
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202204
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Overexpression of Adenovirus E1A Reverses Transforming Growth Factor-β-induced Epithelial-mesenchymal Transition in Human Esophageal Cancer Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The epithelial-mesenchymal transition (EMT), a normal biological process by which epithelial cells acquire a mesenchymal phenotype, is associated with migration, metastasis, and chemoresistance in cancer cells, and with poor prognosis in patients with esophageal cancer. However, therapeutic strategies to inhibit EMT in tumor environments remain elusive. Here, we show the therapeutic potential of telomerase-specific replication- competent oncolytic adenovirus OBP-301 in human esophageal cancer TE4 and TE6 cells with an EMT phenotype. Transforming growth factor-β (TGF-β) administration induced the EMT phenotype with spindleshaped morphology, upregulation of mesenchymal markers and EMT transcription factors, migration, and chemoresistance in TE4 and TE6 cells. OBP-301 significantly inhibited the EMT phenotype via E1 accumulation. EMT cancer cells were susceptible to OBP-301 via massive autophagy induction. OBP-301 suppressed tumor growth and lymph node metastasis of TE4 cells co-inoculated with TGF-β-secreting fibroblasts. Our results suggest that OBP-301 inhibits the TGF-β-induced EMT phenotype in human esophageal cancer cells. OBP-301-mediated E1A overexpression is a promising antitumor strategy to inhibit EMT-mediated esophageal cancer progression.
en-copyright=
kn-copyright=

en-aut-name=MasudaTomoya
en-aut-sei=Masuda
en-aut-mei=Tomoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TazawaHiroshi
en-aut-sei=Tazawa
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HashimotoYuuri
en-aut-sei=Hashimoto
en-aut-mei=Yuuri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IedaTakeshi
en-aut-sei=Ieda
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KikuchiSatoru
en-aut-sei=Kikuchi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KurodaShinji
en-aut-sei=Kuroda
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NomaKazuhiro
en-aut-sei=Noma
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UrataYasuo
en-aut-sei=Urata
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KagawaShunsuke
en-aut-sei=Kagawa
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=FujiwaraToshiyoshi
en-aut-sei=Fujiwara
en-aut-mei=Toshiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

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

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

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

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

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

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

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

affil-num=8
en-affil=Oncolys BioPharma Inc.
kn-affil=

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

affil-num=10
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=esophageal cancer
kn-keyword=esophageal cancer
en-keyword=EMT
kn-keyword=EMT
en-keyword=TGF-β
kn-keyword=TGF-β
en-keyword=oncolytic adenovirus
kn-keyword=oncolytic adenovirus
en-keyword=E1A
kn-keyword=E1A
END

start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=2
article-no=
start-page=129
end-page=135
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202204
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Combination of D-dimer and Glasgow Prognostic Score Can Be Useful in Predicting VTE in Patients with Stage IIIC and IVA Ovarian Cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cancer patients have increased risk of venous thromboembolism (VTE) that must be assessed before treatment. This study aimed to determine effective VTE biomarkers in gynecologic cancer (GC). We investigated the correlation between D-dimer levels, Khorana risk score (KRS), Glasgow prognostic score (GPS), and VTE in 1499 GC patients (583 cervical cancer (CC), 621 endometrial cancer (EC), and 295 ovarian cancer (OC) patients) treated at our institution between January 2008 and December 2019. χ2 and Mann?Whitney U-tests were used to determine statistical significance. We used receiver operating characteristic-curve analysis to evaluate the discriminatory ability of each parameter. D-dimer levels were significantly correlated with KRS and GPS in patients with GC. VTE was diagnosed in 11 CC (1.9%), 27 EC (4.3%), and 39 OC patients (13.2%). Optimal D-dimer cut-off values for VTE were 3.1, 3.2, and 3.9 μg/ml in CC, EC and OC patients, respectively. D-dimer could significantly predict VTE in all GC patients. Furthermore, D-dimer combined with GPS was more accurate in predicting VTE than other VTE biomarkers in stage IIIC and IVA OC (AUC: 0.846; p<0.001). This study demonstrates that combined D-dimer and GPS are useful in predicting VTE in patients with OC.
en-copyright=
kn-copyright=

en-aut-name=KuboKotaro
en-aut-sei=Kubo
en-aut-mei=Kotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKeiichiro
en-aut-sei=Nakamura
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OkamotoKazuhiro
en-aut-sei=Okamoto
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MatsuokaHirofumi
en-aut-sei=Matsuoka
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IdaNaoyuki
en-aut-sei=Ida
en-aut-mei=Naoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HarumaTomoko
en-aut-sei=Haruma
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OgawaChikako
en-aut-sei=Ogawa
en-aut-mei=Chikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MasuyamaHisashi
en-aut-sei=Masuyama
en-aut-mei=Hisashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

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

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

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

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

affil-num=8
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=D-dimer
kn-keyword=D-dimer
en-keyword=gynecologic cancer
kn-keyword=gynecologic cancer
en-keyword=venous thromboembolism
kn-keyword=venous thromboembolism
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=
article-no=
start-page=1
end-page=7
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=COVID-19 mRNA Vaccine?Associated Uveitis Leading to Diagnosis of Sarcoidosis: Case Report and Review of Literature
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<jats:p> A 34-year-old Japanese person with male gender identity who had been taking intramuscular injection of methyltestosterone depot for 11 years after bilateral mastectomy noticed blurred vision 5 days after the second vaccination for COVID-19 (Tozinameran; Pfizer-BioNTech) in the interval of 3 weeks following the first vaccination. The patient was diagnosed as granulomatous iritis with mutton-fat keratic precipitates and small iris nodules at the pupillary margin in the right eye and began to have 0.1% betamethasone eye drops with good response. The patient, however, continued to have fever and malaise and showed a high level of serum soluble interleukin-2 receptor (sIL-2R) even 4 weeks after the second vaccination. Computed tomographic scan disclosed mediastinal and bilateral hilar small lymphadenopathy together with limited granular lesion in the right lung. Gallium-67 scintigraphy demonstrated high uptake not only in mediastinal and hilar lymph nodes but also in bilateral parotid glands. Right parotid gland biopsy revealed noncaseating granulomas and proved pathological diagnosis of sarcoidosis. The systemic symptoms were relieved by oral prednisolone 20 mg daily. Even though the causal relationship remains undetermined, this case is unique at the point that vaccine-associated uveitis led to the detection of pulmonary lesions and lymphadenopathy, resulting in clinical and pathological diagnosis of sarcoidosis. In literature review, 3 patients showed sarcoidosis-like diseases after COVID-19 vaccination: 2 patients were diagnosed clinically as Lofgren syndrome with acute onset of erythema nodosum and ankle swelling, with or without mediastinal and hilar lymphadenopathy, whereas 1 patient with mediastinal lymphadenopathy but no uveitis was diagnosed pathologically by biopsy as sarcoidosis. </jats:p>
en-copyright=
kn-copyright=

en-aut-name=MatsuoToshihiko
en-aut-sei=Matsuo
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HondaHiroyuki
en-aut-sei=Honda
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TanakaTakehiro
en-aut-sei=Tanaka
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=UraguchiKensuke
en-aut-sei=Uraguchi
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KawaharaMasaaki
en-aut-sei=Kawahara
en-aut-mei=Masaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HagiyaHideharu
en-aut-sei=Hagiya
en-aut-mei=Hideharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University, Japan
kn-affil=

affil-num=2
en-affil=Department of General Medicine, Okayama University Hospital, Japan
kn-affil=

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

affil-num=4
en-affil=Department of Otolaryngology, Head & Neck Surgery, Okayama University Hospital, Japan
kn-affil=

affil-num=5
en-affil=Kawahara Eye Clinic, Okayama, Japan
kn-affil=

affil-num=6
en-affil=Department of General Medicine, Okayama University Hospital, Japan
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=137
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cancer-Associated Stromal Cells Promote the Contribution of MMP2-Positive Bone Marrow-Derived Cells to Oral Squamous Cell Carcinoma Invasion
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Simple Summary Based on its invasiveness, oral squamous cell carcinoma (OSCC) shows two different subtypes: less-invasive verrucous squamous carcinoma (VSCC) or highly invasive squamous cell carcinoma (SCC). The stromal component influences OSCC progression and invasion. On the other hand, bone marrow-derived cells (BMDCs) are recruited into tumors and involved in tumor development. We hypothesized that stromal factors might also affect the relation of BMDCs and tumor invasion. We established the OSCC models transplanted with stromal cells from VSCC and SCC, and we compared the potential stromal factors of VSCC and SCC for the involvement of BMDCs in tumor invasion. Our study showed that stromal factors IL6 and IL1B might promote the contribution of MMP-2 positive BMDCs to OSCC invasion. Tumor stromal components contribute to tumor development and invasion. However, the role of stromal cells in the contribution of bone marrow-derived cells (BMDCs) in oral squamous cell carcinoma (OSCC) invasion is unclear. In the present study, we created two different invasive OSCC patient-derived stroma xenografts (PDSXs) and analyzed and compared the effects of stromal cells on the relation of BMDCs and tumor invasion. We isolated stromal cells from two OSCC patients: less invasive verrucous OSCC (VSCC) and highly invasive conventional OSCC (SCC) and co-xenografted with the OSCC cell line (HSC-2) on green fluorescent protein (GFP)-positive bone marrow (BM) cells transplanted mice. We traced the GFP-positive BM cells by immunohistochemistry (IHC) and detected matrix metalloproteinase 2 (MMP2) expression on BM cells by double fluorescent IHC. The results indicated that the SCC-PDSX promotes MMP2-positive BMDCs recruitment to the invasive front line of the tumor. Furthermore, microarray analysis revealed that the expressions of interleukin 6; IL-6 mRNA and interleukin 1 beta; IL1B mRNA were higher in SCC stromal cells than in VSCC stromal cells. Thus, our study first reports that IL-6 and IL1B might be the potential stromal factors promoting the contribution of MMP2-positive BMDCs to OSCC invasion.
en-copyright=
kn-copyright=

en-aut-name=OoMay Wathone
en-aut-sei=Oo
en-aut-mei=May Wathone
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawaiHotaka
en-aut-sei=Kawai
en-aut-mei=Hotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakabatakeKiyofumi
en-aut-sei=Takabatake
en-aut-mei=Kiyofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShanQiusheng
en-aut-sei=Shan
en-aut-mei=Qiusheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=EainHtoo Shwe
en-aut-sei=Eain
en-aut-mei=Htoo Shwe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SukegawaShintaro
en-aut-sei=Sukegawa
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakanoKeisuke
en-aut-sei=Nakano
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NagatsukaHitoshi
en-aut-sei=Nagatsuka
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

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

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

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

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

affil-num=8
en-affil=Department of Oral Pathology and Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=oral squamous cell carcinoma invasion
kn-keyword=oral squamous cell carcinoma invasion
en-keyword=patient-derived stromal cell xenograft (PDSX)
kn-keyword=patient-derived stromal cell xenograft (PDSX)
en-keyword=bone marrow-derived cells (BMDCs)
kn-keyword=bone marrow-derived cells (BMDCs)
en-keyword=MMP2
kn-keyword=MMP2
en-keyword=stromal factor IL-6
kn-keyword=stromal factor IL-6
en-keyword=stromal factor IL1B
kn-keyword=stromal factor IL1B
END

start-ver=1.4
cd-journal=joma
no-vol=22
cd-vols=
no-issue=23
article-no=
start-page=12659
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211123
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Multifaceted Analysis of IL-23A-and/or EBI3-Including Cytokines Produced by Psoriatic Keratinocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Interleukin (IL) 23 (p19/p40) plays a critical role in the pathogenesis of psoriasis and is upregulated in psoriasis skin lesions. In clinical practice, anti-IL-23Ap19 antibodies are highly effective against psoriasis. IL-39 (p19/ Epstein-Barr virus-induced (EBI) 3), a newly discovered cytokine in 2015, shares the p19 subunit with IL-23. Anti-IL-23Ap19 antibodies may bind to IL-39; also, the cytokine may contribute to the pathogenesis of psoriasis. To investigate IL23Ap19- and/or EBI3-including cytokines in psoriatic keratinocytes, we analyzed IL-23Ap19 and EBI3 expressions in psoriasis skin lesions, using immunohistochemistry and normal human epidermal keratinocytes (NHEKs) stimulated with inflammatory cytokines, using quantitative real-time polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), and liquid chromatography-electrospray tandem mass spectrometry (LC-Ms/Ms). Immunohistochemical analysis showed that IL-23Ap19 and EBI3 expressions were upregulated in the psoriasis skin lesions. In vitro, these expressions were synergistically induced by the triple combination of tumor necrosis factor (TNF)-alpha, IL-17A, and interferon (IFN)-gamma, and suppressed by dexamethasone, vitamin D3, and acitretin. In ELISA and LC-Ms/Ms analyses, keratinocyte-derived IL-23Ap19 and EBI3, but not heterodimeric forms, were detected with humanized anti-IL-23Ap19 monoclonal antibodies, tildrakizumab, and anti-EBI3 antibodies, respectively. Psoriatic keratinocytes may express IL-23Ap19 and EBI3 proteins in a monomer or homopolymer, such as homodimer or homotrimer.
en-copyright=
kn-copyright=

en-aut-name=TachibanaKota
en-aut-sei=Tachibana
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TangNina
en-aut-sei=Tang
en-aut-mei=Nina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UrakamiHitoshi
en-aut-sei=Urakami
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KajitaAi
en-aut-sei=Kajita
en-aut-mei=Ai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KobashiMina
en-aut-sei=Kobashi
en-aut-mei=Mina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NomuraHayato
en-aut-sei=Nomura
en-aut-mei=Hayato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SasakuraMinori
en-aut-sei=Sasakura
en-aut-mei=Minori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SugiharaSatoru
en-aut-sei=Sugihara
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=JiangFan
en-aut-sei=Jiang
en-aut-mei=Fan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OuchidaMamoru
en-aut-sei=Ouchida
en-aut-mei=Mamoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MorizaneShin
en-aut-sei=Morizane
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

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

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

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

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

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

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

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

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

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

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

affil-num=11
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science
kn-affil=

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

affil-num=13
en-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science
kn-affil=
en-keyword=psoriasis vulgaris
kn-keyword=psoriasis vulgaris
en-keyword=interleukin (IL) 23
kn-keyword=interleukin (IL) 23
en-keyword=IL-39
kn-keyword=IL-39
en-keyword=p19
kn-keyword=p19
en-keyword=Epstein-Barr virus-induced (EBI) 3
kn-keyword=Epstein-Barr virus-induced (EBI) 3
en-keyword=tildrakizumab
kn-keyword=tildrakizumab
END

start-ver=1.4
cd-journal=joma
no-vol=21
cd-vols=
no-issue=1
article-no=
start-page=339
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211031
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The effects of inhaling hydrogen gas on macrophage polarization, fibrosis, and lung function in mice with bleomycin-induced lung injury
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background : Acute respiratory distress syndrome, which is caused by acute lung injury, is a destructive respiratory disorder caused by a systemic inflammatory response. Persistent inflammation results in irreversible alveolar fibrosis. Because hydrogen gas possesses anti-inflammatory properties, we hypothesized that daily repeated inhalation of hydrogen gas could suppress persistent lung inflammation by inducing functional changes in macrophages, and consequently inhibit lung fibrosis during late-phase lung injury. <br>
Methods : To test this hypothesis, lung injury was induced in mice by intratracheal administration of bleomycin (1.0 mg/kg). Mice were exposed to control gas (air) or hydrogen (3.2% in air) for 6 h every day for 7 or 21 days. Respiratory physiology, tissue pathology, markers of inflammation, and macrophage phenotypes were examined. <br>
Results : Mice with bleomycin-induced lung injury that received daily hydrogen therapy for 21 days (BH group) exhibited higher static compliance (0.056 mL/cmH(2)O, 95% CI 0.047-0.064) than mice with bleomycin-induced lung injury exposed only to air (BA group; 0.042 mL/cmH(2)O, 95% CI 0.031-0.053, p = 0.02) and lower static elastance (BH 18.8 cmH(2)O/mL, [95% CI 15.4-22.2] vs. BA 26.7 cmH(2)O/mL [95% CI 19.6-33.8], p = 0.02). When the mRNA levels of pro-inflammatory cytokines were examined 7 days after bleomycin administration, interleukin (IL)-6, IL-4 and IL-13 were significantly lower in the BH group than in the BA group. There were significantly fewer M2-biased macrophages in the alveolar interstitium of the BH group than in the BA group (3.1% [95% CI 1.6-4.5%] vs. 1.1% [95% CI 0.3-1.8%], p = 0.008). <br>
Conclusions The results suggest that hydrogen inhalation inhibits the deterioration of respiratory physiological function and alveolar fibrosis in this model of lung injury.
en-copyright=
kn-copyright=

en-aut-name=AokageToshiyuki
en-aut-sei=Aokage
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SeyaMizuki
en-aut-sei=Seya
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HirayamaTakahiro
en-aut-sei=Hirayama
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NojimaTsuyoshi
en-aut-sei=Nojima
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IketaniMasumi
en-aut-sei=Iketani
en-aut-mei=Masumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IshikawaMichiko
en-aut-sei=Ishikawa
en-aut-mei=Michiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TerasakiYasuhiro
en-aut-sei=Terasaki
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TaniguchiAkihiko
en-aut-sei=Taniguchi
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MiyaharaNobuaki
en-aut-sei=Miyahara
en-aut-mei=Nobuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakaoAtsunori
en-aut-sei=Nakao
en-aut-mei=Atsunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OhsawaIkuroh
en-aut-sei=Ohsawa
en-aut-mei=Ikuroh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NaitoHiromichi
en-aut-sei=Naito
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

affil-num=4
en-affil=Department of Primary Care and Medical Education, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Biological Process of Aging, Tokyo Metropolitan Institute of Gerontology
kn-affil=

affil-num=6
en-affil=Department of Emergency, Disaster and Critical Care Medicine, Hyogo College of Medicine
kn-affil=

affil-num=7
en-affil=Department of Analytic Human Pathology, Nippon Medical School
kn-affil=

affil-num=8
en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Medical Technology, Okayama University Graduate School of Health Sciences
kn-affil=

affil-num=10
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Biological Process of Aging, Tokyo Metropolitan Institute of Gerontology
kn-affil=

affil-num=12
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Acute respiratory distress syndrome
kn-keyword=Acute respiratory distress syndrome
en-keyword=Bleomycin-induced lung injury
kn-keyword=Bleomycin-induced lung injury
en-keyword=Macrophage
kn-keyword=Macrophage
en-keyword=Molecular hydrogen
kn-keyword=Molecular hydrogen
en-keyword=Lung fibrosis
kn-keyword=Lung fibrosis
END

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

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

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

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

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

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

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

start-ver=1.4
cd-journal=joma
no-vol=22
cd-vols=
no-issue=18
article-no=
start-page=9781
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210910
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Adipose-Derived Extract Suppresses IL-1 beta-Induced Inflammatory Signaling Pathways in Human Chondrocytes and Ameliorates the Cartilage Destruction of Experimental Osteoarthritis in Rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We investigated the effects of adipose-derived extract (AE) on cultured chondrocytes and in vivo cartilage destruction. AE was prepared from human adipose tissues using a nonenzymatic approach. Cultured human chondrocytes were stimulated with interleukin-1 beta (IL-1 beta) with or without different concentrations of AE. The effects of co-treatment with AE on intracellular signaling pathways and their downstream gene and protein expressions were examined using real-time PCR, Western blotting, and immunofluorescence staining. Rat AE prepared from inguinal adipose tissues was intra-articularly delivered to the knee joints of rats with experimental osteoarthritis (OA), and the effect of AE on cartilage destruction was evaluated histologically. In vitro, co-treatment with IL-1 beta combined with AE reduced activation of the p38 and ERK mitogen-activated protein kinase (MAPK) pathway and nuclear translocation of the p65 subunit of nuclear factor-kappa B (NF-kappa B), and subsequently downregulated the expressions of matrix metalloproteinase (MMP)-1, MMP-3, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4, IL-6, and IL-8, whereas it markedly upregulated the expression of IL-1 receptor type 2 (IL-1R2) in chondrocytes. Intra-articular injection of homologous AE significantly ameliorated cartilage destruction six weeks postoperatively in the rat OA model. These results suggested that AE may exert a chondroprotective effect, at least in part, through modulation of the IL-1 beta-induced inflammatory signaling pathway by upregulation of IL-1R2 expression.
en-copyright=
kn-copyright=

en-aut-name=OhashiHideki
en-aut-sei=Ohashi
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishidaKeiichiro
en-aut-sei=Nishida
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YoshidaAki
en-aut-sei=Yoshida
en-aut-mei=Aki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NasuYoshihisa
en-aut-sei=Nasu
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakaharaRyuichi
en-aut-sei=Nakahara
en-aut-mei=Ryuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsumotoYoshinori
en-aut-sei=Matsumoto
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakeshitaAyumu
en-aut-sei=Takeshita
en-aut-mei=Ayumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KanedaDaisuke
en-aut-sei=Kaneda
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SaekiMasanori
en-aut-sei=Saeki
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OzakiToshifumi
en-aut-sei=Ozaki
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

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

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

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

affil-num=4
en-affil=Department of Orthopaedic Surgery, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Orthopaedic Surgery, Okayama University Hospital
kn-affil=

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

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

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

affil-num=9
en-affil=View Clinic Momonosato
kn-affil=

affil-num=10
en-affil=Department of Orthopaedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=adipose tissue
kn-keyword=adipose tissue
en-keyword=cartilage
kn-keyword=cartilage
en-keyword=chondrocyte
kn-keyword=chondrocyte
en-keyword=osteoarthritis
kn-keyword=osteoarthritis
en-keyword=IL-1 receptor type 2
kn-keyword=IL-1 receptor type 2
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=
article-no=
start-page=713358
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210830
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Harnessing Treg Homeostasis to Optimize Posttransplant Immunity: Current Concepts and Future Perspectives
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs) are functionally distinct subsets of mature T cells with broad suppressive activity and have been shown to play an important role in the establishment of immune tolerance after allogeneic hematopoietic stem cell transplantation (HSCT). Tregs exhibit an activated phenotype from the stage of emigration from the thymus and maintain continuous proliferation in the periphery. The distinctive feature in homeostasis enables Tregs to respond sensitively to small environmental changes and exert necessary and sufficient immune suppression; however, on the other hand, it also predisposes Tregs to be susceptible to apoptosis in the inflammatory condition post-transplant. Our studies have attempted to define the intrinsic and extrinsic factors affecting Treg homeostasis from the acute to chronic phases after allogeneic HSCT. We have found that altered cytokine environment in the prolonged post-HSCT lymphopenia or peri-transplant use of immune checkpoint inhibitors could hamper Treg reconstitution, leading to refractory graft-versus-host disease. Using murine models and clinical trials, we have also demonstrated that proper intervention with low-dose interleukin-2 or post-transplant cyclophosphamide could restore Treg homeostasis and further amplify the suppressive function after HSCT. The purpose of this review is to reconsider the distinctive characteristics of post-transplant Treg homeostasis and discuss how to harness Treg homeostasis to optimize posttransplant immunity for developing a safe and efficient therapeutic strategy.</p>
en-copyright=
kn-copyright=

en-aut-name=IkegawaShuntaro
en-aut-sei=Ikegawa
en-aut-mei=Shuntaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuokaKen-ichi
en-aut-sei=Matsuoka
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Hematology and Oncology, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Hematology and Oncology, Okayama University
kn-affil=
en-keyword=regulatory T cell
kn-keyword=regulatory T cell
en-keyword=graft-versus-host disease
kn-keyword=graft-versus-host disease
en-keyword=interleukin 2
kn-keyword=interleukin 2
en-keyword=immune checkpoint inhibitor
kn-keyword=immune checkpoint inhibitor
en-keyword=post-transplant cyclophosphamide
kn-keyword=post-transplant cyclophosphamide
END

start-ver=1.4
cd-journal=joma
no-vol=139
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202110
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Reduction of macrophages by carrageenan decreases oocyst output and modifies local immune reaction in chick cecum with Eimeria tenella
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This study aimed to evaluate the disease severity and local immune responses in macrophage-depleted chicks with Eimeria tenella. Macrophages were reduced by intraperitoneal injection of a carrageenan solution at 12, 13, and 16 days old, whereas the control group received intraperitoneal phosphate-buffered saline. Both chick groups were orally inoculated with E. tenella sporulated oocysts at 14 days old. Feces were collected daily, which were then quantified for oocysts. The chicks were sacrificed on day 5, and the ceca were collected for histopathological observation. The gene expression levels were measured using real-time quantitative reverse transcription-polymerase chain reaction. Macrophage-depleted chicks have been observed to shed a significantly reduced number of fecal oocysts compared to the infected control group. The parasite burden score in cecum specimens of macrophage-depleted chicks was significantly lower than those of infected control on day 5 after infection. Furthermore, macrophage reduction yielded significantly lower cecum histopathological scores and CD4 expression than those of the infected control group. The expression of interleukin (IL)-18, IL-22, interferon-γ, and inducible nitric oxide synthase was also noted to be significantly upregulated in both infected control and macrophage-depleted chicks compared to uninfected chicks. IL-4, IL-13, IL-17, and perforin expressions were also higher with macrophage depletion than in both control groups. These results suggest that macrophages serve as an invasive gate or a transporting vehicle to the site of first merogony. Furthermore, mononuclear phagocytes may play an important role in local immune responses, thus contributing to parasite development during early E. tenella infection.
en-copyright=
kn-copyright=

en-aut-name=HoDung Thi
en-aut-sei=Ho
en-aut-mei=Dung Thi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=PhamHung Hoang Son
en-aut-sei=Pham
en-aut-mei=Hung Hoang Son
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AotaWataru
en-aut-sei=Aota
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MatsubayashiMakoto
en-aut-sei=Matsubayashi
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TsujiNaotoshi
en-aut-sei=Tsuji
en-aut-mei=Naotoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HatabuToshimitsu
en-aut-sei=Hatabu
en-aut-mei=Toshimitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Laboratory of Animal Physiology, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Laboratory of Animal Physiology, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Laboratory of Animal Physiology, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Veterinary Science, Graduate School of Life and Environmental Sciences, Osaka Prefecture University
kn-affil=

affil-num=5
en-affil=Department of Parasitology and Tropical Medicine, Kitasato University School of Medicine
kn-affil=

affil-num=6
en-affil=Laboratory of Animal Physiology, Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=Eimeria tenella
kn-keyword=Eimeria tenella
en-keyword=Local immune response
kn-keyword=Local immune response
en-keyword=Macrophage
kn-keyword=Macrophage
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=4
article-no=
start-page=505
end-page=509
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202108
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Association Between Eosinophilia and Late-onset Circulatory Collapse in Preterm Infants: A case-Control Study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Late-onset circulatory collapse (LCC) in preterm infants is presumably caused by relative adrenal insufficiency. Because eosinophilia is known to be associated with adrenal insufficiency, we attempted to clarify the relation-ship between eosinophilia and LCC in preterm infants. We divided the cases of the infants (born at < 28 weeks’ gestation) admitted to our neonatal intensive care unit in 2008-2010 into 2 groups: those diagnosed with LCC that received glucocorticoids (LCC group), and those who did not receive glucocorticoids (control group). We compared eosinophil counts between the 2 groups and between before and after glucocorticoid treatment in the LCC group. A total of 28 infants were examined: LCC group (n = 12); control group (n = 16). The peak eosin-ophil counts of the LCC group were significantly higher than those of the control group (median: 1.392 × 109/L vs. 1.033 × 109/L, respectively; p = 0.02). Additionally, in the LCC group, the eosinophil counts declined significantly after glucocorticoid treatment (0.877 × 109/L vs. 0.271 × 109/L, p = 0.003). Eosinophil counts in the LCC group were significantly higher than in the control group and decreased rapidly after gluco-corticoid treatment. These results indicate that eosinophilia may be a factor associated with LCC caused by adrenal insufficiency.
en-copyright=
kn-copyright=

en-aut-name=OkamuraTomoka
en-aut-sei=Okamura
en-aut-mei=Tomoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WashioYosuke
en-aut-sei=Washio
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WatanabeHirokazu
en-aut-sei=Watanabe
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakanishiHidehiko
en-aut-sei=Nakanishi
en-aut-mei=Hidehiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UchiyamaAtsushi
en-aut-sei=Uchiyama
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name= TsukaharaHirokazu
en-aut-sei= Tsukahara
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KusudaSatoshi
en-aut-sei=Kusuda
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Neonatology, Maternal and Perinatal Center, Tokyo Women's Medical University
kn-affil=

affil-num=2
en-affil=Department of Neonatology, Maternal and Perinatal Center, Tokyo Women's Medical University
kn-affil=

affil-num=3
en-affil=Department of Neonatology, Maternal and Perinatal Center, Tokyo Women's Medical University
kn-affil=

affil-num=4
en-affil=Department of Neonatology, Maternal and Perinatal Center, Tokyo Women's Medical University
kn-affil=

affil-num=5
en-affil=Department of Neonatology, Maternal and Perinatal Center, Tokyo Women's Medical University
kn-affil=

affil-num=6
en-affil=Department of Pediatrics, Graduate school of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=7
en-affil=Department of Neonatology, Maternal and Perinatal Center, Tokyo Women's Medical University
kn-affil=
en-keyword=late-onset circulatory collapse
kn-keyword=late-onset circulatory collapse
en-keyword=preterm infant
kn-keyword=preterm infant
en-keyword=eosinophilia
kn-keyword=eosinophilia
en-keyword=steroid
kn-keyword=steroid
en-keyword=adrenal insufficiency
kn-keyword=adrenal insufficiency
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=4
article-no=
start-page=461
end-page=469
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202108
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Bendamustine Plus Rituximab as Salvage Treatment for Patients with Relapsed or Refractory Low-grade B-cell Lymphoma and Mantle Cell Lymphoma: A Single-Center Retrospective Study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Bendamustine plus rituximab (B-R) is an effective therapy for relapsed or refractory (r/r) low-grade B-cell  lymphoma (LGBCL) and mantle cell lymphoma (MCL); however, clinical data from Japanese patients treated with B-R therapy are limited. We retrospectively evaluated the efficacy and safety of B-R therapy in 42 patients who received B-R therapy at our hospital for r/r LGBCL and MCL. All patients received intravenous (IV) ritux-imab 375 mg/m2 on day 1 and IV bendamustine 90 mg/m2 on days 2 and 3 every 28 days for up to 6 cycles. The common histologic subtypes were follicular lymphoma (n = 29, 70%), marginal zone lymphoma (n = 6, 14%), and MCL (n = 5, 12%). The overall response rate was 93%, with 62% complete response and complete response unconfirmed. The median progression-free survival (PFS) was 38 months (95% confidence interval [CI], 24.6 to not reached [NR]), and the median overall survival (OS) was 80 months (95% CI, 60.7 to NR). Patients receiving a cumulative dose of bendamustine ? 720 mg/m2 showed a significantly longer PFS and OS. Grade 3/4 adverse events (? 10%) included neutropenia (55%), lymphopenia (69%), and nausea (24%). B-R therapy was effective and well tolerated, and the cumulative dose of bendamustine was associated with a favorable outcome.
en-copyright=
kn-copyright=

en-aut-name=MurakamiHiroyuki
en-aut-sei=Murakami
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YoshiokaTakanori
en-aut-sei=Yoshioka
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoriyamaTakashi
en-aut-sei=Moriyama
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshikawaTatsunori
en-aut-sei=Ishikawa
en-aut-mei=Tatsunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MakitaMasanori
en-aut-sei=Makita
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SunamiKazutaka
en-aut-sei=Sunami
en-aut-mei=Kazutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Hematology, National Hospital Organization Okayama Medical Center
kn-affil=

affil-num=2
en-affil=Department of Hematology, National Hospital Organization Okayama Medical Center
kn-affil=

affil-num=3
en-affil=Department of Hematology, National Hospital Organization Okayama Medical Center
kn-affil=

affil-num=4
en-affil=Department of Hematology, National Hospital Organization Okayama Medical Center
kn-affil=

affil-num=5
en-affil=Department of Hematology, National Hospital Organization Okayama Medical Center
kn-affil=

affil-num=6
en-affil=Department of Hematology, National Hospital Organization Okayama Medical Center
kn-affil=
en-keyword=bendamustine
kn-keyword=bendamustine
en-keyword=low grade B-cell lymphoma
kn-keyword=low grade B-cell lymphoma
en-keyword=mantle cell lymphoma
kn-keyword=mantle cell lymphoma
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=13
article-no=
start-page=2125
end-page=2128
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210701
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Unique Case of Encephalopathy with an Elevated IgG-4 and Extremely High Interleukin-6 Level and Delayed Myelodysplastic Syndrome
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We herein report a 75-year-old man who developed disturbed consciousness with polynuclear cell dominant pleocytosis and low glucose and extremely high interleukin (IL)-6 levels in his cerebrospinal fluid. The biopsy specimen from his right supraclavicular lymph node showed the infiltration of inflammatory cells positive for IgG, IgG4 and IL-6. Prednisolone and azathioprine administered under suspicion of IgG4-related disease (IgG4-RD) or multicentric Castleman's disease (MCD) successfully remitted the symptoms. However, he developed myelodysplastic syndrome (MDS) and died 18 months later. The extremely high IL-6 may have been related to the rare neurological manifestations and development of MDS in the present case.
en-copyright=
kn-copyright=

en-aut-name=MatsumotoNamiko
en-aut-sei=Matsumoto
en-aut-mei=Namiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IkegamiKen
en-aut-sei=Ikegami
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OmoteYoshio
en-aut-sei=Omote
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakemotoMami
en-aut-sei=Takemoto
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamashitaTom
en-aut-sei=Yamashita
en-aut-mei=Tom
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TaniguchiKohei
en-aut-sei=Taniguchi
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

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

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

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

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

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

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

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

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

affil-num=9
en-affil=Departments of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=encephalopathy
kn-keyword=encephalopathy
en-keyword=IgG4 related disease
kn-keyword=IgG4 related disease
en-keyword=interleukin-6
kn-keyword=interleukin-6
en-keyword=multicentric Castleman's disease
kn-keyword=multicentric Castleman's disease
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=3
article-no=
start-page=363
end-page=372
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202106
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Role of the Transcription Factor BTB and CNC Homology 1 in a Rat Model of Acute Liver Injury Induced by Experimental Endotoxemia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Hepatic oxidative stress plays an important role in the pathogenesis of several acute liver diseases, and free heme is thought to contribute to endotoxemia-induced acute liver injury. The heme oxygenase 1 (HO-1) gene is upregulated and the δ-aminolevulinate synthase (ALAS1) gene is downregulated in the rat liver following lipopolysaccharide (LPS) treatment. BTB and CNC homology 1 (Bach1) is a heme-responsive transcription factor that normally represses HO-1 expression. In this study, we evaluated the changes in HO-1, ALAS1, and Bach1 expression and nuclear Bach1 expression in rat livers following intravenous LPS administration (10 mg/kg body weight). LPS significantly upregulated HO-1 mRNA and downregulated ALAS1 mRNA in the rat livers, suggesting that hepatic free heme concentrations are increased after LPS treatment. Bach1 mRNA was strongly induced after LPS injection. In contrast, nuclear Bach1 was significantly but transiently decreased after LPS treatment. Rats were also administered hemin (50 mg/kg body weight) intravenously to elevate heme concentrations, which decreased nuclear Bach1 levels. Our results suggest that elevated hepatic free heme may be associated with a decline of nuclear Bach1, and induction of Bach1 mRNA may compensate for the decreased nuclear Bach1 after LPS treatment in the rat liver.
en-copyright=
kn-copyright=

en-aut-name=TaniokaNohito
en-aut-sei=Tanioka
en-aut-mei=Nohito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShimizuHiroko
en-aut-sei=Shimizu
en-aut-mei=Hiroko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OmoriEmiko
en-aut-sei=Omori
en-aut-mei=Emiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakahashiToru
en-aut-sei=Takahashi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamaokaMasakazu
en-aut-sei=Yamaoka
en-aut-mei=Masakazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MorimatsuHiroshi
en-aut-sei=Morimatsu
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

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

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

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

affil-num=4
en-affil=Faculty of Health and Welfare Science, Okayama Prefectural University
kn-affil=

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

affil-num=6
en-affil=Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=heme oxygenase-1
kn-keyword=heme oxygenase-1
en-keyword=BTB and CNC homology 1
kn-keyword=BTB and CNC homology 1
en-keyword= heme, 
kn-keyword= heme, 
en-keyword=lipopolysaccharide
kn-keyword=lipopolysaccharide
en-keyword= liver injury
kn-keyword= liver injury
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=3
article-no=
start-page=299
end-page=306
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202106
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Interrelationships Between Serum Levels of Procalcitonin and Inflammatory Markers in Patients Who Visited a General Medicine Department
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Various laboratory markers of inflammation are utilized in general practice, but their clinical diagnostic significance is often ambiguous. In the present study, we determined the clinical significance of the examination of serum levels of procalcitonin (PCT) by comparing the PCT levels with the levels of other inflammatory markers,
based on a retrospective review of 332 PCT-positive patients, including cases of bacterial infection (20.5%), non-specific inflammation (20.8%), neoplasm (9.9%), connective tissue diseases (8.4%), and non-bacterial infection (7.2%), were analyzed. The serum PCT level was highest in the bacterial infection group (1.94 ng/ml) followed by the non-specific inflammatory group (0.58 ng/ml) and neoplastic diseases group (0.34 ng/ml). The serum PCT level was positively correlated with serum levels of C-reactive protein (rho=0.62), soluble interleukin-2 receptor (sIL-2R; rho=0.69), and ferritin, the plasma level of D-dimer, and white blood cell count, and negatively correlated with the serum albumin level (rho=?0.52), hemoglobin concentration, and platelet count. The serum PCT level showed a stronger positive correlation with the serum sIL-2R level than the other biomarkers. The results suggest that an increased PCT level may indicate not only an infectious state but also a non-bacterial inflammatory condition in the diagnostic process in general practice.
en-copyright=
kn-copyright=

en-aut-name=ArakiJo
en-aut-sei=Araki
en-aut-mei=Jo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OkaKosuke
en-aut-sei=Oka
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamamotoKoichiro
en-aut-sei=Yamamoto
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HanayamaYoshihisa 
en-aut-sei=Hanayama
en-aut-mei=Yoshihisa 
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TokumasuKazuki
en-aut-sei=Tokumasu
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HagiyaHideharu
en-aut-sei=Hagiya
en-aut-mei=Hideharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OgawaHiroko
en-aut-sei=Ogawa
en-aut-mei=Hiroko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ItoshimaKoichi
en-aut-sei=Itoshima
en-aut-mei=Koichi
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=

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

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

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

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

affil-num=5
en-affil=
kn-affil=

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

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

affil-num=8
en-affil=Department of Laboratory Medicine, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=bacterial infection
kn-keyword=bacterial infection
en-keyword=inflammation
kn-keyword=inflammation
en-keyword=malignant lymphoma
kn-keyword=malignant lymphoma
en-keyword=procalcitonin
kn-keyword=procalcitonin
en-keyword=soluble interleukin-2 receptor
kn-keyword=soluble interleukin-2 receptor
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=2021
dt-pub=20210325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=インターロイキン6シグナル伝達の阻害は、インターロイキン1受容体アンタゴニスト欠損マウスにおいて、大動脈炎、左心室肥大、関節炎を軽減する
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=
en-copyright=
kn-copyright=

en-aut-name=HadaYoshiko
en-aut-sei=Hada
en-aut-mei=Yoshiko
kn-aut-name=秦昌紫子
kn-aut-sei=秦
kn-aut-mei=昌紫子
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=22
cd-vols=
no-issue=1
article-no=
start-page=150
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210515
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Loss of IL-33 enhances elastase-induced and cigarette smoke extract-induced emphysema in mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background IL-33, which is known to induce type 2 immune responses via group 2 innate lymphoid cells, has been reported to contribute to neutrophilic airway inflammation in chronic obstructive pulmonary disease. However, its role in the pathogenesis of emphysema remains unclear. Methods We determined the role of interleukin (IL)-33 in the development of emphysema using porcine pancreas elastase (PPE) and cigarette smoke extract (CSE) in mice. First, IL-33(-/-) mice and wild-type (WT) mice were given PPE intratracheally. The numbers of inflammatory cells, and the levels of cytokines and chemokines in the bronchoalveolar lavage (BAL) fluid and lung homogenates, were analyzed; quantitative morphometry of lung sections was also performed. Second, mice received CSE by intratracheal instillation. Quantitative morphometry of lung sections was then performed again. Results Intratracheal instillation of PPE induced emphysematous changes and increased IL-33 levels in the lungs. Compared to WT mice, IL-33(-/-) mice showed significantly greater PPE-induced emphysematous changes. No differences were observed between IL-33(-/-) and WT mice in the numbers of macrophages or neutrophils in BAL fluid. The levels of hepatocyte growth factor were lower in the BAL fluid of PPE-treated IL-33(-/-) mice than WT mice. IL-33(-/-) mice also showed significantly greater emphysematous changes in the lungs, compared to WT mice, following intratracheal instillation of CSE. Conclusion These observations suggest that loss of IL-33 promotes the development of emphysema and may be potentially harmful to patients with COPD.
en-copyright=
kn-copyright=

en-aut-name=MorichikaDaisuke
en-aut-sei=Morichika
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TaniguchiAkihiko
en-aut-sei=Taniguchi
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OdaNaohiro
en-aut-sei=Oda
en-aut-mei=Naohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FujiiUtako
en-aut-sei=Fujii
en-aut-mei=Utako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SenooSatoru
en-aut-sei=Senoo
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ItanoJunko
en-aut-sei=Itano
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KanehiroArihiko
en-aut-sei=Kanehiro
en-aut-mei=Arihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KitaguchiYoshiaki
en-aut-sei=Kitaguchi
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YasuoMasanori
en-aut-sei=Yasuo
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HanaokaMasayuki
en-aut-sei=Hanaoka
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SatohTakashi
en-aut-sei=Satoh
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=AkiraShizuo
en-aut-sei=Akira
en-aut-mei=Shizuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KiuraKatsuyuki
en-aut-sei=Kiura
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=MiyaharaNobuaki
en-aut-sei=Miyahara
en-aut-mei=Nobuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=First Department of Internal Medicine, Shinshu University School of Medicine
kn-affil=

affil-num=9
en-affil=First Department of Internal Medicine, Shinshu University School of Medicine
kn-affil=

affil-num=10
en-affil=First Department of Internal Medicine, Shinshu University School of Medicine
kn-affil=

affil-num=11
en-affil=Laboratory of Host Defense, World Premier Institute Immunology Frontier Research Center (WPI?IFReC), Osaka University
kn-affil=

affil-num=12
en-affil=Laboratory of Host Defense, World Premier Institute Immunology Frontier Research Center (WPI?IFReC), Osaka University
kn-affil=

affil-num=13
en-affil=Department of Allergy and Respiratory Medicine, Okayama University
kn-affil=

affil-num=14
en-affil=Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Allergy and Respiratory Medicine, Okayama University
kn-affil=
en-keyword=Chronic obstructive pulmonary disease
kn-keyword=Chronic obstructive pulmonary disease
en-keyword=COPD
kn-keyword=COPD
en-keyword=HGF
kn-keyword=HGF
en-keyword=VEGF
kn-keyword=VEGF
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=2
article-no=
start-page=153
end-page=167
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202104
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Lactoferrin-like Immunoreactivity in Distinct Neuronal Populations in the Mouse Central Nervous System
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Lactoferrin (Lf) is an iron-binding glycoprotein mainly found in exocrine secretions and the secondary granules of neutrophils. In the central nervous system (CNS), expression of the Lf protein has been reported in the lesions of some neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis, as well as in the aged brain. Lf is primarily considered an iron chelator, protecting cells from potentially toxic iron or iron-requiring microorganisms. Other biological functions of Lf include immunomodulation and transcriptional regulation. However, the roles of Lf in the CNS have yet to be fully clarified. In this study, we raised an antiserum against mouse Lf and investigated the immunohistochemical localization of Lf-like immunoreactivity (Lf-LI) throughout the CNS of adult mice. Lf-LI was found in some neuronal populations throughout the CNS. Intense labeling was found in neurons in the olfactory systems, hypothalamic nuclei, entorhinal cortex, and a variety of brainstem nuclei. This study provides detailed information on the Lf-LI distribution in the CNS, and the findings should promote further understanding of both the physiological and pathological significance of Lf in the CNS.
en-copyright=
kn-copyright=

en-aut-name=ShimaokaShigeyoshi
en-aut-sei=Shimaoka
en-aut-mei=Shigeyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HamaokaHitomi
en-aut-sei=Hamaoka
en-aut-mei=Hitomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=InoueJunji
en-aut-sei=Inoue
en-aut-mei=Junji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TooyamaIkuo
en-aut-sei=Tooyama
en-aut-mei=Ikuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KondoYoichi
en-aut-sei=Kondo
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Anatomy and Cell Biology, Division of Life Sciences, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=2
en-affil=Department of Anatomy and Cell Biology, Division of Life Sciences, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=3
en-affil=Department of Anatomy and Cell Biology, Division of Life Sciences, Osaka Medical and Pharmaceutical University
kn-affil=

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

affil-num=5
en-affil=Molecular Neuroscience Research Center, Shiga University of Medical Science
kn-affil=

affil-num=6
en-affil=Molecular Neuroscience Research Center, Shiga University of Medical Science
kn-affil=
en-keyword=lactoferrin
kn-keyword=lactoferrin
en-keyword=immunohistochemistry
kn-keyword=immunohistochemistry
en-keyword=brain mapping
kn-keyword=brain mapping
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=6
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=2020
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Hemosiderin deposition in lymph nodes of patients with plasma cell-type Castleman disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Plasma cell-type Castleman disease (PCD) is a rare idiopathic atypical lymphoproliferative disorder. It is difficult to differentiate between PCD and IgG4-related disease (IgG4-RD) based on histology alone. As PCD often presents with abundant hemosiderin deposition, lymph node lesions obtained from 22 PCD patients and 12 IgG4-RD patients were analyzed using Prussian blue staining to clarify whether hemosiderin deposition is effective in distinguishing between these two diseases. The analysis disclosed that hemosiderin was more densely deposited in PCD than in IgG4-RD. The median number of Prussian blue-positive cells ± standard deviation (SD) in PCD and IgG4-RD cases was 13 ± 36 cells/3HPFs and 4 ± 8 cells/3HPFs (P = 0.034), respectively. In addition, we analyzed the relationship between hemosiderin deposition and levels of serum interleukin (IL)-6, serum C-reactive protein (CRP), and anemia-related biomarkers. We found that hemosiderin deposition was significantly correlated with the level of serum CRP (P = 0.045); however, no significant correlation was observed between hemosiderin deposition and serum IL-6 levels (P = 0.204). A non-significant positive correlation was observed between hemosiderin deposition and serum hemoglobin levels (P=0.09). Furthermore, no significant correlation was observed between hemosiderin deposition and serum iron levels (P = 0.799). In conclusion, hemosiderin deposition characteristically observed in PCD may be related to the inflammatory aggressiveness of the disease and could be used for its differential diagnosis.
en-copyright=
kn-copyright=

en-aut-name=HanYanyan
en-aut-sei=Han
en-aut-mei=Yanyan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IgawaTakuro
en-aut-sei=Igawa
en-aut-mei=Takuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OginoKyohei
en-aut-sei=Ogino
en-aut-mei=Kyohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NishikoriAsami
en-aut-sei=Nishikori
en-aut-mei=Asami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=GionYuka
en-aut-sei=Gion
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YoshinoTadashi
en-aut-sei=Yoshino
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SatoYasuharu
en-aut-sei=Sato
en-aut-mei=Yasuharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

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

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

affil-num=3
en-affil=Department of Pathology, Fukuyama City Hospital
kn-affil=

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

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

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

affil-num=7
en-affil=Division of Pathophysiology, Okayama University Graduate School of Health Sciences
kn-affil=
en-keyword=hemosiderin deposition
kn-keyword=hemosiderin deposition
en-keyword=plasma cell-type Castleman disease
kn-keyword=plasma cell-type Castleman disease
en-keyword=IgG4-related disease
kn-keyword=IgG4-related disease
en-keyword=serum IL-6
kn-keyword=serum IL-6
en-keyword=serum C-reactive protein
kn-keyword=serum C-reactive protein
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=3
article-no=
start-page=78
end-page=86
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=2020
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinicopathological significance of CD79a expression in classic Hodgkin lymphoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Classic Hodgkin lymphoma (CHL) is a lymphoid neoplasia characterized by the presence of large tumor cells, referred to as Hodgkin and Reed-Sternberg (HRS) cells, originating from B-cells in an inflammatory background. As the clinical significance of B-cell markers has yet to be fully elucidated, this study aimed to clarify the clinicopathological significance of CD79a in 55 patients with CHL. They were immunohistochemically divided into two groups, comprising of 20 CD79a-positive and 35 CD79a-negative patients. There was no significant correlation between CD79a and CD20 expression (rs = 0.125, P = 0.362). CD79a-positive patients were significantly older at onset (P = 0.011). There was no significant correlation between CD79a-positivity and clinical stage (P = 0.203), mediastinal involvement (P = 0.399), extranodal involvement (P = 0.749), or laboratory findings, including serum levels of lactate dehydrogenase (P = 1) and soluble interleukin-2 receptor (P = 0.251). There were significant differences in overall survival (OS) (P = 0.005) and progression-free survival (PFS) (P = 0.007) between CD79a-positive and CD79a-negative patients (5-year OS: 64.6% and 90.5%; 5-year PFS: 44.0% and 76.6%, respectively). Five patients in whom the majority (> 80%) of HRS cells expressed CD79a consisted of 4 males and 1 female aged between 52 and 81 years; 4 of them were in a limited clinical stage. We concluded that CD79a-positive CHL may have unique clinicopathological features.
en-copyright=
kn-copyright=

en-aut-name=SakataniAkio
en-aut-sei=Sakatani
en-aut-mei=Akio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=Igawaakuro
en-aut-sei=Igawa
en-aut-mei=akuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OkataniTakeshi
en-aut-sei=Okatani
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FujiharaMegumu
en-aut-sei=Fujihara
en-aut-mei=Megumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AsaokuHideki
en-aut-sei=Asaoku
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SatoYasuharu
en-aut-sei=Sato
en-aut-mei=Yasuharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshinoTadashi
en-aut-sei=Yoshino
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

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

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

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

affil-num=4
en-affil=Department of Pathology, Hiroshima Red Cross Hospital & Atomic-bomb Survivors Hospital
kn-affil=

affil-num=5
en-affil=Department of Hematology, Hiroshima Red Cross Hospital & Atomic-bomb Survivors Hospital
kn-affil=

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

affil-num=7
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=classic Hodgkin lymphoma
kn-keyword=classic Hodgkin lymphoma
en-keyword=CD79a
kn-keyword=CD79a
en-keyword=prognosis
kn-keyword=prognosis
en-keyword=immunohistochemistry
kn-keyword=immunohistochemistry
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=4
article-no=
start-page=269
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20201210
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pulmonary Manifestations of Plasma Cell Type Idiopathic Multicentric Castleman Disease: A Clinicopathological Study in Comparison with IgG4-Related Disease 
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Plasma cell type idiopathic multicentric Castleman disease (PC-iMCD) occasionally manifests as parenchymal lung disease. This study aimed to elucidate the detailed clinicopathological features of lung lesions in PC-iMCD and compare the findings with those in immunoglobulin (Ig) G4-related disease (IgG4-RD), the most difficult differential diagnosis of PC-iMCD. We analyzed the clinicopathological findings and immunohistochemical expression patterns of interleukin-6 (IL-6) and Igs in lung specimens from 16 patients with PC-iMCD and 7 patients with IgG4-RD. Histologically, pulmonary PC-iMCD could not be differentiated from IgG4-RD based on lesion distribution patterns, the number of lymphoid follicles and obliterative vasculitis, or fibrosis types. The eosinophil count was higher in the IgG4-RD group than in the PC-iMCD group (p = 0.004). The IgG4/IgG-positive cell ratio was significantly higher in the IgG4-RD group (p < 0.001). The IgA-positive cell count and IL-6 expression intensity were higher in the PC-iMCD group than in the IgG4-RD group (p < 0.001). Based on these findings, we proposed a new diagnostic approach to differentiate lung lesions of PC-iMCD and IgG4-RD. Our approach can be utilized to stratify patients with suspected lung-dominant PC-iMCD to identify candidates for strong immunosuppressive treatment, including IL-6 blockade, at an early stage.
en-copyright=
kn-copyright=

en-aut-name=NishimuraMidori Filiz
en-aut-sei=Nishimura
en-aut-mei=Midori Filiz
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IgawaTakuro
en-aut-sei=Igawa
en-aut-mei=Takuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=GionYuka
en-aut-sei=Gion
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TomitaSakura
en-aut-sei=Tomita
en-aut-mei=Sakura
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=InoueDai
en-aut-sei=Inoue
en-aut-mei=Dai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IzumozakiAkira
en-aut-sei=Izumozaki
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=UbaraYoshifumi
en-aut-sei=Ubara
en-aut-mei=Yoshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NishimuraYoshito
en-aut-sei=Nishimura
en-aut-mei=Yoshito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YoshinoTadashi
en-aut-sei=Yoshino
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SatoYasuharu
en-aut-sei=Sato
en-aut-mei=Yasuharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

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

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

affil-num=3
en-affil=Division of Pathophysiology, Okayama University Graduate School of Health Sciences
kn-affil=

affil-num=4
en-affil=Department of Pathology, Tokai University School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Radiology, Kanazawa University Graduate School of Medical Sciences
kn-affil=

affil-num=6
en-affil=Department of Radiology, Kanazawa University Graduate School of Medical Sciences
kn-affil=

affil-num=7
en-affil=Nephrology Center, Toranomon Hospital Kajigaya
kn-affil=

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

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

affil-num=10
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=plasma cell type idiopathic multicentric Castleman disease
kn-keyword=plasma cell type idiopathic multicentric Castleman disease
en-keyword=IL-6
kn-keyword=IL-6
en-keyword=IgG4-related disease
kn-keyword=IgG4-related disease
en-keyword=immunohistochemistry
kn-keyword=immunohistochemistry
en-keyword=hyper IL-6 syndrome
kn-keyword=hyper IL-6 syndrome
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=6
cd-vols=
no-issue=12
article-no=
start-page=e05743
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=202012
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Antioxidative attributes of rice bran extracts in ameliorative effects of atherosclerosis-associated risk factors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Oxidative stress, chronic inflammation, dyslipidemia, hyperglycemia, and shear stress (physical effect) are risk factors associated with the pathogenesis of atherosclerosis. Rice bran, a by-product of rice milling process, is known to house polyphenols and vitamins which exhibit potent antioxidant and anti-inflammatory properties. Through recent emerging knowledge of rice bran in health and wellness, the present study was aimed to assess the ameliorative effects of rice bran extracts (RBE) derived from Japanese colored rice varieties in modulating risk factors of atherosclerosis via in vitro and in vivo study models. Pre-treatment of lipopolysaccharide (LPS)-stimulated murine J774A.1 macrophage-like cells with RBE alleviated nitric oxide (NO) overproduction and downregulated gene expressions of pro-inflammatory modulators: tumor necrosis factor-α (TNF-α), interleukin (IL)-α (IL-1α), IL-1β, IL-6, and inducible nitric oxide synthase (iNOS). In addition, RBE also significantly attenuated LPS-stimulated protein expressions of iNOS, TNF-α, IL-1α, and IL-6 in J774A.1 macrophage-like cells as compared to non-treated LPS control group. In in vivo, 12 weeks of RBE dietary supplementations significantly reduced (p < 0.05) total cholesterol, triglycerides, and pro-atherogenic oxidized LDL/β2-glycoprotein I (oxLDL/β2GPI) complexes at plasma levels, in high fat diet (HFD) induced low density lipoprotein receptor knockout (Ldlr?/-) mice. En face pathological assessments of murine aortas also revealed significant reductions by 38% (p < 0.05) in plaque sizes of RBE-supplemented HFD mice groups as compared to non RBE-supplemented HFD control mice group. Moreover, gene expressions of aortic (iNOS, TNF-α, IL-1β) and hepatic (TNF-α, IL-1α, IL-1β) pro-inflammatory modulators were also downregulated in RBE-supplemented mice groups. Present study has revealed the potent health attributes and application of RBE as a dietary supplement to attenuate risks of inadvertent oxidative damage and chronic inflammation underlying the pathogenesis of atherosclerosis. Intrinsically, present preliminary findings may provide global health prospects for future dietary implementation of RBE in management of atherosclerosis.
en-copyright=
kn-copyright=

en-aut-name=XianWen Tan
en-aut-sei=Xian
en-aut-mei=Wen Tan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KobayashiKazuko
en-aut-sei=Kobayashi
en-aut-mei=Kazuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LianhuaShen
en-aut-sei=Lianhua
en-aut-mei=Shen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=InagakiJunko
en-aut-sei=Inagaki
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IdeMasahiro
en-aut-sei=Ide
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HwangSiaw San
en-aut-sei=Hwang
en-aut-mei=Siaw San
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsuuraEiji
en-aut-sei=Matsuura
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

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

affil-num=2
en-affil=Collaborative Research Center for OMIC, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Pathophysiology, Zunyi Medical University
kn-affil=

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

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

affil-num=6
en-affil=School of Chemical Engineering and Science, Faculty of Engineering, Computing and Science, Swinburne University of Technology Sarawak Campus
kn-affil=

affil-num=7
en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=Food science
kn-keyword=Food science
en-keyword=Food analysis
kn-keyword=Food analysis
en-keyword=Rice bran extract (RBE)
kn-keyword=Rice bran extract (RBE)
en-keyword=Functional food
kn-keyword=Functional food
en-keyword=Phytochemicals
kn-keyword=Phytochemicals
en-keyword=Atherosclerosis
kn-keyword=Atherosclerosis
en-keyword=Oxidative stress
kn-keyword=Oxidative stress
en-keyword=Inflammation
kn-keyword=Inflammation
en-keyword=Antioxidant
kn-keyword=Antioxidant
en-keyword=Anti-inflammation
kn-keyword=Anti-inflammation
en-keyword=Oxidized lipoprotein (oxLDL)
kn-keyword=Oxidized lipoprotein (oxLDL)
END

start-ver=1.4
cd-journal=joma
no-vol=39
cd-vols=
no-issue=3
article-no=
start-page=188
end-page=196
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=2020
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cyclic nigerosylnigerose ameliorates DSS-induced colitis with restoration of goblet cell number and increase in IgA reactivity against gut microbiota in mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cyclic nigerosylnigerose (CNN) is a cyclic oligosaccharide. Oral administration of CNN promotes immunoglobulin A (IgA) secretion in the gut. IgA is a major antibody secreted into the gut and plays a crucial role in suppressing gut inflammation due to commensal gut microbiota. To investigate the effect of administration of CNN to promote IgA secretion on gut inflammation, experimental colitis was induced with dextran sulfate sodium (DSS) in Balb/c mice after 6 weeks of CNN pre-feeding. The severity of colitis was evaluated based on a disease activity index (DAI), the gene expression of inflammatory cytokines, and a histological examination. The CNN-treated mice with DSS-induced colitis (CNN-DSS group) showed significantly lower DAI scores and mRNA levels of interleukin-1 compared with the CNN-untreated mice with DSS-induced colitis (DSS group). Histological examination of the colon revealed that the pathological score was significantly lower in the CNN-DSS group compared with the DSS group due to the reduced infiltration of immune cells. The number of goblet cells was significantly higher in the CNN-DSS group compared with the DSS group. The IgA concentration and the ratio of microbiota coated with IgA were evaluated in the cecal content. Although there was no difference in the IgA concentration among groups, a higher proportion of cecal microbiota were coated with IgA in the CNN-DSS group compared with that in the DSS group. These results suggest that CNN might preserve goblet cells in the colon and promote IgA coating of gut microbiota, which synergistically ameliorate gut inflammation in mice with DSS-induced colitis.
en-copyright=
kn-copyright=

en-aut-name=TsurutaTakeshi
en-aut-sei=Tsuruta
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KatsumataEmiko
en-aut-sei=Katsumata
en-aut-mei=Emiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MizoteAkiko
en-aut-sei=Mizote
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=JianHou Jian
en-aut-sei=Jian
en-aut-mei=Hou Jian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MuhomahTeresia Aluoch
en-aut-sei=Muhomah
en-aut-mei=Teresia Aluoch
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NishinoNaoki
en-aut-sei=Nishino
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Laboratory of Animal Nutrition, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Laboratory of Animal Nutrition, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Hayashibara Co., Ltd.
kn-affil=

affil-num=4
en-affil=Laboratory of Animal Nutrition, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=5
en-affil=Laboratory of Animal Nutrition, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=6
en-affil=Laboratory of Animal Nutrition, Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=oligosaccharide
kn-keyword=oligosaccharide
en-keyword=DSS-induced colitis
kn-keyword=DSS-induced colitis
en-keyword=goblet cell
kn-keyword=goblet cell
en-keyword=gut microbiota
kn-keyword=gut microbiota
en-keyword=immunoglobulin A
kn-keyword=immunoglobulin A
END

start-ver=1.4
cd-journal=joma
no-vol=39
cd-vols=
no-issue=3
article-no=
start-page=117
end-page=122
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200227
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Oral administration of the probiotic bacterium Lactobacillus acidophilus strain L-55 modulates the immunological parameters of the laying hen inoculated with a Newcastle disease virus-based live attenuated vaccine
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Probiotic supplements containing living bacteria have attracted interest as a potential source of health benefits for humans and livestock. The aim of this study was to determine whether administration of Lactobacillus acidophilus strain L-55 (LaL-55) enhances the immune response among chicks exposed to a Newcastle disease virus (NDV)-based live attenuated vaccine. Oral administration of LaL-55 augmented the elevation in the total numbers of leukocytes and lymphocytes following inoculation with the NDV-based live attenuated vaccine. Monocyte counts increased after LaL-55 administration independent of inoculation with the NDV vaccine. Among chicks that were administered LaL-55, there was a dose-dependent increase in the NK cell activity measured by a 51Cr release assay at 2 weeks after the secondary NDV vaccine inoculation. Two weeks after the secondary inoculation with the NDV vaccine, interferon (IFN)-γ-mRNA expression was significantly elevated in mononuclear splenocytes from chicks that were administered LaL-55. Meanwhile, LaL-55 administration did not change the mRNA levels of IFN-α, IFN-β, and interleukin-1β. These results may suggest that coadministration of LaL-55 with an NDV vaccine augments the immune response against the virus. Therefore, LaL-55 may help protect against viral diseases in poultry.
en-copyright=
kn-copyright=

en-aut-name=HoDung Thi
en-aut-sei=Ho
en-aut-mei=Dung Thi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HatabuToshimitsu
en-aut-sei=Hatabu
en-aut-mei=Toshimitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SunadaYosuke
en-aut-sei=Sunada
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoYasuhiro
en-aut-sei=Kondo
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Research & Development, Ohayo Dairy Products Co., Ltd.
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=Lactobacillus acidophilus L-55
kn-keyword=Lactobacillus acidophilus L-55
en-keyword=chicken
kn-keyword=chicken
en-keyword=Newcastle disease vaccine
kn-keyword=Newcastle disease vaccine
en-keyword=immunomodulatory
kn-keyword=immunomodulatory
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=1
article-no=
start-page=6869
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200422
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Deficiency of CD44 prevents thoracic aortic dissection in a murine model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Thoracic aortic dissection (TAD) is a life-threatening vascular disease. We showed that CD44, a widely distributed cell surface adhesion molecule, has an important role in inflammation. In this study, we examined the role of CD44 in the development of TAD. TAD was induced by the continuous infusion of beta-aminopropionitrile (BAPN), a lysyl oxidase inhibitor, and angiotensin II (AngII) for 7 days in wild type (WT) mice and CD44 deficient (CD44(-/-)) mice. The incidence of TAD in CD44(-/-) mice was significantly reduced compared with WT mice (44% and 6%, p<0.01). Next, to evaluate the initial changes, aortic tissues at 24hours after BAPN/AngII infusion were examined. Neutrophil accumulation into thoracic aortic adventitia in CD44(-/-) mice was significantly decreased compared with that in WT mice (5.7 +/- 0.3% and 1.6 +/- 0.4%, p<0.01). In addition, BAPN/AngII induced interleukin-6, interleukin-1 beta, matrix metalloproteinase-2 and matrix metalloproteinase-9 in WT mice, all of which were significantly reduced in CD44(-/-) mice (all p<0.01). In vitro transmigration of neutrophils from CD44(-/-) mice through an endothelial monolayer was significantly decreased by 18% compared with WT mice (p<0.01). Our findings indicate that CD44 has a critical role in TAD development in association with neutrophil infiltration into adventitia.
en-copyright=
kn-copyright=

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

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YonezawaTomoko
en-aut-sei=Yonezawa
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoMegumi
en-aut-sei=Kondo
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AmiokaNaofumi
en-aut-sei=Amioka
en-aut-mei=Naofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

en-aut-name=HirohataSatoshi
en-aut-sei=Hirohata
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
ORCID=

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

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

affil-num=3
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

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

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

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

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

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

affil-num=9
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
en-keyword=Aneurysm
kn-keyword=Aneurysm
en-keyword=Aortic diseases
kn-keyword=Aortic diseases
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=
article-no=
start-page=1461
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200714
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=High Mobility Group Box 1 Expression in Oral Inflammation and Regeneration
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=High mobility group box 1 (HMGB1) is a non-histone DNA-binding protein of about 30 kDa. It is released from a variety of cells into the extracellular milieu in response to inflammatory stimuli and acts on specific cell-surface receptors, such as receptors for advanced glycation end-products (RAGE), Toll-like receptor (TLR)2, TLR4, with or without forming a complex with other molecules. HMGB1 mediates various mechanisms such as inflammation, cell migration, proliferation, and differentiation. On the other hand, HMGB1 enhances chemotaxis acting through the C-X-C motif chemokine ligand (CXCL)12/C-X-C chemokine receptor (CXCR)4 axis and is involved in regeneration. In the oral cavity, high levels of HMGB1 have been detected in the gingival tissue from periodontitis and peri-implantitis patients, and it has been shown that secreted HMGB1 induces pro-inflammatory cytokine expression, such as interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha, which prolong inflammation. In contrast, wound healing after tooth extraction or titanium dental implant osseointegration requires an initial acute inflammation, which is regulated by secreted HMGB1. This indicates that secreted HMGB1 regulates angiogenesis and bone remodeling by osteoclast and osteoblast activation and promotes bone healing in oral tissue repair. Therefore, HMGB1 can prolong inflammation in the periodontal tissue and, conversely, can regenerate or repair damaged tissues in the oral cavity. In this review, we highlight the role of HMGB1 in the oral cavity by comparing its function and regulation with its function in other diseases. We also discuss the necessity for further studies in this field to provide more specific scientific evidence for dentistry.
en-copyright=
kn-copyright=

en-aut-name=YamashiroKeisuke
en-aut-sei=Yamashiro
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IdeguchiHidetaka
en-aut-sei=Ideguchi
en-aut-mei=Hidetaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AoyagiHiroaki
en-aut-sei=Aoyagi
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=Yoshihara-HirataChiaki
en-aut-sei=Yoshihara-Hirata
en-aut-mei=Chiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HiraiAnna
en-aut-sei=Hirai
en-aut-mei=Anna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=Suzuki-KyoshimaRisa
en-aut-sei=Suzuki-Kyoshima
en-aut-mei=Risa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ZhangYao
en-aut-sei=Zhang
en-aut-mei=Yao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WakeHidenori
en-aut-sei=Wake
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

en-aut-name=YamamotoTadashi
en-aut-sei=Yamamoto
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakashibaShogo
en-aut-sei=Takashiba
en-aut-mei=Shogo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Periodontics and Endodontics, Okayama University Hospital
kn-affil=

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

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

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

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

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

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

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

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

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

affil-num=11
en-affil=Department of Pathophysiology-Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=high mobility group box 1
kn-keyword=high mobility group box 1
en-keyword=inflammation
kn-keyword=inflammation
en-keyword=periodontal regeneration
kn-keyword=periodontal regeneration
en-keyword=periodontitis
kn-keyword=periodontitis
en-keyword=osseointegration
kn-keyword=osseointegration
en-keyword=tooth movement
kn-keyword=tooth movement
en-keyword=wound healing
kn-keyword=wound healing
END

start-ver=1.4
cd-journal=joma
no-vol=33
cd-vols=
no-issue=12
article-no=
start-page=2437
end-page=2448
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200619
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinicopathological analysis of 34 Japanese patients with EBV-positive mucocutaneous ulcer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Epstein?Barr virus (EBV)-positive mucocutaneous ulcer (EBVMCU) is a unifocal mucosal or cutaneous ulcer that is histologically characterized by proliferating EBV-positive atypical B cells. While EBVMCU demonstrates a histology similar to that of EBV-positive diffuse large B-cell lymphoma (DLBCL), their clinical behavior differs. Thus, characterizing distinguishing features of EBVMCU and EBV-positive DLBCL is critical. To identify unique characteristics between EBVMCU and lymphoma, we analyzed the clinicopathological and genetic features of 34 Japanese patients with EBVMCU and compared them to those of 24 EBV-positive DLBCL patients and 25 EBV-negative DLBCL patients. All patients with EBVMCU had localized ulcerative lesions, and 31 patients (91%) were using immunosuppressants, such as methotrexate (MTX) or hydroxycarbamide. All patients that were followed up with exhibited good prognosis following immunosuppressant reduction or chemotherapy. In addition, 17 EBV-positive DLBCL patients, and 15 EBV-negative DLBCL patients, received chemotherapy (P?<?0.001, P?<?0.001, respectively). Our data showed that EBVMCU did not increase indicators associated with lymphoma prognosis, such as soluble interleukin 2 receptor (sIL-2R) and lactate dehydrogenase (LDH) compared to those in the EBV-positive DLBCL or EBV-negative DLBCL groups (sIL-2R, P?<?0.001, P?=?0.025; LDH, P?=?0.018, P?=?0.038, respectively). However, histologically, EBVMCU exhibited EBV-positive, variable-sized, atypical B-cell proliferation. Thus, EBVMCU was histologically classified as: (1) polymorphous; (2) large cell-rich; (3) classic Hodgkin lymphoma-like; and (4) mucosa-associated lymphoid tissue lymphoma-like. Moreover, genetic analysis showed that immunoglobin heavy chain (IGH) gene rearrangement did not differ significantly between EBVMCU and EBV-positive DLBCL (44% vs. 32%; P?=?0.377), or between EBVMCU and EBV-negative DLBCL (44% vs. 58%; P?=?0.280). Therefore, it is difficult to distinguish EBVMCU from EBV-positive DLBCL using only pathological and genetic findings, suggesting that clinical information is important in accurately distinguishing between EBVMCU and EBV-positive DLBCL.
en-copyright=
kn-copyright=

en-aut-name=IkedaTomoka
en-aut-sei=Ikeda
en-aut-mei=Tomoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=GionYuka
en-aut-sei=Gion
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SakamotoMisa
en-aut-sei=Sakamoto
en-aut-mei=Misa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TachibanaTomoyasu
en-aut-sei=Tachibana
en-aut-mei=Tomoyasu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NishikoriAsami
en-aut-sei=Nishikori
en-aut-mei=Asami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NishimuraMidori Filiz
en-aut-sei=Nishimura
en-aut-mei=Midori Filiz
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshinoTadashi
en-aut-sei=Yoshino
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SatoYasuharu
en-aut-sei=Sato
en-aut-mei=Yasuharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

affil-num=3
en-affil=Okayama University Graduate School of Health Sciences
kn-affil=

affil-num=4
en-affil=Department of Otolaryngology, Japanese Red Cross Society Himeji Hospital
kn-affil=

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

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

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

affil-num=8
en-affil=Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Lymphoid tissues
kn-keyword=Lymphoid tissues
en-keyword=Lymphoma
kn-keyword=Lymphoma
END

start-ver=1.4
cd-journal=joma
no-vol=21
cd-vols=
no-issue=9
article-no=
start-page=3140
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200429
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Induction of CEMIP in Chondrocytes by Inflammatory Cytokines: Underlying Mechanisms and Potential Involvement in Osteoarthritis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In patients with osteoarthritis (OA), there is a decrease in both the concentration and molecular size of hyaluronan (HA) in the synovial fluid and cartilage. Cell migration-inducing hyaluronidase 1 (CEMIP), also known as hyaluronan (HA)-binding protein involved in HA depolymerization (HYBID), was recently reported as an HA depolymerization-related molecule expressed in the cartilage of patients with OA. However, the underlying mechanism of CEMIP regulation is not well understood. We found that CEMIP expression was transiently increased by interleukine-1 beta (IL-1 beta) stimulation in chondrocytic cells. We also observed that ERK activation and NF-kappa B nuclear translocation were involved in the induction of CEMIP by IL-1 beta. In addition, both administration of HA and mechanical strain attenuated the CEMIP induction in IL-1 beta-stimulated chondrocytes. In conclusion, we clarified the regulatory mechanism of CEMIP in chondrocytes by inflammatory cytokines and suggested the potential involvement in osteoarthritis development.
en-copyright=
kn-copyright=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HatipogluOmer F.
en-aut-sei=Hatipoglu
en-aut-mei=Omer F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AsanoKeiichi
en-aut-sei=Asano
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=InagakiJunko
en-aut-sei=Inagaki
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NishidaKeiichiro
en-aut-sei=Nishida
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HirohataSatoshi
en-aut-sei=Hirohata
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

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

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

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

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

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

affil-num=6
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=
en-keyword=cell migration-inducing hyaluronidase 1 (CEMIP)
kn-keyword=cell migration-inducing hyaluronidase 1 (CEMIP)
en-keyword=chondrocyte
kn-keyword=chondrocyte
en-keyword=hyaluronan
kn-keyword=hyaluronan
en-keyword=mechanical strain
kn-keyword=mechanical strain
en-keyword=nuclear factor kappa B (NF-kappa B)
kn-keyword=nuclear factor kappa B (NF-kappa B)
en-keyword=osteoarthritis
kn-keyword=osteoarthritis
END

start-ver=1.4
cd-journal=joma
no-vol=83
cd-vols=
no-issue=
article-no=
start-page=106429
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=202006
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The fungal metabolite (+)-terrein abrogates osteoclast differentiation via suppression of the RANKL signaling pathway through NFATc1
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pathophysiological bone resorption is commonly associated with periodontal disease and involves the excessive resorption of bone matrix by activated osteoclasts. Receptor activator of nuclear factor (NF)-κB ligand (RANKL) signaling pathways have been proposed as targets for inhibiting osteoclast differentiation and bone resorption. The fungal secondary metabolite (+)-terrein is a natural compound derived from Aspergillus terreus that has previously shown anti-interleukin-6 properties related to inflammatory bone resorption. However, its effects and molecular mechanism of action on osteoclastogenesis and bone resorption remain unclear. In the present study, we showed that 10 ?M synthetic (+)-terrein inhibited RANKL-induced osteoclast formation and bone resorption in a dose-dependent manner and without cytotoxicity. RANKL-induced messenger RNA expression of osteoclast-specific markers including nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), the master regulator of osteoclastogenesis, cathepsin K, tartrate-resistant acid phosphatase (Trap) was completely inhibited by synthetic (+)-terrein treatment. Furthermore, synthetic (+)-terrein decreased RANKL-induced NFATc1 protein expression. This study revealed that synthetic (+)-terrein attenuated osteoclast formation and bone resorption by mediating RANKL signaling pathways, especially NFATc1, and indicated the potential effect of (+)-terrein on inflammatory bone resorption including periodontal disease.
en-copyright=
kn-copyright=

en-aut-name=NakagawaSaki
en-aut-sei=Nakagawa
en-aut-mei=Saki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OmoriKazuhiro
en-aut-sei=Omori
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakayamaMasaaki
en-aut-sei=Nakayama
en-aut-mei=Masaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MandaiHiroki
en-aut-sei=Mandai
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamamotoSatoshi
en-aut-sei=Yamamoto
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KobayashiHiroya
en-aut-sei=Kobayashi
en-aut-mei=Hiroya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakoHidefumi
en-aut-sei=Sako
en-aut-mei=Hidefumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SakaidaKyosuke
en-aut-sei=Sakaida
en-aut-mei=Kyosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YoshimuraHiroshi
en-aut-sei=Yoshimura
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=IshiiSatoki
en-aut-sei=Ishii
en-aut-mei=Satoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=IbaragiSoichiro
en-aut-sei=Ibaragi
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=HiraiKimito
en-aut-sei=Hirai
en-aut-mei=Kimito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=YamashiroKeisuke
en-aut-sei=Yamashiro
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=YamamotoTadashi
en-aut-sei=Yamamoto
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=SugaSeiji
en-aut-sei=Suga
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=TakashibaShogo
en-aut-sei=Takashiba
en-aut-mei=Shogo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

affil-num=1
en-affil=Department of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Periodontics and Endodontics, Okayama University Hospital
kn-affil=

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

affil-num=4
en-affil=Department of Medical Technology, School of Health Science, Gifu University of Medical Science
kn-affil=

affil-num=5
en-affil=Department of Periodontics and Endodontics, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Department of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama Universit
kn-affil=

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

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

affil-num=9
en-affil=ivision of Applied Chemistry, Graduate School of Natural Sciences and Technology, Okayama University
kn-affil=

affil-num=10
en-affil=Division of Applied Chemistry, Graduate School of Natural Sciences and Technology, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Oral Maxillofacial Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

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

affil-num=13
en-affil=Department of Periodontics and Endodontics, Okayama University Hospital
kn-affil=

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

affil-num=15
en-affil=Division of Applied Chemistry, Graduate School of Natural Sciences and Technology, Okayama University
kn-affil=

affil-num=16
en-affil=Department of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Synthetic (+)-terrein
kn-keyword=Synthetic (+)-terrein
en-keyword=Osteoclast
kn-keyword=Osteoclast
en-keyword=RANKL
kn-keyword=RANKL
en-keyword=NFATc1
kn-keyword=NFATc1
END

start-ver=1.4
cd-journal=joma
no-vol=41
cd-vols=
no-issue=3
article-no=
start-page=364
end-page=370
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=202003
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Role of Macrophage Migration Inhibitory Factor in NLRP3 Inflammasome Expression in Otitis Media
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Hypothesis: 

Macrophage migration inhibitory factor plays an important role in the expression of interleukin (IL)-1β and the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome in lipopolysaccharide-induced otitis media.

Background: 

NLRP3 inflammasome and macrophage migration inhibitory factor are critical molecules mediating inflammation. However, the interaction between the NLRP3 inflammasome and macrophage migration inhibitory factor has not been fully examined.

Methods: 

Wild-type mice and macrophage migration inhibitory factor gene-deficient (MIF?/?) mice received a transtympanic injection of either lipopolysaccharide or phosphate-buffered saline. The mice were sacrificed 24 hours after the injection. Concentrations of IL-1β, NLRP3, ASC (apoptosis-associated speck-like protein containing a caspase recruitment domain and a pyrin domain), and caspase-1 in the middle ear effusions were measured by enzyme-linked immunosorbent assay. Temporal bones were processed for histologic examination and immunohistochemistry.

Results: 

In the immunohistochemical study using the wild-type mice, positive staining of macrophage migration inhibitory factor, NLRP3, ASC, and caspase-1 were observed in infiltrating inflammatory cells induced by lipopolysaccharide in the middle ear. The number of inflammatory cells caused by lipopolysaccharide administration decreased remarkably in the MIF?/? mice as compared with the wild-type mice. The concentrations of IL-1β, NLRP3, ASC, and caspase-1 increased in the lipopolysaccharide-treated wild-type mice. The MIF?/? mice with lipopolysaccharide had decreased levels of IL-1β, NLRP3, ASC, and caspase-1 as compared with the wild-type mice.

Conclusion: 

Macrophage migration inhibitory factor has an important role in the production of IL-1β and the NLRP3 inflammasome. Controlling the inflammation by modulating macrophage migration inhibitory factor and the NLRP3 inflammasome may be a novel therapeutic strategy for otitis media.
en-copyright=
kn-copyright=

en-aut-name=KariyaShin
en-aut-sei=Kariya
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OkanoMitsuhiro
en-aut-sei=Okano
en-aut-mei=Mitsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ZhaoPengfei
en-aut-sei=Zhao
en-aut-mei=Pengfei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MaedaYukihide
en-aut-sei=Maeda
en-aut-mei=Yukihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KataokaYuko
en-aut-sei=Kataoka
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HigakiTakaya
en-aut-sei=Higaki
en-aut-mei=Takaya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MakiharaSeiichiro
en-aut-sei=Makihara
en-aut-mei=Seiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NishihiraJun
en-aut-sei=Nishihira
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TachibanaTomoyasu
en-aut-sei=Tachibana
en-aut-mei=Tomoyasu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NishizakiKazunori
en-aut-sei=Nishizaki
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Otolaryngology?Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Otolaryngology?Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Otolaryngology?Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Otolaryngology?Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Otolaryngology?Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Otolaryngology?Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Otolaryngology?Head and Neck Surgery, Kagawa Rosai Hospital
kn-affil=

affil-num=8
en-affil=Department of Medical Bioinformatics, Hokkaido Information University
kn-affil=

affil-num=9
en-affil=Departments of Otolaryngology, Japanese Red Cross Society Himeji Hospital
kn-affil=

affil-num=10
en-affil=Department of Otolaryngology?Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Cytokine
kn-keyword=Cytokine
en-keyword=Infection
kn-keyword=Infection
en-keyword=Inflammation
kn-keyword=Inflammation
en-keyword=Interleukin
kn-keyword=Interleukin
en-keyword=NOD-like receptor
kn-keyword=NOD-like receptor
en-keyword=Toll-like receptor
kn-keyword=Toll-like receptor
END

start-ver=1.4
cd-journal=joma
no-vol=20
cd-vols=
no-issue=1
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200113
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Hemophagocytic lymphohistiocytosis complicating invasive pneumococcal disease: a pediatric case report
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background<br/>
Hemophagocytic lymphohistiocytosis (HLH) is an infrequent but life-threatening disease due to excessive immune activation. Secondary HLH can be triggered by infections, autoimmune diseases, and malignant diseases. Streptococcus pneumoniae is a pathogenic bacterium responsible for invasive pneumococcal disease (IPD) such as meningitis and bacteremia. Although the pneumococcal conjugate vaccine (PCV) has led to reductions in IPD incidence, cases of IPD caused by serotypes not included in PCV are increasing. There are few reports of secondary HLH caused by IPD in previously healthy children. We herein report a rare case of a previously healthy boy with secondary HLH complicating IPD of serotype 23A, which is not included in the pneumococcal 13-valent conjugate vaccine (PCV-13).<br/>
Case presentation<br/>
An 11-month-old boy who had received three doses of PCV-13 was hospitalized with prolonged fever, bilateral otitis media, neutropenia and elevated C-reactive protein (CRP) levels. Blood culture on admission revealed S. pneumoniae, leading to a diagnosis of IPD. HLH was diagnosed based on a prolonged fever, neutropenia, anemia, hepatosplenomegaly, hemophagocytosis in the bone marrow, and elevated serum levels of triglycerides, ferritin, and soluble interleukin-2 receptor. He received broad-spectrum antibiotics and intravenous immunoglobulins for IPD and high-dose steroid pulse therapy and cyclosporine A for HLH; thereafter, his fever resolved, and laboratory findings improved. The serotype of the isolated S. pneumoniae was 23A, which is not included in PCV-13.<br/>
Conclusions<br/>
It is important to consider secondary HLH as a complication of IPD cases with febrile cytopenia or hepatosplenomegaly, and appropriate treatment for HLH should be started without delay.
en-copyright=
kn-copyright=

en-aut-name=TsugeMitsuru
en-aut-sei=Tsuge
en-aut-mei=Mitsuru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyamotoMachiko
en-aut-sei=Miyamoto
en-aut-mei=Machiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MiyawakiReiji
en-aut-sei=Miyawaki
en-aut-mei=Reiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoYoichi
en-aut-sei=Kondo
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TsukaharaHirokazu
en-aut-sei=Tsukahara
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

affil-num=2
en-affil=Department of Pediatrics, Matsuyama Red Cross Hospital
kn-affil=

affil-num=3
en-affil=Department of Pediatrics,Ehime University Graduate School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Pediatrics, Matsuyama Red Cross Hospital
kn-affil=

affil-num=5
en-affil=Department of Pediatrics, Matsuyama Red Cross Hospital
kn-affil=
en-keyword=Child
kn-keyword=Child
en-keyword=Hemophagocytic lymphohistiocytosis
kn-keyword=Hemophagocytic lymphohistiocytosis
en-keyword=Invasive pneumococcal disease
kn-keyword=Invasive pneumococcal disease
en-keyword=Pneumococcal conjugate vaccine
kn-keyword=Pneumococcal conjugate vaccine
en-keyword=Serotype replacement
kn-keyword=Serotype replacement
END

start-ver=1.4
cd-journal=joma
no-vol=383
cd-vols=
no-issue=2
article-no=
start-page=111556
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20191015
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mechanical strain attenuates cytokine-induced ADAMTS9 expression via transient receptor potential vanilloid type 1
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= The synovial fluids of patients with osteoarthritis (OA) contain elevated levels of inflammatory cytokines, which induce the expression of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) and of the matrix metalloproteinase (MMP) in chondrocytes. Mechanical strain has varying effects on organisms depending on the strength, cycle, and duration of the stressor; however, it is unclear under inflammatory stimulation how mechanical strain act on. Here, we show that mechanical strain attenuates inflammatory cytokine-induced expression of matrix-degrading enzymes. Cyclic tensile strain (CTS), as a mechanical stressor, attenuated interleukin (IL)-1β and tumor necrosis factor (TNF)-α-induced mRNA expression of ADAMTS4, ADAMTS9, and MMP-13 in normal chondrocytes (NHAC-kn) and in a chondrocytic cell line (OUMS-27). This effect was abolished by treating cells with mechano-gated channel inhibitors, such as gadolinium, transient receptor potential (TRP) family inhibitor, ruthenium red, and with pharmacological and small interfering RNA-mediated TRPV1 inhibition. Furthermore, nuclear factor κB (NF-κB) translocation from the cytoplasm to the nucleus resulting from cytokine stimulation was also abolished by CTS. These findings suggest that mechanosensors such as the TRPV protein are potential therapeutic targets in treating OA.
en-copyright=
kn-copyright=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShinaokaAkira
en-aut-sei=Shinaoka
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Kumagishi-ShinaokaKanae
en-aut-sei=Kumagishi-Shinaoka
en-aut-mei=Kanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AsanoKeiichi
en-aut-sei=Asano
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HatipogluOmer Faruk
en-aut-sei=Hatipoglu
en-aut-mei=Omer Faruk
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=InagakiJunko
en-aut-sei=Inagaki
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakahashiKen
en-aut-sei=Takahashi
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NishidaKeiichiro
en-aut-sei=Nishida
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HirohataSatoshi
en-aut-sei=Hirohata
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

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

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

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

affil-num=4
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

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

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

affil-num=8
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

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

affil-num=11
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=5
article-no=
start-page=433
end-page=440
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=201910
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Relationship between Intracellular Signaling of the (Pro)renin Receptor and the Pathogenesis of Preeclampsia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= An association between preeclampsia and (pro)renin was recently reported. Intracellular signaling of the (pro) renin receptor [(P)RR] increases the expressions of TGF-β and PAI-1. In this study we sought to clarify the involvement of (pro)renin in the pathogenesis of preeclampsia via the intracellular signaling of (P)RR on preeclampsia placentas. Activated (pro)renin plasma concentrations were compared between pregnant women with (n=15) and without (n=28) preeclampsia. The placentas were immunohistochemically evaluated with anti-HIF-1α and anti-(P)RR antibodies. HTR-8/SVneo cells were cultured under hypoxic conditions and treated with human recombinant (pro)renin. The mRNA expressions of HIF-1α, (P)RR, PAI-1, TGF-β, and ET-1 were also examined by real-time RCR. The activated (pro)renin plasma concentration was significantly higher in the third vs. the second trimester in the preeclampsia patients. HIF-1α and (P)RR expressions were significantly increased in the preeclampsia placentas. The mRNA expressions of PAI-1, TGF-β, and ET-1 were significantly increased in the experiments using recombinant (pro)renin vs. hypoxic conditions. (P)RR expression in preeclampsia placentas is increased by persistent hypoxia through the second and third trimesters, and PAI-1, TGF-β, and ET-1 production is increased via (P)RR. Our results suggest that ET-1 production via the intracellular signaling of (P)RR is important in the pathogenesis of preeclampsia.
en-copyright=
kn-copyright=

en-aut-name=TamadaShoko
en-aut-sei=Tamada
en-aut-mei=Shoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MitsuiTakashi
en-aut-sei=Mitsui
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OhiraAkiko
en-aut-sei=Ohira
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TaniKazumasa
en-aut-sei=Tani
en-aut-mei=Kazumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MakiJota
en-aut-sei=Maki
en-aut-mei=Jota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=EguchiTakeshi
en-aut-sei=Eguchi
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=EtoEriko
en-aut-sei=Eto
en-aut-mei=Eriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HayataKei
en-aut-sei=Hayata
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MasuyamaHisashi
en-aut-sei=Masuyama
en-aut-mei=Hisashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

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

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

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

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

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

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

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

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

affil-num=9
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=preeclampsia
kn-keyword=preeclampsia
en-keyword=(pro)renin
kn-keyword=(pro)renin
en-keyword=(pro)renin receptor
kn-keyword=(pro)renin receptor
en-keyword=endothelin-1
kn-keyword=endothelin-1
en-keyword=HTR-8/SVneo
kn-keyword=HTR-8/SVneo
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=5
article-no=
start-page=383
end-page=386
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=201910
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Role of High Mobility Group Box-1 in Epileptogenesis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= High mobility group box-1 (HMGB1) is a non-histone, DNA-binding nuclear protein belonging to the family of damage-associated molecular patterns (DAMPs). HMGB1 has been reported to play an important role during epileptogenesis although the mechanisms of its actions are still not clear. Many hypotheses have been suggested especially about the relationship between HMGB1 and inflammation responses and blood-brain barrier disruption during epileptogenesis. In this review, we will mainly discuss the role of HMGB1 in epileptogenesis.
en-copyright=
kn-copyright=

en-aut-name=FuLi
en-aut-sei=Fu
en-aut-mei=Li
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishiboriMasahiro
en-aut-sei=Nishibori
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

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

affil-num=2
en-affil=Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=HMGB1
kn-keyword=HMGB1
en-keyword=epileptogenesis
kn-keyword=epileptogenesis
en-keyword=inflammation
kn-keyword=inflammation
en-keyword=blood-brain barrier
kn-keyword=blood-brain barrier
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=1
article-no=
start-page=41
end-page=50
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=201902
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Predictive Factors for Successful Vaccination Against Hepatitis B Surface Antigen in Patients Who Have Undergone Orthotopic Liver Transplantation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Post-orthotopic liver transplantation (OLT) hepatitis B recurrence is well-controlled with a nucleos(t)ide analogue and hepatitis B immunoglobulin (HBIG) combination, but the high cost and the potential risk of unknown infection associated with HBIG remain unresolved issues. Low-cost recombinant hepatitis B virus (HBV) vaccine administration is a potential solution to these problems. We retrospectively analyzed the rate and predictive factors of HBV vaccine success in 49 post-OLT patients: liver cirrhosis-type B (LC-B), n=28 patients; acute liver failure-type B (ALF-B), n=8; and non-HBV-related end-stage liver disease (non-B ESLD) who received a liver from anti-hepatitis B core antibody-positive donors, n=13. A positive anti-hepatitis B surface antibody response was achieved in 29% (8/28) of the LC-B group, 88% (7/8) of the ALF-B group, and 44% (4/9) of the adult non-B ESLD group. All four non-B ESLD infants showed vaccine success. The predictive factors for a good response in LC-B were young age, marital donor, and high donor age. ALF-B and non-B ESLD infants are thus good vaccination candidates. LC-B patients with marital donors are also good candidates, perhaps because the donated liver maintains an efficient immune memory to HBV, as the donors had already been infected in adulthood and showed adequate anti-HBV immune responses.
en-copyright=
kn-copyright=

en-aut-name=IkedaAilee
en-aut-sei=Ikeda
en-aut-mei=Ailee
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakakiAkinobu
en-aut-sei=Takaki
en-aut-mei=Akinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YasunakaTetsuya
en-aut-sei=Yasunaka
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OyamaAtsushi
en-aut-sei=Oyama
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AdachiTakuya
en-aut-sei=Adachi
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WadaNozomu
en-aut-sei=Wada
en-aut-mei=Nozomu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OnishiHideki
en-aut-sei=Onishi
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IkedaFusao
en-aut-sei=Ikeda
en-aut-mei=Fusao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShirahaHidenori
en-aut-sei=Shiraha
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YoshidaKazuhiro
en-aut-sei=Yoshida
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KuiseTakashi
en-aut-sei=Kuise
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NobuokaDaisuke
en-aut-sei=Nobuoka
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=YoshidaRyuichi
en-aut-sei=Yoshida
en-aut-mei=Ryuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=UmedaYuzo
en-aut-sei=Umeda
en-aut-mei=Yuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=YagiTakahito
en-aut-sei=Yagi
en-aut-mei=Takahito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=FujiwaraToshiyoshi
en-aut-sei=Fujiwara
en-aut-mei=Toshiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=OkadaHiroyuki
en-aut-sei=Okada
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

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

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

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

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

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

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

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

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

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

affil-num=10
en-affil=Department of Gastroenterological Surgery, Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Gastroenterological Surgery, Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Gastroenterological Surgery, Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Gastroenterological Surgery, Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Gastroenterological Surgery, Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Gastroenterological Surgery, Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of Gastroenterological Surgery, Transplant and Surgical Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=17
en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=acute liver failure
kn-keyword=acute liver failure
en-keyword=hepatitis B
kn-keyword=hepatitis B
en-keyword=hepatitis B vaccine
kn-keyword=hepatitis B vaccine
en-keyword=liver cirrhosis
kn-keyword=liver cirrhosis
en-keyword=liver transplantation
kn-keyword=liver transplantation
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=1
article-no=
start-page=29
end-page=39
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=201902
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Histidine-rich Glycoprotein Could Be an Early Predictor of Vasospasm after Aneurysmal Subarachnoid Hemorrhage
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Cerebral vasospasm (CVS) is a major contributor to the high morbidity and mortality of aneurysmal subarachnoid hemorrhage (aSAH) patients. We measured histidine-rich glycoprotein (HRG), a new biomarker of aSAH, in cerebrospinal fluid (CSF) to investigate whether HRG might be an early predictor of CVS. A total of seven controls and 14 aSAH patients (8 males, 6 females aged 53.4±15.4 years) were enrolled, and serial CSF and serum samples were taken. We allocated these samples to three phases (T1-T3) and measured HRG, interleukin (IL)-6, fibrinopeptide A (FpA), and 8-hydroxy-2’-deoxyguanosine (8OHdG) in the CSF, and the HRG in serum. We also examined the release of HRG in rat blood incubated in artificial CSF. In contrast to the other biomarkers examined, the change in the CSF HRG concentration was significantly different between the nonspasm and spasm groups (p<0.01). The rat blood/CSF model revealed a time course similar to that of the human CSF samples in the non-spasm group. HRG thus appears to have the potential to become an early predictor of CVS. In addition, the interaction of HRG with IL-6, FpA, and 8OHdG may form the pathology of CVS.
en-copyright=
kn-copyright=

en-aut-name=MatsumotoAtsushi
en-aut-sei=Matsumoto
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraTakehiro
en-aut-sei=Nakamura
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShinomiyaAya
en-aut-sei=Shinomiya
en-aut-mei=Aya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawakitaKenya
en-aut-sei=Kawakita
en-aut-mei=Kenya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KawanishiMasahiko
en-aut-sei=Kawanishi
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyakeKeisuke
en-aut-sei=Miyake
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KurodaYasuhiro
en-aut-sei=Kuroda
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KeepRichard F.
en-aut-sei=Keep
en-aut-mei=Richard F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TamiyaTakashi
en-aut-sei=Tamiya
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Neurological Surgery, Kagawa University Faculty of Medicine
kn-affil=

affil-num=2
en-affil=Department of Medical Technology, Kagawa Prefectural University of Health Sciences
kn-affil=

affil-num=3
en-affil=Department of Neurological Surgery, Kagawa University Faculty of Medicine
kn-affil=

affil-num=4
en-affil=Emergency Medical Center, Kagawa University Hospital
kn-affil=

affil-num=5
en-affil=Department of Neurological Surgery, Kagawa University Faculty of Medicine
kn-affil=

affil-num=6
en-affil=Department of Neurological Surgery, Kagawa University Faculty of Medicine
kn-affil=

affil-num=7
en-affil=Emergency Medical Center, Kagawa University Hospital
kn-affil=

affil-num=8
en-affil=Department of Neurosurgery, University of Michigan
kn-affil=

affil-num=9
en-affil=Department of Neurological Surgery, Kagawa University Faculty of Medicine
kn-affil=
en-keyword=biomarker
kn-keyword=biomarker
en-keyword=histidine-rich glycoprotein
kn-keyword=histidine-rich glycoprotein
en-keyword=predictor
kn-keyword=predictor
en-keyword=subarachnoid hemorrhage
kn-keyword=subarachnoid hemorrhage
en-keyword=vasospasm
kn-keyword=vasospasm
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=6
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=201902
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Role of Kallikrein-Related Peptidases in Atopic Dermatitis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Excessive protease activity is a characteristic abnormality that affects the epidermal barrier in patients with atopic dermatitis (AD). Kallikrein-related peptidases (KLKs) are excessively expressed in AD lesions, and it is suggested that the abnormal action of KLKs is involved in the skin barrier dysfunction in AD. In other words, overexpressed KLKs disrupt the normal barrier function, and due to that breakdown, external substances that can become antigens of AD easily invade the epidermis, resulting in dermatitis, coupled with the induction of Th2 cytokines. Further investigations are required to elucidate the role of KLKs in AD; this knowledge could contribute to the design of new therapeutic and prophylactic drugs for AD.
en-copyright=
kn-copyright=

en-aut-name=MorizaneShin
en-aut-sei=Morizane
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=atopic dermatitis
kn-keyword=atopic dermatitis
en-keyword=kallikrein-related peptidases
kn-keyword=kallikrein-related peptidases
en-keyword=epidermal barrier dysfunction
kn-keyword=epidermal barrier dysfunction
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2018
dt-pub=20180323
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=EGFR遺伝子変異を有する進行非小細胞肺癌患者におけるInterleukin-6のgefitinibの治療効果における影響
kn-title=Potential influence of interleukin-6 on the therapeutic effect of gefitinib in patients with  advanced non-small cell lung cancer harbouring EGFR mutations
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TamuraTomoki
en-aut-sei=Tamura
en-aut-mei=Tomoki
kn-aut-name=田村朋季
kn-aut-sei=田村
kn-aut-mei=朋季
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2017
dt-pub=20170929
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=PD-1は低用量インターロイキン2療法における制御性T細胞のホメオスターシスを制御する
kn-title=PD-1 modulates regulatory T-cell homeostasis during low-dose interleukin-2 therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=AsanoTakeru
en-aut-sei=Asano
en-aut-mei=Takeru
kn-aut-name=淺野豪
kn-aut-sei=淺野
kn-aut-mei=豪
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=50
cd-vols=
no-issue=1
article-no=
start-page=66
end-page=74
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20161122
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Accelerated cell cycle progression of human regulatory T cell-like cell line caused by continuous exposure to asbestos fibers
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Asbestos exposure causes malignant tumors such as lung cancer and malignant mesothelioma. Based on our hypothesis in which continuous exposure to asbestos of immune cells cause reduction of antitumor immunity, the decrease of natural killer cell killing activity with reduction of NKp46 activating receptor expression, inhibition of cytotoxic T cell clonal expansion, reduced CXCR3 chemokine receptor expression and production of interferon-γ production in CD4+ T cells were reported using cell line models, freshly isolated peripheral blood immune cells from health donors as well as asbestos exposed patients such as pleural plaque and mesothelioma. In addition to these findings, regulatory T cells (Treg) showed enhanced function through cell-cell contact and increased secretion of typical soluble factors, interleukin (IL)-10 and transforming growth factor (TGF)-β, in a cell line model using the MT-2 human polyclonal T cells and its sublines exposed continuously to asbestos fibers. Since these sublines showed a remarkable reduction of FoxO1 transcription factor, which regulates various cell cycle regulators in asbestos-exposed sublines, the cell cycle progression in these sublines was examined and compared with that of the original MT-2 cells. Results showed that cyclin D1 expression was markedly enhanced, and various cyclin-dependent kinase-inhibitors were reduced with increased S phases in the sublines. Furthermore, the increase of cyclin D1 expression was regulated by FoxO1. The overall findings indicate that antitumor immunity in asbestos-exposed individuals may be reduced in Treg through changes in the function and volume of Treg.
en-copyright=
kn-copyright=

en-aut-name=LeeSuni
en-aut-sei=Lee
en-aut-mei=Suni
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuzakiHidenori
en-aut-sei=Matsuzaki
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MaedaMegumi
en-aut-sei=Maeda
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamamotoShoko
en-aut-sei=Yamamoto
en-aut-mei=Shoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=Kumagai-TakeiNaoko
en-aut-sei=Kumagai-Takei
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HatayamaTamayo
en-aut-sei=Hatayama
en-aut-mei=Tamayo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IkedaMiho
en-aut-sei=Ikeda
en-aut-mei=Miho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YoshitomeKei
en-aut-sei=Yoshitome
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NishimuraYasumitsu
en-aut-sei=Nishimura
en-aut-mei=Yasumitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OtsukiTakemi
en-aut-sei=Otsuki
en-aut-mei=Takemi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Hygiene, Kawasaki Medical School
kn-affil=

affil-num=2
en-affil=Department of Hygiene, Kawasaki Medical School
kn-affil=

affil-num=3
en-affil=Department of Biofunctional Chemistry, Division of Bioscience, Okayama University Graduate School of Natural Science and Technology
kn-affil=

affil-num=4
en-affil=Department of Hygiene, Kawasaki Medical School
kn-affil=

affil-num=5
en-affil=
kn-affil=

affil-num=6
en-affil=Department of Hygiene, Kawasaki Medical School
kn-affil=

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

affil-num=8
en-affil=Department of Hygiene, Kawasaki Medical School
kn-affil=

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

affil-num=10
en-affil=Department of Hygiene, Kawasaki Medical School
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=49
cd-vols=
no-issue=2
article-no=
start-page=499
end-page=508
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20160531
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=TGF-β in jaw tumor fluids induces RANKL expression in stromal fibroblasts
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Odontogenic tumors and cysts, arising in the jawbones, grow by resorption and destruction of the jawbones. However, mechanisms underlying bone resorption by odontogenic tumors/cysts remain unclear. Odontogenic tumors/cysts comprise odontogenic epithelial cells and stromal fibroblasts, which originate from the developing tooth germ. It has been demonstrated that odontogenic epithelial cells of the developing tooth germ induce osteoclastogenesis to prevent the tooth germ from invading the developing bone to maintain its structure in developing bones. Thus, we hypothesized that odontogenic epithelial cells of odontogenic tumors/cysts induce osteoclast formation, which plays potential roles in tumor/cyst outgrowth into the jawbone. The purpose of this study was to examine osteoclastogenesis by cytokines, focusing on transforming growth factor-β (TGF-β), produced by odontogenic epithelial cells. We observed two pathways for receptor activator of NF-κB ligand (RANKL) induction by keratocystic odontogenic tumor fluid: the cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) pathway through interleukin-1α (IL-1α) signaling and non-COX-2/PGE2 pathway through TGF-β receptor signaling. TGF-β1 and IL-1α produced by odontogenic tumors/cysts induced osteoclastogenesis directly in the osteoclast precursor cells and indirectly via increased RANKL induction in the stroma.
en-copyright=
kn-copyright=

en-aut-name=YamadaChiaki
en-aut-sei=Yamada
en-aut-mei=Chiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AikawaTomonao
en-aut-sei=Aikawa
en-aut-mei=Tomonao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OkunoEmi
en-aut-sei=Okuno
en-aut-mei=Emi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyagawaKazuaki
en-aut-sei=Miyagawa
en-aut-mei=Kazuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AmanoKatsuhiko
en-aut-sei=Amano
en-aut-mei=Katsuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakahataSosuke
en-aut-sei=Takahata
en-aut-mei=Sosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KimataMasaaki
en-aut-sei=Kimata
en-aut-mei=Masaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OkuraMasaya
en-aut-sei=Okura
en-aut-mei=Masaya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IidaSeiji
en-aut-sei=Iida
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KogoMikihiko
en-aut-sei=Kogo
en-aut-mei=Mikihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Oral and Maxillofacial Reconstructive Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
kn-affil=

affil-num=3
en-affil=Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
kn-affil=

affil-num=4
en-affil=Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
kn-affil=

affil-num=5
en-affil=Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
kn-affil=

affil-num=7
en-affil=Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
kn-affil=

affil-num=8
en-affil=Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
kn-affil=

affil-num=9
en-affil=Department of Oral and Maxillofacial Reconstructive Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2017
dt-pub=20170324
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Effects of synthetic (+)-terrein on secretion of proteins induced by interleukin-6 and the target molecules on signaling pathway in human gingival fibroblasts
kn-title=真菌二次代謝産物である(+)-terrein がヒト歯肉線維芽細胞におけるinterleukin-6 誘導性タンパク質の産生に及ぼす影響とその標的分子の解明
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=YamamotoSatoshi
en-aut-sei=Yamamoto
en-aut-mei=Satoshi
kn-aut-name=山本総司
kn-aut-sei=山本
kn-aut-mei=総司
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=71
cd-vols=
no-issue=1
article-no=
start-page=49
end-page=57
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2017
dt-pub=201702
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Verification of Implant Surface Modification by a Novel Processing Method
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Metals have been used clinically as biomaterials, especially in the orthopaedic and dental fields. Metals used as implants wear at contact surfaces, producing metal particles and metal ions that may be harmful. Newly developed metal implants and methods of implant surface modification are currently under scrutiny. We evaluated the use of electrolytic in-process dressing (ELID) as a surface finishing method for metal implants. Metal implants processed using the ELID method (ELID group) or not processed (Non-ELID group) were inserted surgically into rabbit femurs. The rabbits were sacrificed postoperatively over a 24-week period. We assessed the concentrations of the cytokines, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α, the resistance to implant pull-out, and histopathology at the implant site. There was no significant difference between the groups regarding the cytokine concentrations or implant pull-out resistance. Many particles indicating wear around the implant were noted in the Non-ELID group (n=10) but not the ELID group (n=13), while a fibrous membrane adhering to the every implant was noted in the ELID group. The formation of a fibrous membrane rather than metal particles in the ELID group may indicate improved biocompatibility, and it suggests that ELID may prevent corrosion in the areas of contact.
en-copyright=
kn-copyright=

en-aut-name=OkadaYoshiki
en-aut-sei=Okada
en-aut-mei=Yoshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AbeNobuhiro
en-aut-sei=Abe
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HisamoriNoriyuki
en-aut-sei=Hisamori
en-aut-mei=Noriyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KaneedaToshiaki
en-aut-sei=Kaneeda
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MoriyamaShigeaki
en-aut-sei=Moriyama
en-aut-mei=Shigeaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OhmoriHitoshi
en-aut-sei=Ohmori
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MizutaniMasayoshi
en-aut-sei=Mizutani
en-aut-mei=Masayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YanaiHiroyuki
en-aut-sei=Yanai
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakashimaYoshio
en-aut-sei=Nakashima
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YokoyamaYusuke
en-aut-sei=Yokoyama
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OzakiToshifumi
en-aut-sei=Ozaki
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

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

affil-num=2
en-affil=Department of Orthopaedic Surgery and Sport Medicine, General Medical Center Kawasaki Medical School
kn-affil=

affil-num=3
en-affil=Department of Science and Engineering, Sophia University
kn-affil=

affil-num=4
en-affil=Department of Mechanical System Engineering, Okayama University of Science
kn-affil=

affil-num=5
en-affil=Department of Mechanical Engineering, Fukuoka University
kn-affil=

affil-num=6
en-affil=Riken Ohmori Materials Fabrication Laboratory
kn-affil=

affil-num=7
en-affil=Department of Mechanical Systems and Design, Graduate School of Engineering, Tohoku University
kn-affil=

affil-num=8
en-affil=Department of Pathology, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Nakashima Medical Co., Ltd.
kn-affil=

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

affil-num=11
en-affil=Department of Orthopaedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=biomaterial
kn-keyword=biomaterial
en-keyword=surface modification
kn-keyword=surface modification
en-keyword=metal implant
kn-keyword=metal implant
en-keyword=wear
kn-keyword=wear
en-keyword=metal ion
kn-keyword=metal ion
END

start-ver=1.4
cd-journal=joma
no-vol=70
cd-vols=
no-issue=5
article-no=
start-page=429
end-page=433
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=201610
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Phase I/IIa Study of Low Dose Subcutaneous Interleukin-2 (IL-2) for Treatment of Refractory Chronic Graft Versus Host Disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Chronic graft versus host disease (cGVHD) remains a major problem for long survivors after allogeneic hematopoietic stem cell transplantation (HSCT). Currently, corticosteroid therapy is effective for cGVHD as the first line therapy. However, prolonged therapy with corticosteroids causes various severe adverse events. To develop the new therapeutic strategy of cGVHD, we have launched a multicenter phase I/IIa clinical trial of low dose subcutaneous interleukin-2 (IL-2) for treatment of steroid refractory cGVHD, which is constituted of 2 sequential phases (induction phase and maitanance phase). This study will provide the new therapeutic option for patients with refractory cGVHD after allogeneic HSCT.
en-copyright=
kn-copyright=

en-aut-name=AsanoTakeru
en-aut-sei=Asano
en-aut-mei=Takeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuokaKen-ichi
en-aut-sei=Matsuoka
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IyamaSatoshi
en-aut-sei=Iyama
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OhashiKazuteru
en-aut-sei=Ohashi
en-aut-mei=Kazuteru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=InamotoYoshihiro
en-aut-sei=Inamoto
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OhwadaChikako
en-aut-sei=Ohwada
en-aut-mei=Chikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MurataMakoto
en-aut-sei=Murata
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SatakeAtsushi
en-aut-sei=Satake
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YoshidaChikamasa
en-aut-sei=Yoshida
en-aut-mei=Chikamasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakaseKoichi
en-aut-sei=Nakase
en-aut-mei=Koichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MoriYasuo
en-aut-sei=Mori
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TanimotoMitsune
en-aut-sei=Tanimoto
en-aut-mei=Mitsune
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Medical Oncology and Hematology, Sapporo Medical University Hospital
kn-affil=

affil-num=4
en-affil=Hematology division, Tokyo Metropolitan Cancer and Infectious Diseases Center, Komagome Hospital
kn-affil=

affil-num=5
en-affil=Department of Hematopoietic Stem Cell Transplantation, National Cancer Center Hospital
kn-affil=

affil-num=6
en-affil=Department of Hematology, Chiba University Hospital
kn-affil=

affil-num=7
en-affil=Department of Hematology and Oncology, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=First Department of Internal Medicine, Kansai Medical University
kn-affil=

affil-num=9
en-affil=Division of Hematology, National Hospital Organization Minami-Okayama Medical Center
kn-affil=

affil-num=10
en-affil=Division of Hematology, Ehime Prefectural Central Hospital
kn-affil=

affil-num=11
en-affil=Department of Hematology and Oncology, Kyushu University Hospital
kn-affil=

affil-num=12
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=
en-keyword=chronic GVHD
kn-keyword=chronic GVHD
en-keyword=allogeneic HSCT
kn-keyword=allogeneic HSCT
en-keyword=steroid refractory
kn-keyword=steroid refractory
en-keyword=IL-2
kn-keyword=IL-2
END

start-ver=1.4
cd-journal=joma
no-vol=128
cd-vols=
no-issue=2
article-no=
start-page=91
end-page=94
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20160801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The 2015 Incentive Award of the Okayama Medical Association in General Medical Science (2015 Yuuki Prize)
kn-title=平成27年度岡山医学会賞 総合研究奨励賞（結城賞）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KajitaAi
en-aut-sei=Kajita
en-aut-mei=Ai
kn-aut-name=梶田藍
kn-aut-sei=梶田
kn-aut-mei=藍
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Dermatology, Okayama University Hospital
kn-affil=岡山大学病院　皮膚科
END

start-ver=1.4
cd-journal=joma
no-vol=128
cd-vols=
no-issue=1
article-no=
start-page=9
end-page=11
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20160401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The 2014 Incentive Award of the Okayama Medical Association in General Medical Science (2014 Yuuki Prize)
kn-title=平成26年度岡山医学会賞 総合研究奨励賞（結城賞）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TakeuchiMai
en-aut-sei=Takeuchi
en-aut-mei=Mai
kn-aut-name=竹内真衣
kn-aut-sei=竹内
kn-aut-mei=真衣
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　病理学
END

start-ver=1.4
cd-journal=joma
no-vol=70
cd-vols=
no-issue=1
article-no=
start-page=37
end-page=43
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=201602
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effects of Dexmedetomidine on Serum Interleukin-6, Hemodynamic Stability, and Postoperative Pain Relief in Elderly Patients under Spinal Anesthesia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The beneficial effects of dexmedetomidine (DEX) have not been extensively investigated in elderly patients receiving spinal anesthesia. This study evaluated the effects of intravenous DEX infusion on stress and hemodynamic response, as well as on postoperative analgesia in elderly patients undergoing total knee arthroplasty (TKA). We randomly allocated 45 adult patients to 3 patient groups (n=15 each): uni-saline group patients underwent unilateral TKA with saline administration, uni-DEX group patients underwent unilateral TKA with DEX administration, and bilateral-DEX group patients underwent bilateral TKA with DEX administration. Serum interleukin-6 (IL-6) levels were significantly lower in the bilateral-DEX group than in the uni-saline group 6 and 24h postoperatively, and were negatively correlated with total DEX dosage 24h postoperatively. Bradycardia occurred more frequently in the uni-DEX and bilateral-DEX groups than in the uni-saline group. The total dose of required supplementary analgesics was significantly higher in the uni-saline group than in the uni-DEX and bilateral-DEX groups 6h postoperatively. The results indicate that perioperative intravenous DEX administration decreases postoperative serum IL-6 levels in patients undergoing bilateral TKA, and has a postoperative analgesic effect in patients undergoing unilateral or bilateral TKA.
en-copyright=
kn-copyright=

en-aut-name=YunSo Hui
en-aut-sei=Yun
en-aut-mei=So Hui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ParkJong Cook
en-aut-sei=Park
en-aut-mei=Jong Cook
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KimSang Rim
en-aut-sei=Kim
en-aut-mei=Sang Rim
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ChoiYun Suk
en-aut-sei=Choi
en-aut-mei=Yun Suk
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Anesthesiology and Pain Medicine, Jeju National University School of Medicine

affil-num=2
en-affil=
kn-affil=Department of Anesthesiology and Pain Medicine, Jeju National University School of Medicine

affil-num=3
en-affil=
kn-affil=Department of Orthopedic Surgery, Jeju National University School of Medicine

affil-num=4
en-affil=
kn-affil=Department of Anesthesiology and Pain Medicine, Jeju National University School of Medicine
en-keyword=analgesic effect
kn-keyword=analgesic effect
en-keyword=dexmedetomidine
kn-keyword=dexmedetomidine
en-keyword=hemodynamic response
kn-keyword=hemodynamic response
en-keyword=stress response
kn-keyword=stress response
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=20150930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=リンパ芽球性リンパ腫患者における可溶性インターロイキン2受容体血清値とCD25発現の関連性
kn-title=Serum level of soluble interleukin-2 recepter correlates with CD25 expression in patients with T lymphoblastic lymphoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TojiTomohiro
en-aut-sei=Toji
en-aut-mei=Tomohiro
kn-aut-name=都地友紘
kn-aut-sei=都地
kn-aut-mei=友紘
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=69
cd-vols=
no-issue=5
article-no=
start-page=279
end-page=290
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=201510
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Inhibitory Effects of Edaravone, a Free Radical Scavenger, on Cytokine-induced Hyperpermeability of Human Pulmonary Microvascular Endothelial Cells:A Comparison with Dexamethasone and Nitric Oxide Synthase Inhibitor
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Lung hyperpermeability affects the development of acute respiratory distress syndrome (ARDS), but therapeutic strategies for the control of microvascular permeability have not been established. We examined the effects of edaravone, dexamethasone, and N-monomethyl-L-arginine (L-NMMA) on permeability changes in human pulmonary microvascular endothelial cells (PMVEC) under a hypercytokinemic state. Human PMVEC were seeded in a Boyden chamber. After monolayer confluence was achieved, the culture media were replaced respectively by culture media containing edaravone, dexamethasone, and L-NMMA. After 24-h incubation, the monolayer was stimulated with tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Fluorescein-labeled dextran was added. Then the trans-human PMVEC leak was measured. Expressions of vascular endothelial-cadherin (VE-cadherin) and zonula occludens-1 protein (ZO-1) were evaluated using real-time quantitative polymerase chain reaction and immunofluorescence microscopy. The results showed that TNF-α＋IL-1β markedly increased pulmonary microvascular permeability. Pretreatment with edaravone, dexamethasone, or L-NMMA attenuated the hyperpermeability and inhibited the cytokine-induced reduction of VE-cadherin expression on immunofluorescence staining. Edaravone and dexamethasone increased the expression of ZO-1 at both the mRNA and protein levels. Edaravone and dexamethasone inhibited the permeability changes of human PMVEC, at least partly through an enhancement of VE-cadherin. Collectively, these results suggest a potential therapeutic approach for intervention in patients with ARDS.
en-copyright=
kn-copyright=

en-aut-name=SaitoYukie
en-aut-sei=Saito
en-aut-mei=Yukie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujiiYousuke
en-aut-sei=Fujii
en-aut-mei=Yousuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YashiroMasato
en-aut-sei=Yashiro
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TsugeMitsuru
en-aut-sei=Tsuge
en-aut-mei=Mitsuru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NosakaNobuyuki
en-aut-sei=Nosaka
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamashitaNobuko
en-aut-sei=Yamashita
en-aut-mei=Nobuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamadaMutsuko
en-aut-sei=Yamada
en-aut-mei=Mutsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TsukaharaHirokazu
en-aut-sei=Tsukahara
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MorishimaTsuneo
en-aut-sei=Morishima
en-aut-mei=Tsuneo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

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

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

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

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

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

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

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

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

affil-num=9
en-affil=
kn-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=pulmonary microvascular endothelial cells
kn-keyword=pulmonary microvascular endothelial cells
en-keyword=permeability
kn-keyword=permeability
en-keyword=edaravone
kn-keyword=edaravone
en-keyword=vascular endothelial-cadherin
kn-keyword=vascular endothelial-cadherin
en-keyword=zonula occludens-1 protein
kn-keyword=zonula occludens-1 protein
END

start-ver=1.4
cd-journal=joma
no-vol=5
cd-vols=
no-issue=
article-no=
start-page=13539
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=2015
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A subset of ocular adnexal marginal zone lymphomas may arise in association with IgG4-related disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We previously suggested a relationship between ocular immunoglobulin (Ig)G4-related disease (IgG4-RD) and marginal zone lymphomas (MZLs). However, the cytokine background associated with these disorders and whether it differs between ocular adnexal MZLs with (IgG4-associated MZL) and without (IgG4-negative MZL) numerous IgG4+ plasma cells are unknown. In this study, we identified the mRNA expression pattern of Th2 and regulatory T-cell (Treg) cytokines in IgG4-RD and in IgG4-associated MZL and IgG4-negative MZL using real-time polymerase chain reaction analysis. Ocular IgG4-RD and IgG4-associated MZL exhibited significantly higher expression ratios of interleukin (IL)-4/β-actin, IL-10/β-actin, IL-13/β-actin, transforming growth factor (TGF) β1/β-actin, and FOXP3/β-actin than did IgG4-negative MZL (p?<?0.05). This finding further supports our prior observations that a significant subset of ocular MZLs arises in the setting of IgG4-RD. Furthermore, the presence of a different inflammatory background in IgG4-negative MZLs suggests that IgG4-associated MZLs may have a different pathogenesis.
en-copyright=
kn-copyright=

en-aut-name=KyotaroOhno
en-aut-sei=Kyotaro
en-aut-mei=Ohno
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YasuharuSato
en-aut-sei=Yasuharu
en-aut-mei=Sato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Koh-ichiOhshima
en-aut-sei=Koh-ichi
en-aut-mei=Ohshima
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KatsuyoshiTakata
en-aut-sei=Katsuyoshi
en-aut-mei=Takata
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TomokoMiyata-Takata
en-aut-sei=Tomoko
en-aut-mei=Miyata-Takata
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MaiTakeuchi
en-aut-sei=Mai
en-aut-mei=Takeuchi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YukaGion
en-aut-sei=Yuka
en-aut-mei=Gion
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TomoyasuTachibana
en-aut-sei=Tomoyasu
en-aut-mei=Tachibana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YorihisaOrita
en-aut-sei=Yorihisa
en-aut-mei=Orita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ToshihiroIto
en-aut-sei=Toshihiro
en-aut-mei=Ito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=StevenH. Swerdlow
en-aut-sei=Steven
en-aut-mei=H. Swerdlow
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TadashiYoshino
en-aut-sei=Tadashi
en-aut-mei=Yoshino
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

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

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

affil-num=3
en-affil=
kn-affil=Department of Ophthalmology, National Hospital Organization Okayama Medical Center

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

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

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

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

affil-num=8
en-affil=
kn-affil=Department of Otolaryngology, Himeji Red Cross Hospital

affil-num=9
en-affil=
kn-affil=Department of Otolaryngology, Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=10
en-affil=
kn-affil=Department of Immunology, Nara Medical University

affil-num=11
en-affil=
kn-affil=Department of Pathology, Division of Hematopathology, University of Pittsburgh School of Medicine

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

start-ver=1.4
cd-journal=joma
no-vol=127
cd-vols=
no-issue=2
article-no=
start-page=133
end-page=137
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=20150803
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=An investigator initiated phase II clinical trial of tamibarotene (AM80G) for chronic graft-versus-host disease
kn-title=慢性移植片対宿主病に対するタミバロテン（AM80G）の医師主導臨床第�U相試験
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NishimoriHisakazu
en-aut-sei=Nishimori
en-aut-mei=Hisakazu
kn-aut-name=西森久和
kn-aut-sei=西森
kn-aut-mei=久和
aut-affil-num=1
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=前田嘉信
kn-aut-sei=前田
kn-aut-mei=嘉信
aut-affil-num=2
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学病院

affil-num=2
en-affil=
kn-affil=岡山大学病院
en-keyword=臨床研究中核病院
kn-keyword=臨床研究中核病院
en-keyword=慢性GVHD
kn-keyword=慢性GVHD
en-keyword=タミバロテン
kn-keyword=タミバロテン
en-keyword=同種造血幹細胞移植
kn-keyword=同種造血幹細胞移植
en-keyword=Th17
kn-keyword=Th17
END

start-ver=1.4
cd-journal=joma
no-vol=127
cd-vols=
no-issue=1
article-no=
start-page=47
end-page=50
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=20150401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Gene therapy using REIC/Dkk-3-encoding adenoviral vector for the treatment of malignant pleural mesothelioma
kn-title=REIC/Dkk-3遺伝子発現アデノウイルスベクターを用いた悪性胸膜中皮腫に対する遺伝子治療
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=豊岡伸一
kn-aut-sei=豊岡
kn-aut-mei=伸一
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　臨床遺伝子医療学
en-keyword=悪性胸膜中皮腫
kn-keyword=悪性胸膜中皮腫
en-keyword=REIC/DKK-3
kn-keyword=REIC/DKK-3
en-keyword=遺伝子治療
kn-keyword=遺伝子治療
END

start-ver=1.4
cd-journal=joma
no-vol=4
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140702
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effects of hydrogen-rich water on aging periodontal tissues in rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Oxidative damage is involved in age-related inflammatory reactions. The anti-oxidative effects of hydrogen-rich water suppress oxidative damage, which may aid in inhibiting age-related inflammatory reactions. We investigated the effects of drinking hydrogen-rich water on aging periodontal tissues in healthy rats. Four-month-old male Fischer 344 rats (n = 12) were divided into two groups: the experimental group (hydrogen-rich water treatment) and the control group (distilled water treatment). The rats consumed hydrogen-rich water or distilled water until 16 months of age. The experimental group exhibited lower periodontal oxidative damage at 16 months of age than the control group. Although protein expression of interleukin-1 beta did not differ, gene expression of Nod-like receptor protein 3 inflammasomes was activated in periodontal tissues from the experimental group as compared with the control group. Drinking hydrogen-rich water is proposed to have anti-aging effects on periodontal oxidative damage, but not on inflammatory reactions in healthy rats.
en-copyright=
kn-copyright=

en-aut-name=TomofujiTakaaki
en-aut-sei=Tomofuji
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawabataYuya
en-aut-sei=Kawabata
en-aut-mei=Yuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KasuyamaKenta
en-aut-sei=Kasuyama
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=EndoYasumasa
en-aut-sei=Endo
en-aut-mei=Yasumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YonedaToshiki
en-aut-sei=Yoneda
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamaneMayu
en-aut-sei=Yamane
en-aut-mei=Mayu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AzumaTetsuji
en-aut-sei=Azuma
en-aut-mei=Tetsuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=EkuniDaisuke
en-aut-sei=Ekuni
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MoritaManabu
en-aut-sei=Morita
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

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

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

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

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

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

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

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

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

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

start-ver=1.4
cd-journal=joma
no-vol=156
cd-vols=
no-issue=1-2
article-no=
start-page=82
end-page=93
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201312
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=IL-7 promotes long-term in vitro survival of unique long-lived memory subset generated from mucosal effector memory CD4(+) T cells in chronic colitis mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Colitogenic memory CD4(+) T cells are important in the pathogenesis of inflammatory bowel disease (IBD). Although memory stem cells with high survival and self-renewal capacity were recently identified in both mice and humans, it is unclear whether a similar subset is present in chronic colitis mice. We sought to identify and purify a long-lived subset of colitogenic memory CD4(+) T cells, which may be targets for treatment of IBD. A long-lived subset of colitogenic memory CD4(+) T cells was purified using a long-term culture system. The characteristics of these cells were assessed. Interleukin (IL)-7 promoted the in vitro survival for >8 weeks of lamina propria (LP) CD4(+) T cells from colitic SOD mice previously injected with CD4(+)CD45RB(high) T cells. These cells were in a quiescent state and divided a maximum of 5 times in 4 weeks. LP CD4(+) T cells expressed higher levels of Bcl-2, integrin-alpha 4 beta 7, CXCR3 and CD25 after than before culture, as well as secreting high concentrations of IL-2 and low concentrations of IFN-gamma and IL-17 in response to intestinal bacterial antigens. LP CD4(+) T cells from colitic mice cultured with IL-7 for 8 weeks induced more severe colitis than LP CD4(+) T cells cultured for 4 weeks. We developed a novel culture system to purify a long-lived, highly pathogenic memory subset from activated LP CD4(+) T cells. IL-7 promoted long-term in vitro survival of this subset in a quiescent state. This subset will be a novel, effective target for the treatment of IBD.
en-copyright=
kn-copyright=

en-aut-name=TakaharaMasahiro
en-aut-sei=Takahara
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NemotoYasuhiro
en-aut-sei=Nemoto
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OshimaShigeru
en-aut-sei=Oshima
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MatsuzawaYu
en-aut-sei=Matsuzawa
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KanaiTakanori
en-aut-sei=Kanai
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OkamotoRyuichi
en-aut-sei=Okamoto
en-aut-mei=Ryuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TsuchiyaKiichiro
en-aut-sei=Tsuchiya
en-aut-mei=Kiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakamuraTetsuya
en-aut-sei=Nakamura
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YamamotoKazuhide
en-aut-sei=Yamamoto
en-aut-mei=Kazuhide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=WatanabeMamoru
en-aut-sei=Watanabe
en-aut-mei=Mamoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Tokyo Med & Dent Univ, Dept Gastroenterol & Hepatol, Grad Sch

affil-num=2
en-affil=
kn-affil=Tokyo Med & Dent Univ, Dept Gastroenterol & Hepatol, Grad Sch

affil-num=3
en-affil=
kn-affil=Tokyo Med & Dent Univ, Dept Gastroenterol & Hepatol, Grad Sch

affil-num=4
en-affil=
kn-affil=Tokyo Med & Dent Univ, Dept Gastroenterol & Hepatol, Grad Sch

affil-num=5
en-affil=
kn-affil=Keio Univ, Dept Internal Med, Div Gastroenterol & Hepatol, Sch Med

affil-num=6
en-affil=
kn-affil=Tokyo Med & Dent Univ, Dept Gastroenterol & Hepatol, Grad Sch

affil-num=7
en-affil=
kn-affil=Tokyo Med & Dent Univ, Dept Gastroenterol & Hepatol, Grad Sch

affil-num=8
en-affil=
kn-affil=Tokyo Med & Dent Univ, Dept Gastroenterol & Hepatol, Grad Sch

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

affil-num=10
en-affil=
kn-affil=Tokyo Med & Dent Univ, Dept Gastroenterol & Hepatol, Grad Sch
en-keyword=Inflammatory bowel disease
kn-keyword=Inflammatory bowel disease
en-keyword=Memory T cells
kn-keyword=Memory T cells
en-keyword=CD4
kn-keyword=CD4
en-keyword=IL-7
kn-keyword=IL-7
en-keyword=Cell culture
kn-keyword=Cell culture
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=1
article-no=
start-page=116
end-page=121
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=201101
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Serum levels of platelet-derived growth factor-BB and vascular endothelial growth factor as prognostic factors for patients with fulminant hepatic failure
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background and Aims: 

In animal models for acute liver injury, the administration of some angiogenic factors such as vascular endothelial growth factor (VEGF) and granulocyte-colony stimulating factor (G-CSF) are shown to reduce liver injury and improve liver proliferative capacity. The aim of the present study was to assess the role of angiogenic factors in fulminant hepatic failure (FHF). 

Methods: 

Serum levels of nine angiogenic factors (angiopoietin-2, follistatin, G-CSF, hepatocyte growth factor [HGF], interleukin-8, leptin, platelet-derived growth factor [PDGF]-BB, platelet endothelial cell adhesion molecule-1 and VEGF) were measured using the Bio-Plex Protein Array System in 30 patients, 17 of whom were diagnosed with FHF, 13 with acute hepatitis (AH), and 20 controls. 

Results: 

Serum levels of PDGF-BB and VEGF were lower in FHF patients than AH patients and controls (PDGF-BB; 2050 +/- 1572 pg/mL vs 4521 +/- 2419 pg/mL vs 8506 +/- 5500 pg/mL, VEGF; 39 +/- 38 pg/mL vs 144 +/- 122 pg/mL vs 205 +/- 121 pg/mL). By using univariate logistic regression models, serum levels of PDGF-BB and VEGF were associated with poor outcomes. Serum PDGF-BB levels were strongly correlated with serum VEGF levels (r = 0.70). Furthermore, serum PDGF-BB levels were significantly correlated with platelet counts (r = 0.79), PT activity (r = 0.37) and D.Bil/T.Bil ratio (r = 0.50), while serum VEGF levels were significantly correlated with platelet counts (r = 0.68) and PT activity (r = 0.38). 

Conclusions: 

We consider that serum levels of PDGF-BB and VEGF are worth investigating as biomarkers for predicting outcomes of FHF patients.
en-copyright=
kn-copyright=

en-aut-name=TakayamaHiroki
en-aut-sei=Takayama
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyakeYasuhiro
en-aut-sei=Miyake
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NousoKazuhiro
en-aut-sei=Nouso
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IkedaFusao
en-aut-sei=Ikeda
en-aut-mei=Fusao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShirahaHidenori
en-aut-sei=Shiraha
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakakiAkinobu
en-aut-sei=Takaki
en-aut-mei=Akinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KobashiHaruhiko
en-aut-sei=Kobashi
en-aut-mei=Haruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamamotoKazuhide
en-aut-sei=Yamamoto
en-aut-mei=Kazuhide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

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

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

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

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

affil-num=8
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Gastroenterol & Hepatol
en-keyword=fulminant hepatic failure
kn-keyword=fulminant hepatic failure
en-keyword=hepatocyte growth factor
kn-keyword=hepatocyte growth factor
en-keyword=platelet-derived growth factor-BB
kn-keyword=platelet-derived growth factor-BB
en-keyword=prognostic factor
kn-keyword=prognostic factor
en-keyword=vascular endothelial growth factor
kn-keyword=vascular endothelial growth factor
END

start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=4
article-no=
start-page=938
end-page=944
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201310
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Inhibition of RAGE signaling through the intracellular delivery of inhibitor peptides by PEI cationization
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The receptor for advanced glycation end products (RAGE) is a multi-ligand cell surface receptor and a member of the immunoglobulin superfamily. RAGE is involved in a wide range of inflammatory, degenerative and hyper-proliferative disorders which span over different organs by engaging diverse ligands, including advanced glycation end products, S100 family proteins, high-mobility group protein B1 (HMGB1) and amyloid beta. We previously demonstrated that the cytoplasmic domain of RAGE is phosphorylated upon the binding of ligands, enabling the recruitment of two distinct pairs of adaptor proteins, Toll-interleukin 1 receptor domain-containing adaptor protein (TIRAP) and myeloid differentiation protein 88 (MyD88). This engagement allows the activation of downstream effector molecules, and thereby mediates a wide variety of cellular processes, such as inflammatory responses, apoptotic cell death, migration and cell growth. Therefore, inhibition of the binding of TIRAP to RAGE may abrogate intracellular signaling from ligand-activated RAGE. In the present study, we developed inhibitor peptides for RAGE signaling (RAGE-I) by mimicking the phosphorylatable cytosolic domain of RAGE. RAGE-I was efficiently delivered into the cells by polyethylenimine (PEI) cationization. We demonstrated that RAGE-I specifically bound to TIRAP and abrogated the activation of Cdc42 induced by ligand-activated RAGE. Furthermore, we were able to reduce neuronal cell death induced by an excess amount of S100B and to inhibit the migration and invasion of glioma cells in vitro. Our results indicate that RAGE-I provides a powerful tool for therapeutics to block RAGE-mediated multiple signaling.
en-copyright=
kn-copyright=

en-aut-name=PutrantoEndy Widya
en-aut-sei=Putranto
en-aut-mei=Endy Widya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamamotoKen-Ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KataokaKen
en-aut-sei=Kataoka
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamadaHidenori
en-aut-sei=Yamada
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FutamiJun-Ichiro
en-aut-sei=Futami
en-aut-mei=Jun-Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HuhNam-Ho
en-aut-sei=Huh
en-aut-mei=Nam-Ho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

affil-num=4
en-affil=
kn-affil=Okayama Univ Sci, Fac Sci, Dept Life Sci

affil-num=5
en-affil=
kn-affil=Okayama Univ, Grad Sch Nat Sci & Biotechnol, Dept Med Bioengn Sci

affil-num=6
en-affil=
kn-affil=Okayama Univ, Grad Sch Nat Sci & Biotechnol, Dept Med Bioengn Sci

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

affil-num=8
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cell Biol
en-keyword=receptor for advanced glycation end products
kn-keyword=receptor for advanced glycation end products
en-keyword=Toll-interleukin 1 receptor domain-containing adaptor protein
kn-keyword=Toll-interleukin 1 receptor domain-containing adaptor protein
en-keyword=cationization
kn-keyword=cationization
en-keyword=S100B
kn-keyword=S100B
en-keyword=cell death
kn-keyword=cell death
en-keyword=cell migration
kn-keyword=cell migration
END

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

start-ver=1.4
cd-journal=joma
no-vol=67
cd-vols=
no-issue=4
article-no=
start-page=227
end-page=237
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Comprehensive Analysis of 174 Febrile Patients Admitted to Okayama University Hospital
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Primary care physicians often encounter patients with fever of unknown origin and without apparent causes. Recent advances in laboratory medicine have facilitated diagnostic procedures;however, it is still difficult to determine the critical febrile factor at an early stage. We reviewed the medical records of 174 patients who were admitted due to a chief complaint of fever (＞37.5℃) to our hospital during the period from 2004 to 2010. The patients were categorized into patients with infection, inflammation, neoplasm and drug-induced fever. Based on the analysis done by category, it was revealed that the patient's age, body temperature and duration of fever were closely related to the final diagnosis. Serum CRP levels were significantly low in the nonbacterial infection group, while serum levels of sIL-2R were high in neoplasm and drug-induced cases. CRP level on admission was weakly but significantly correlated with body temperature, while duration of fever was inversely related to body temperature. The effectiveness of PET-CT and tissue biopsy for diagnosis was considerably high, particularly in the categories of neoplasm and nonspecific inflammation, respectively, though the effectiveness of bacterial culture was low. Thus, a careful review of physical and laboratory information including body temperature, CRP level, duration of fever, gender difference and history of medication is indispensable for diagnosis. Stepwise categorization and disease classification by comprehensive and systemic checkup are very helpful for determining the causes of fever.
en-copyright=
kn-copyright=

en-aut-name=RyukoHiromasa
en-aut-sei=Ryuko
en-aut-mei=Hiromasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

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

affil-num=2
en-affil=
kn-affil=Department of General Medicine, Okayama University Graduate School of Medicine,Dentistry and Pharmaceutical Sciences
en-keyword=computed tomography (CT)
kn-keyword=computed tomography (CT)
en-keyword=C-reactive protein (CRP)
kn-keyword=C-reactive protein (CRP)
en-keyword=fluorodeoxyglucose positron emission tomography (FDG-PET)
kn-keyword=fluorodeoxyglucose positron emission tomography (FDG-PET)
en-keyword=fever of unknown origin (FUO)
kn-keyword=fever of unknown origin (FUO)
en-keyword=soluble interleukin-2 receptor (sIL-2R)
kn-keyword=soluble interleukin-2 receptor (sIL-2R)
END

start-ver=1.4
cd-journal=joma
no-vol=124
cd-vols=
no-issue=3
article-no=
start-page=197
end-page=201
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20121203
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Synthetic retinoid Am80 ameliorates chronic graft-versus-host disease by downregulating Th1 and Th17
kn-title=合成レチノイドAm80はTh1とTh17を抑制することにより慢性移植片対宿主病を改善する
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NishimoriHisakazu
en-aut-sei=Nishimori
en-aut-mei=Hisakazu
kn-aut-name=西森久和
kn-aut-sei=西森
kn-aut-mei=久和
aut-affil-num=1
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=前田嘉信
kn-aut-sei=前田
kn-aut-mei=嘉信
aut-affil-num=2
ORCID=

en-aut-name=TanimotoMitsune
en-aut-sei=Tanimoto
en-aut-mei=Mitsune
kn-aut-name=谷本光音
kn-aut-sei=谷本
kn-aut-mei=光音
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学
en-keyword=慢性移植片対宿主病
kn-keyword=慢性移植片対宿主病
en-keyword=同種造血幹細胞移植
kn-keyword=同種造血幹細胞移植
en-keyword=Th17細胞
kn-keyword=Th17細胞
en-keyword=Th1細胞
kn-keyword=Th1細胞
en-keyword=Am80
kn-keyword=Am80
END

start-ver=1.4
cd-journal=joma
no-vol=17
cd-vols=
no-issue=7
article-no=
start-page=484
end-page=491
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=201007
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Potent antitumor effects of combined therapy with a telomerase-specific, replication-competent adenovirus (OBP-301) and IL-2 in a mouse model of renal cell carcinoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=OBP-301 (a telomerase-specific, replication-competent adenovirus with hTERT promoter) was constructed in a previous study and it showed a strong anticancer effect by inducing cell lysis in human lung and prostate cancer cells. This study investigated the effectiveness of a combination therapy of OBP-301 and interleukin-2 (IL-2) in a mouse model of renal cell carcinoma (RCC). The cell-killing effect of OBP-301 was confirmed in vitro in the RENCA cancer cells. In in vivo experiment, luciferase-expressing RENCA cells were implanted in the left kidney and lung of BALB/c mice to prepare the RCC metastatic model. The animals were randomly divided into four treatment groups: PBS, IL-2 alone, OBP-301 alone and the combination. The analyses of orthotopic tumor weight, lung metastasis and luciferin-stained tumor images 14 days after each treatment showed significant tumor growth inhibition in the combination group in comparison with that in the OBP-301- or IL-2-treated groups. In addition, the percentage of regulatory T-cells (Tregs) in the combination group was significantly suppressed in comparison with that in the PBS and single-agent treatment groups. The outcomes of this study suggest that tumor-specific oncolytic immunovirotherapy may become an attractive strategy for the treatment of human RCC.
en-copyright=
kn-copyright=

en-aut-name=HuangP
en-aut-sei=Huang
en-aut-mei=P
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KakuH
en-aut-sei=Kaku
en-aut-mei=H
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ChenJ
en-aut-sei=Chen
en-aut-mei=J
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KashiwakuraY
en-aut-sei=Kashiwakura
en-aut-mei=Y
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SaikaT
en-aut-sei=Saika
en-aut-mei=T
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NasuY
en-aut-sei=Nasu
en-aut-mei=Y
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=UrataY
en-aut-sei=Urata
en-aut-mei=Y
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FujiwaraT
en-aut-sei=Fujiwara
en-aut-mei=T
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=WatanabeM
en-aut-sei=Watanabe
en-aut-mei=M
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KumonH
en-aut-sei=Kumon
en-aut-mei=H
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

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

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

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

affil-num=4
en-affil=
kn-affil=Innovation Center Okayama for Nanobio-Targeted Therapy, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

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

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

affil-num=7
en-affil=
kn-affil=Oncolys BioPharma Inc.

affil-num=8
en-affil=
kn-affil=Center for Gene and Cell Therapy, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

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

affil-num=10
en-affil=
kn-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
en-keyword=renal cell carcinoma
kn-keyword=renal cell carcinoma
en-keyword=OBP-301
kn-keyword=OBP-301
en-keyword=adenovirus
kn-keyword=adenovirus
en-keyword=hTERT
kn-keyword=hTERT
en-keyword=interleukin-2
kn-keyword=interleukin-2
END

start-ver=1.4
cd-journal=joma
no-vol=284
cd-vols=
no-issue=21
article-no=
start-page=14236
end-page=14244
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=20090522
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Overexpression of REIC/Dkk-3 in Normal Fibroblasts Suppresses Tumor Growth via Induction of Interleukin-7
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We previously showed that the tumor suppressor gene REIC/Dkk-3, when overexpressed by an adenovirus (Ad-REIC), exhibited a dramatic therapeutic effect on human cancers through a mechanism triggered by endoplasmic reticulum stress. Adenovirus vectors show no target cell specificity and thus may elicit unfavorable side effects through infection of normal cells even upon intra-tumoral injection. In this study, we examined possible effects of Ad-REIC on normal cells. We found that infection of normal human fibroblasts (NHF) did not cause apoptosis but induced production of interleukin (IL)-7. The induction was triggered by endoplasmic reticulum stress and mediated through IRE1 alpha, ASK1, p38, and IRF-1. When Ad-REIC-infected NHF were transplanted in a mixture with untreated human prostate cancer cells, the growth of the cancer cells was significantly suppressed. Injection of an IL-7 antibody partially abrogated the suppressive effect of Ad-REIC-infected NHF. These results indicate that Ad-REIC has another arm against human cancer, an indirect host-mediated effect because of overproduction of IL-7 by mis-targeted NHF, in addition to its direct effect on cancer cells.
en-copyright=
kn-copyright=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KataokaKen
en-aut-sei=Kataoka
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AbarzuaFernando
en-aut-sei=Abarzua
en-aut-mei=Fernando
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TanimotoRyuta
en-aut-sei=Tanimoto
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WatanabeMasami
en-aut-sei=Watanabe
en-aut-mei=Masami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ThanSwe Swe
en-aut-sei=Than
en-aut-mei=Swe Swe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KuroseKaoru
en-aut-sei=Kurose
en-aut-mei=Kaoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KashiwakuraYuji
en-aut-sei=Kashiwakura
en-aut-mei=Yuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OchiaiKazuhiko
en-aut-sei=Ochiai
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NasuYasutomo
en-aut-sei=Nasu
en-aut-mei=Yasutomo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KumonHiromi
en-aut-sei=Kumon
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=HuhNam-ho
en-aut-sei=Huh
en-aut-mei=Nam-ho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

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

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

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

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

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

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

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

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

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

affil-num=10
en-affil=
kn-affil=Innovation Center Okayama for Nanobio-Targeted Therapy, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

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

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

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

start-ver=1.4
cd-journal=joma
no-vol=122
cd-vols=
no-issue=2
article-no=
start-page=219
end-page=226
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=20090221
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Promotion of IL-4- and IL-5-dependent differentiation of anti-μ-primed B cells by ascorbic acid 2-glucoside
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The stable ascorbic acid derivative 2-O-alpha-D-glucopyranosyl-L-ascorbic acid (AA-2G) was used to investigate the role of ascorbic acid (AA) in B cell differentiation in vitro. AA-2G is stable in a solution unlike AA but is hydrolyzed by cellular alpha-glucosidase to release AA. Mouse spleen B cells were primed for 2 days with an anti-mu antibody in the presence of interleukin (IL)-4 and IL-5 and then washed and recultured with AA-2G in the presence of IL-4 and IL-5. AA-2G, but not AA, dose-dependently increased IgM production, the greatest enhancement being 150% at concentrations of more than 0.5 mM. In the absence of IL-4 and IL-5, primed B cells produced a negligible amount of IgM, and AA-2G had no effect. AA-2G-induced IgM production in the presence of IL-4 and IL-5 was inhibited by the alpha-glucosidase inhibitor castanospermine. Intracellular AA content, depleted during the priming period, increased by adding AA-2G at the start of reculture. Treatment of B cells with AA-2G resulted in an increase in the number of IgM-secreting cells, CD138-positive cells and CD45R/B220-negative cells. The number of viable cells in untreated cultures decreased gradually, but the decrease was significantly attenuated by AA-2G, resulting in about 70% more viable cells in AA-2G-treated cultures. AA-2G caused a slight but reproducible enhancement of DNA synthesis and a slight decrease in the number of cells with a sub-G1 DNA content. These results demonstrated that AA released from AA-2G enhanced cytokine-dependent IgM production in anti-mu-primed B cells and suggest that its effect is caused through promoting the differentiation of B cells to plasma cells and attenuating the gradual decrease in the number of viable cells.
en-copyright=
kn-copyright=

en-aut-name=IchiyamaKenji
en-aut-sei=Ichiyama
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MitsuzumiHitoshi
en-aut-sei=Mitsuzumi
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ZhongMing
en-aut-sei=Zhong
en-aut-mei=Ming
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TaiAkihiro
en-aut-sei=Tai
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TsuchiokaAkihiro
en-aut-sei=Tsuchioka
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KawaiSaeko
en-aut-sei=Kawai
en-aut-mei=Saeko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamamotoItaru
en-aut-sei=Yamamoto
en-aut-mei=Itaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=GohdaEiichi
en-aut-sei=Gohda
en-aut-mei=Eiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

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

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

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

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

affil-num=8
en-affil=
kn-affil=Department of Immunochemistry, Division of Pharmaceutical Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=2-O-α-D-Glucopyranosyl-l-ascorbic acid (AA-2G)
kn-keyword=2-O-α-D-Glucopyranosyl-l-ascorbic acid (AA-2G)
en-keyword=Ascorbic acid
kn-keyword=Ascorbic acid
en-keyword=Anti-μ antibody
kn-keyword=Anti-μ antibody
en-keyword=IgM production
kn-keyword=IgM production
en-keyword=B cell differentiation
kn-keyword=B cell differentiation
END

start-ver=1.4
cd-journal=joma
no-vol=22
cd-vols=
no-issue=9
article-no=
start-page=1003
end-page=1010
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2005
dt-pub=200509
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Interleukin-18 (IL-18) mRNA Expression and Localization of IL-18 mRNA-Expressing Cells in the Mouse Uterus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Interleukin-18 (IL-18) belongs to the interleukin-1 family and was identified as an interferon gamma inducing factor. We investigated IL-18 mRNA-expressing cells in the mouse uterus. By RNase protection assay, IL-18 mRNA and a subunit of IL-18 receptor mRNA were detected in the uterus. In the uterus, IL-18 mRNA levels increased during sexual maturation. In situ hybridization analysis demonstrated IL-18 mRNA-expressing cells in the mouse uterus of different ages. At 21 days of age, IL-18 mRNA-expressing cells were detected in the luminal epithelial cells and stromal cells although the IL-18 mRNA signal was weak. At 42 days of age, IL-18 mRNA signal was mainly detected in the stromal cells located near the myometrium, and in some of the luminal and glandular epithelial cells. In the uterus of 63-day-old adult mice, a strong hybridization signal for IL-18 mRNA was detected at estrus, but was weak at diestrus. IL-18 mRNA was mainly detected in the glandular epithelial cells and stromal cells. The effect of estradiol-17 beta (E-2) on IL-18 mRNA-expressing cells in the uterus was examined in ovariectomized mice. In oil-treated mice IL-18 mRNA signal was localized in luminal epithelial cells and stromal cells, while in E-2-treated mice IL-18 mRNA signal was localized in stromal cells alone. These results suggest that the mouse uterus has an IL-18 system, and IL-18 exerts a physiological role within the uterus in a paracrine manner, and that IL-18 gene expression is regulated by estrogen.
en-copyright=
kn-copyright=

en-aut-name=KusumotoKenji
en-aut-sei=Kusumoto
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MurakamiYousuke
en-aut-sei=Murakami
en-aut-mei=Yousuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OtsukiMariko
en-aut-sei=Otsuki
en-aut-mei=Mariko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KanayamaMunetoshi
en-aut-sei=Kanayama
en-aut-mei=Munetoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakeuchiSakae
en-aut-sei=Takeuchi
en-aut-mei=Sakae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakahashiSumio
en-aut-sei=Takahashi
en-aut-mei=Sumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Biology, Faculty of Science, Okayama University

affil-num=2
en-affil=
kn-affil=Department of Biology, Faculty of Science, Okayama University

affil-num=3
en-affil=
kn-affil=Department of Biology, Faculty of Science, Okayama University

affil-num=4
en-affil=
kn-affil=Tsushima Facility, Advanced Science Research Center, Okayama University

affil-num=5
en-affil=
kn-affil=Department of Biology, Faculty of Science, Okayama University

affil-num=6
en-affil=
kn-affil=Department of Biology, Faculty of Science, Okayama University
en-keyword=interleukin-18 (IL-18)
kn-keyword=interleukin-18 (IL-18)
en-keyword=uterus
kn-keyword=uterus
en-keyword=estrogen
kn-keyword=estrogen
en-keyword=mouse
kn-keyword=mouse
END

start-ver=1.4
cd-journal=joma
no-vol=118
cd-vols=
no-issue=3
article-no=
start-page=187
end-page=192
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2007
dt-pub=20070104
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=原発性肺高血圧症の進行メカニズムの解明と治療薬の開発
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=小川愛子
kn-aut-sei=小川
kn-aut-mei=愛子
aut-affil-num=1
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=中村一文
kn-aut-sei=中村
kn-aut-mei=一文
aut-affil-num=2
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=松原広己
kn-aut-sei=松原
kn-aut-mei=広己
aut-affil-num=3
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=藤尾栄起
kn-aut-sei=藤尾
kn-aut-mei=栄起
aut-affil-num=4
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=池田哲也
kn-aut-sei=池田
kn-aut-mei=哲也
aut-affil-num=5
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=宮地克維
kn-aut-sei=宮地
kn-aut-mei=克維
aut-affil-num=6
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=三浦大志
kn-aut-sei=三浦
kn-aut-mei=大志
aut-affil-num=7
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=三浦綾
kn-aut-sei=三浦
kn-aut-mei=綾
aut-affil-num=8
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=永瀬聡
kn-aut-sei=永瀬
kn-aut-mei=聡
aut-affil-num=9
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=草野研吾
kn-aut-sei=草野
kn-aut-mei=研吾
aut-affil-num=10
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=伊達洋至
kn-aut-sei=伊達
kn-aut-mei=洋至
aut-affil-num=11
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=大江透
kn-aut-sei=大江
kn-aut-mei=透
aut-affil-num=12
ORCID=

affil-num=1
en-affil=
kn-affil=University of California, San Diego, Division of Pulmonary and Critical Care Medicine

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科

affil-num=3
en-affil=
kn-affil=国立病院機構岡山医療センター循環器科

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科

affil-num=6
en-affil=
kn-affil=国立病院機構岡山医療センター循環器科

affil-num=7
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科

affil-num=8
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科

affil-num=9
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科

affil-num=10
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科

affil-num=11
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科腫瘍・胸部外科

affil-num=12
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科循環器内科
en-keyword=原発性肺高血圧症
kn-keyword=原発性肺高血圧症
en-keyword=平滑筋細胞
kn-keyword=平滑筋細胞
en-keyword=prednisolone
kn-keyword=prednisolone
en-keyword=細胞周期
kn-keyword=細胞周期
END

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

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

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

start-ver=1.4
cd-journal=joma
no-vol=102
cd-vols=
no-issue=11-12
article-no=
start-page=1323
end-page=1332
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199012
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on the treatment for intractable asthma Part 2. Evaluation of the pharmacological action of various Kampo Medicines on lymphocyte and neutrophil functions in intractable asthmatics
kn-title=難治性喘息の治療に関する研究 第2編 重症難治性喘息におけるリンパ球および好中球に及ぼす各種漢方薬の薬理作用に関する検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The pharmacological action of Sho-saiko-to and Hange-koboku-to, components of Saiboku-to, as well as that of Sho-seiryu-to were compared with that of Saiboku-to and examined in intractable asthmatics with respect to both lymphocyte functions, including interleukin 2 (IL-2) production and IL-2 receptor expression in peripheral blood lymphocytes stimulated by Candida, and on neutrophil functions, including leukotriene C(4) (LTC(4)) and superoxide (O(2)(-)) production by peripheral blood neutrophils. The results revealed, first, that, Sho-saiko-to, Hange-koboku-to, and Sho-seiryu-to did not have significant suppressive effects on IL-2 production and IL-2 receptor expression by Candia, though Saiboku-to caused significant suppression of these same parameters. Second, after 2 or 3 months oral administration to intractable asthmatics Saiboku-to (TJ-96) suppressed LTC(4) production by peripheral blood neutrophils in response to Candida and Ca-ionophore. Third, in vitro, Saiboku-to caused dose-dependent suppression of both LTC(4) and O(2)(-) production by peripheral blood neutrophils. Sho-saiko-to and Sho-seiryu-to also had suppressive effects on both LTC(4) and O(2)(-) production, with Sho-saiko-to causing the strongest suppression among these drugs. These results indicate that Saiboku-to might be useful in the treatment of intractable asthma due to its suppressive effect on type IV allergy caused by lymphocyte activation by Candida. Moreover, its inhibitory effect of LTC(4) and O(2)(-) production by neutrophils prevents prolonged broncho-constriction and irreversible changes in small airways.
en-copyright=
kn-copyright=

en-aut-name=EdaRyosuke
en-aut-sei=Eda
en-aut-mei=Ryosuke
kn-aut-name=江田良輔
kn-aut-sei=江田
kn-aut-mei=良輔
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=難治性喘息
kn-keyword=難治性喘息
en-keyword=柴朴湯
kn-keyword=柴朴湯
en-keyword=漢方薬
kn-keyword=漢方薬
en-keyword=リンパ球
kn-keyword=リンパ球
en-keyword=好中球
kn-keyword=好中球
END

start-ver=1.4
cd-journal=joma
no-vol=102
cd-vols=
no-issue=11-12
article-no=
start-page=1309
end-page=1321
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199012
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on the treatment for intractable asthma Part 1. Inhibitory effect of Saiboku-to on type IV allergy in intractable asthma
kn-title=難治性喘息の治療に関する研究 第1編 重症難治性喘息における柴朴湯 (TJ-96) の臨床劾果並びにIV型アレルギー反応に及ぼす影響
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In an effort to clarify the clinical and pharmacological effects of Saiboku-to in intractable asthmatics, the effect of a 6 month administration of Saiboku-to on the production of antigen-specific lymphokines were studied. The results revealed, first, that a significant decrease in attacks and steroid-sparing effects were obtained after 3 to 4 months administration of Saiboku-to (P<0.05). Second, peripheral blood lymphocyte blastogenesis by Candida was significantly suppressed after 3 months (P<0.05), though it was not by PHA. Moreover interleukin 2 (IL-2) production and neutrophil chemotatic activity (NCA) in peripheral blood mononuclear cells stimulated by Candida were significantly decreased after 3 months (P<0.01), but not by PHA. Third, in vitro production of both IL-2 and NCA by Candida were suppressed in a dose dependent manner and the augmented expression of IL-2 receptors by Candida was decreased by Saiboku-to. These results suggest that the action mechanism of Saiboku-to in intractable asthma seems to be the suppression of type IV allergy. Therefore Saiboku-to therapy might be a useful treatment for intractable asthma due to its relatively less serious side effects as compared with corticosteroids.
en-copyright=
kn-copyright=

en-aut-name=EdaRyosuke
en-aut-sei=Eda
en-aut-mei=Ryosuke
kn-aut-name=江田良輔
kn-aut-sei=江田
kn-aut-mei=良輔
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=難治性喘息
kn-keyword=難治性喘息
en-keyword=柴朴湯
kn-keyword=柴朴湯
en-keyword=カンジダ抗原
kn-keyword=カンジダ抗原
en-keyword=IV型アレルギー反応
kn-keyword=IV型アレルギー反応
END

start-ver=1.4
cd-journal=joma
no-vol=102
cd-vols=
no-issue=5-6
article-no=
start-page=719
end-page=732
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199006
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on cellular immunity in interstitial lung diseases Part 2. Interleukin-2 receptor in peripheral blood from idiopathic interstitial pneumonia
kn-title=間質性肺疾患における細胞性免疫に関する研究 第2編 特発性間質性肺炎・膠原病肺における末梢血インターロイキン2レセプター（IL-2R）の検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In this study, the Interleukin-2 receptor (IL-2R) and lymphocyte subsets in the patients with idiopathic interstitial pneumonia (IIP), interstitial pneumonia with collagen vascular disease (IPCVD) and alveolar type of HTLV-I associated bronchiolo-alveolar disorder (HABA-A) were evaluated. Soluble IL-2R (sIL-2R) in the lymphocyte culture supernatant increased in IIP, while the sIL-2R in sera and IL-2R positive lymphocyte showed no increase. In HABA-A, the serum sIL-2R level, the responsiveness to IL-2 and percentage of IL-2R positive lymphocytes and helper-T lymphocytes were increased. In IPCVD, the serum sIL-2R level increased but the percentage of IL-2R positive lymphocytes and helper-T lymphocytes decreased. The CD4/CD8 ratio was low in IIP and IPCVD, but high in HABA-A. In patients with IIP or IPCVD treated with steroids, the percentage of IL-2R positive lymphocytes and helper-T lymphocytes decreased more than in those not treated with steroids. Therefore, cellular immunity regulated by the IL-2 and IL-2R system might play an important role in the pathogenesis of IPCVD and HABA-A.
en-copyright=
kn-copyright=

en-aut-name=KawabataHidetoshi
en-aut-sei=Kawabata
en-aut-mei=Hidetoshi
kn-aut-name=川畑秀俊
kn-aut-sei=川畑
kn-aut-mei=秀俊
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=diffuse panbronchiolitis
kn-keyword=diffuse panbronchiolitis
en-keyword=interleukin-2 receptor
kn-keyword=interleukin-2 receptor
en-keyword=soluble interleukin-2 receptor
kn-keyword=soluble interleukin-2 receptor
END

start-ver=1.4
cd-journal=joma
no-vol=102
cd-vols=
no-issue=5-6
article-no=
start-page=705
end-page=718
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199006
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on cellular immunity in interstitial lung diseases Part 1. Interleukin-2 receptor in peripheral blood from diffuse panbronchiolitis
kn-title=間質性肺疾患における細胞性免疫に関する研究 第1編 びまん性汎細気管支炎における末梢血インターロイキン2レセプター（IL-2R）の検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In this study, patients with diffuse panbronchiolitis (DPB) and bronchiolar type of HTLV-I associated bronchiolo-alveolar disorder (HABA-B) were evaluated in regard to regulation of interleukin-2 receptor (IL-2R) and lymphocyte subsets. The levels of soluble IL-2R in sera and lymphocyte culture supernatant, the responsiveness of lymphocytes to IL-2 and the percentage of IL-2R positive lymphocytes and helper-T lymphocytes were higher in DPB than in normal controls. Furthermore in HABA-B, the levels of IL-2R were much higher than those of DPB. The correlation coefficient between the percentage of IL-2R positive lymphocytes or helper-T lymphocytes and the CD4/CD8 ratio were statistically significant. In the patients with DPB, the percentage of IL-2R positive lymphocytes and helper-T lymphocytes were increased with the progress in clinical stage of DPB or the serum titer of cold hemagglutinin increase. Therefore, the cellular immunity regulated by the IL-2 and IL-2R system might play an important role in the pathogenesis of DPB and HABA-B.
en-copyright=
kn-copyright=

en-aut-name=KawabataHidetoshi
en-aut-sei=Kawabata
en-aut-mei=Hidetoshi
kn-aut-name=川畑秀俊
kn-aut-sei=川畑
kn-aut-mei=秀俊
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=diffuse panbronchiolitis
kn-keyword=diffuse panbronchiolitis
en-keyword=interleukin-2 receptor soluble interleukin-2 receptor
kn-keyword=interleukin-2 receptor soluble interleukin-2 receptor
END

start-ver=1.4
cd-journal=joma
no-vol=122
cd-vols=
no-issue=3
article-no=
start-page=231
end-page=236
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20101201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=A case of transverse colon cancer with remarkable extramural invasion to stomach and jejunum
kn-title=壁外性に腫瘤を形成し胃・小腸浸潤を示した横行結腸癌の１例
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A 77-year-old woman was admitted to our hospital due to abdominal pain and body weight loss. A palpable mass the size of an infant's head was tender on palpation and identified as an epigastric lesion. Colonoscopic examination revealed stenosis of the transverse colon, although no intraluminal growth of the tumor was found. The histologic findings of the biopsy material were poorly differentiated and/or undifferentiated cells. Abdominal CT scan showed an irregular-shaped tumor with a diameter of 10cm invading the stomach and jejunum. We performed an operation under a diagnosis of extramurally growing cancer or malignant lymphoma of the colon. Partial resection of the transverse colon was done by distal gastrectomy and partial resection of the jejunum. Histologic examination of the operative specimens revealed moderately differentiated adenocarcinoma of the transverse colon, prominently proliferating into the surrounding tissues. The finding of a long stenotic lesion and extramural compression by colonography are characteristic of this tumor, based on a review of 43 literature reports in Japan.
en-copyright=
kn-copyright=

en-aut-name=HamanoRyosuke
en-aut-sei=Hamano
en-aut-mei=Ryosuke
kn-aut-name=濱野亮輔
kn-aut-sei=濱野
kn-aut-mei=亮輔
aut-affil-num=1
ORCID=

en-aut-name=OtsukaShinya
en-aut-sei=Otsuka
en-aut-mei=Shinya
kn-aut-name=大塚眞哉
kn-aut-sei=大塚
kn-aut-mei=眞哉
aut-affil-num=2
ORCID=

en-aut-name=KimuraYuuji
en-aut-sei=Kimura
en-aut-mei=Yuuji
kn-aut-name=木村裕司
kn-aut-sei=木村
kn-aut-mei=裕司
aut-affil-num=3
ORCID=

en-aut-name=NishieManabu
en-aut-sei=Nishie
en-aut-mei=Manabu
kn-aut-name=西江学
kn-aut-sei=西江
kn-aut-mei=学
aut-affil-num=4
ORCID=

en-aut-name=TokunagaNaoyuki
en-aut-sei=Tokunaga
en-aut-mei=Naoyuki
kn-aut-name=徳永尚之
kn-aut-sei=徳永
kn-aut-mei=尚之
aut-affil-num=5
ORCID=

en-aut-name=MiyasouHideaki
en-aut-sei=Miyasou
en-aut-mei=Hideaki
kn-aut-name=宮宗秀明
kn-aut-sei=宮宗
kn-aut-mei=秀明
aut-affil-num=6
ORCID=

en-aut-name=TsunemituYousuke
en-aut-sei=Tsunemitu
en-aut-mei=Yousuke
kn-aut-name=常光洋輔
kn-aut-sei=常光
kn-aut-mei=洋輔
aut-affil-num=7
ORCID=

en-aut-name=InagakiMasaru
en-aut-sei=Inagaki
en-aut-mei=Masaru
kn-aut-name=稲垣優
kn-aut-sei=稲垣
kn-aut-mei=優
aut-affil-num=8
ORCID=

en-aut-name=IwakawaKazuhide
en-aut-sei=Iwakawa
en-aut-mei=Kazuhide
kn-aut-name=岩川和秀
kn-aut-sei=岩川
kn-aut-mei=和秀
aut-affil-num=9
ORCID=

en-aut-name=IwagakiHiromi
en-aut-sei=Iwagaki
en-aut-mei=Hiromi
kn-aut-name=岩垣博巳
kn-aut-sei=岩垣
kn-aut-mei=博巳
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=国立病院機構福山医療センター　外科

affil-num=2
en-affil=
kn-affil=国立病院機構福山医療センター　外科

affil-num=3
en-affil=
kn-affil=国立病院機構福山医療センター　外科

affil-num=4
en-affil=
kn-affil=国立病院機構福山医療センター　外科

affil-num=5
en-affil=
kn-affil=国立病院機構福山医療センター　外科

affil-num=6
en-affil=
kn-affil=国立病院機構福山医療センター　外科

affil-num=7
en-affil=
kn-affil=国立病院機構福山医療センター　外科

affil-num=8
en-affil=
kn-affil=国立病院機構福山医療センター　外科

affil-num=9
en-affil=
kn-affil=国立病院機構福山医療センター　外科

affil-num=10
en-affil=
kn-affil=国立病院機構福山医療センター　外科
en-keyword=大腸癌 (colon cancer)
kn-keyword=大腸癌 (colon cancer)
en-keyword=壁外性発育 (extraluminal growth)
kn-keyword=壁外性発育 (extraluminal growth)
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=3
article-no=
start-page=508
end-page=513
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Induction of cytolytic activity and interferon-gamma production in murine natural killer cells by polymyxins B and E
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Natural killer (NK) cells are the primary effector cells of the innate immune system and have well-established roles in tumor rejection and resistance to viruses, bacteria and certain parasites. There is a need for more specific immune modulators of NK cell activity that tack the wide-ranging side effects of NK cell-stimulatory interleukins. The polycationic antibiotic polymyxin B (PMB) has been shown to have a unique ability to enhance activities of some immune cells, independent of its antibiotic properties. Here we report that both PMB and its analog potymyxin E (PME) markedly enhanced the activity of NK cells enriched from the murine spleen. Maximal activation of NK cell activity was obtained after 24 h of incubation with PMB at a dose of 300 mu g/ml. PMB nonapeptide, one of the two PMB domains, and PME methanesulfonate, the negatively charged derivative of PME, had little effect on NK cell activity. PMB induced interferon (IFN)-gamma and tumor necrosis factor-a production in NK cells. Proliferation of NK cells in vitro was significantly stimulated by being incubated with PMB. Administration of PMB to mice for 7 consecutive days stimulated splenic NK cell activity and increased NK cell populations in the spleen. These results suggest that the polycationic antibiotics PMB and PME may up-regulate innate and adaptive immune responses by induction of NK cell activity and IFN-gamma production.</p>
en-copyright=
kn-copyright=

en-aut-name=ZhongMing
en-aut-sei=Zhong
en-aut-mei=Ming
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KadotaYusuke
en-aut-sei=Kadota
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShimizuYoshio
en-aut-sei=Shimizu
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=GohdaEiichi
en-aut-sei=Gohda
en-aut-mei=Eiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

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

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

affil-num=3
en-affil=
kn-affil=Bizen Chemical Co., Ltd

affil-num=4
en-affil=
kn-affil=Department of Immunochemistry, Division of Pharmaceutical Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=polymyxin B (PMB)
kn-keyword=polymyxin B (PMB)
en-keyword=polymyxin E (PME)
kn-keyword=polymyxin E (PME)
en-keyword=NK cells
kn-keyword=NK cells
en-keyword=IFN-gamma
kn-keyword=IFN-gamma
END

start-ver=1.4
cd-journal=joma
no-vol=43
cd-vols=
no-issue=2
article-no=
start-page=125
end-page=131
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2005
dt-pub=20050201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neutrophil and lymphocyte responses to oral Streptococcus in Adamantiades-Behcet's disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Immune reactions against microorganisms play an important pathogenic role in Adamantiades-Beh?et’s disease (ABD). We had previously obtained Streptococcus sanguinis (strain BD113-20) isolated from the oral cavity of patients with ABD. To investigate the pathogenesis of this isolate, we examined neutrophil 5 reactions and level of cytokine production by lymphocytes after stimulation with the strain. The reactions
of neutrophils were examined by chemiluminescence assay using whole blood. The
amounts of interferon gamma (IFN-g) and interleukin (IL)-4, IL-8, IL-10, and IL-12
produced by peripheral blood mononuclear cells (PBMCs) were measured by ELISA. 10 Strain BD113-20 activated neutrophils from patients with ABD and healthy volunteers, and, in addition it increased IFN-g production by lymphocytes. Lymphocyte from the patients with ABD showed a dominant T helper 1 (Th-1) immune response. Results indicated that both bacterial stimulation and host hypersensitivity might be involved in the symptoms and pathogenesis of ABD.
en-copyright=
kn-copyright=

en-aut-name=KurauchiTomomi
en-aut-sei=Kurauchi
en-aut-mei=Tomomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YokotaKenji
en-aut-sei=Yokota
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MatsuoToshihiko
en-aut-sei=Matsuo
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FujinamiYoshihito
en-aut-sei=Fujinami
en-aut-mei=Yoshihito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IsogaiEmiko
en-aut-sei=Isogai
en-aut-mei=Emiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IsogaiHiroshi
en-aut-sei=Isogai
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OhtsukiHiroshi
en-aut-sei=Ohtsuki
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OgumaKeiji
en-aut-sei=Oguma
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

affil-num=2
en-affil=
kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine and Dentistry

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

affil-num=4
en-affil=
kn-affil=Department of Ophthalmology, Okayama University Graduate School of Medicine and Dentistry

affil-num=5
en-affil=
kn-affil=Department of Preventive Dentistry, Health Sciences University of Hokkaido

affil-num=6
en-affil=
kn-affil=Division of Animal Experimentation, Sapporo Medical University

affil-num=7
en-affil=
kn-affil=Department of Ophthalmology, Okayama University Graduate School of Medicine and Dentistry

affil-num=8
en-affil=
kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine and Dentistry
en-keyword=Adamantiades-Behcet's disease
kn-keyword=Adamantiades-Behcet's disease
en-keyword=Streptococcus sanguinis
kn-keyword=Streptococcus sanguinis
en-keyword=neutrophil
kn-keyword=neutrophil
en-keyword=chemiluminescence
kn-keyword=chemiluminescence
en-keyword=IL-8
kn-keyword=IL-8
en-keyword=T helper-1
kn-keyword=T helper-1
en-keyword=IFN-gamma
kn-keyword=IFN-gamma
en-keyword=IL-12
kn-keyword=IL-12
END

start-ver=1.4
cd-journal=joma
no-vol=250
cd-vols=
no-issue=1-2
article-no=
start-page=14
end-page=23
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Differentiation of murine B cells induced by chondroitin sulfate B
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>A two-step culture system was used to investigate the role of chondroitin sulfate (CS) B, which is mitogenic to B cells, in differentiation of B cells. Mouse spleen B cells were incubated for 3 days with CSB in the presence of interleukin (IL)-4 and IL-5. After washing, the cells were replated at 10(5) viable cells/well and recultured without CSB in the presence of IL-4 and IL-5. CSB dose-dependently increased IgM production, the greatest enhancement being 450%. Dextran sulfate had a similar effect, whereas other glycosaminoglycans, CSA, CSC, heparin and hyaluronic acid, were marginally effective. Treatment of B cells with CSB resulted in increases in the number of IgM-secreting cells and numbers of CD138-positive cells and CD45R/B220-negative cells. CSB-induced IgM production was inhibited by the protein kinase C (PKC) inhibitor GF109203X but not by the phosphatidylinositol 3-kinase (P13K) inhibitor wortmannin. These results demonstrated that CSB promoted differentiation of B cells in the presence of IL-4 and IL-5 and suggested that PKC but not P13K is crucial for CSB-induced IgM production.</p>
en-copyright=
kn-copyright=

en-aut-name=YoshiharaRitsuko
en-aut-sei=Yoshihara
en-aut-mei=Ritsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AoyamaEriko
en-aut-sei=Aoyama
en-aut-mei=Eriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KadotaYusuke
en-aut-sei=Kadota
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawaiSaeko
en-aut-sei=Kawai
en-aut-mei=Saeko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=GotoTomomi
en-aut-sei=Goto
en-aut-mei=Tomomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ZhongMing
en-aut-sei=Zhong
en-aut-mei=Ming
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=GohdaEiichi
en-aut-sei=Gohda
en-aut-mei=Eiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

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

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

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

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

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

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

affil-num=7
en-affil=
kn-affil=Department of Immunochemistry, Division of Pharmaceutical Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=chondroitin sulfate B (CSB)
kn-keyword=chondroitin sulfate B (CSB)
en-keyword=murine B cells
kn-keyword=murine B cells
en-keyword=IgM
kn-keyword=IgM
en-keyword=differentiation
kn-keyword=differentiation
en-keyword=CD138
kn-keyword=CD138
en-keyword=protein kinase C
kn-keyword=protein kinase C
END

start-ver=1.4
cd-journal=joma
no-vol=52
cd-vols=
no-issue=5
article-no=
start-page=1451
end-page=1460
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2005
dt-pub=20055
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=ADAMTS-9 is synergistically induced by interleukin-1 and tumor necrosis factor  in OUMS-27 chondrosarcoma cells and in human chondrocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p><b>Objective</b><br />
To compare induction of the aggrecanases (ADAMTS-1, ADAMTS-4, ADAMTS-5, ADAMTS-8, ADAMTS-9, and ADAMTS-15) by interleukin-1 (IL-1) and tumor necrosis factor (TNF) in chondrocyte-like OUMS-27 cells and human chondrocytes, and to determine the mechanism of induction of the most responsive aggrecanase gene.</p>
<p><b>Methods</b><br />
OUMS-27 cells were stimulated for different periods of time and with various concentrations of IL-1 and/or TNF. Human chondrocytes obtained from osteoarthritic joints and human skin fibroblasts were also stimulated with IL-1 and/or TNF. Total RNA was extracted, reverse transcribed, and analyzed by quantitative real-time polymerase chain reaction and Northern blotting. ADAMTS-9 protein was examined by Western blotting, and the role of the MAPK signaling pathway for ADAMTS9 induction in IL-1-stimulated OUMS-27 cells was investigated.</p>
<p><b>Results</b><pr>
IL-1 increased messenger RNA (mRNA) levels of ADAMTS4, ADAMTS5, and ADAMTS9 but not ADAMTS1 and ADAMTS8. The fold increase for ADAMTS9 mRNA was greater than that for mRNA of the other aggrecanase genes. The increase of ADAMTS9 mRNA by IL-1 stimulation was greater in chondrocytes than in fibroblasts. The combination of IL-1 and TNF had a synergistic effect, resulting in a considerable elevation in the level of ADAMTS9 mRNA. ADAMTS-9 protein was also induced in IL-1-stimulated OUMS-27 cells. The MAPK inhibitors SB203580 and PD98059 decreased ADAMTS9 up-regulation in OUMS-27 cells.</p>
<p><b>Conclusion</b><br />
ADAMTS9 is an IL-1- and TNF-inducible gene that appears to be more responsive to these proinflammatory cytokines than are other aggrecanase genes. Furthermore, these cytokines had a synergistic effect on ADAMTS9. Together with the known ability of ADAMTS-9 to proteolytically degrade aggrecan and its potential to cleave other cartilage molecules, the data suggest that ADAMTS-9 may have a pathologic role in arthritis.</p>
en-copyright=
kn-copyright=

en-aut-name=DemircanKadir
en-aut-sei=Demircan
en-aut-mei=Kadir
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HirohataSatoshi
en-aut-sei=Hirohata
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NishidaKeiichiro
en-aut-sei=Nishida
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HatipogluOmer F.
en-aut-sei=Hatipoglu
en-aut-mei=Omer F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YonezawaTomoko
en-aut-sei=Yonezawa
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ApteSuneel S.
en-aut-sei=Apte
en-aut-mei=Suneel S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NinomiyaYoshifumi
en-aut-sei=Ninomiya
en-aut-mei=Yoshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

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

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

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

affil-num=7
en-affil=
kn-affil=Lerner Research Institute, Cleveland Clinic Foundation

affil-num=8
en-affil=
kn-affil=Okayama University Graduate School of Medicine and Dentistry
en-keyword=ADAMTS
kn-keyword=ADAMTS
en-keyword=aggrecanase
kn-keyword=aggrecanase
en-keyword=arthritis
kn-keyword=arthritis
en-keyword=chondrocyte
kn-keyword=chondrocyte
en-keyword=metalloproteinases
kn-keyword=metalloproteinases
en-keyword=IL-1
kn-keyword=IL-1
END

start-ver=1.4
cd-journal=joma
no-vol=57
cd-vols=
no-issue=6
article-no=
start-page=267
end-page=277
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2003
dt-pub=200312
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pathophysiological functions of CD30+ CD4+ T cells in rheumatoid arthritis.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>High levels of soluble CD30 (sCD30) were detected in the serum and synovial fluid of patients with rheumatoid arthritis (RA), indicating the involvement of CD30+ T cells in the pathogenesis. We investigated the induction of CD30 and its functions in CD4+T cells from patients with established RA (disease duration &#62;_2 years). CD4+ T cells from both the peripheral blood (PB) and synovial tissue (ST) of RA patients expressed surface CD30 when stimulated with anti-CD3 antibody (Ab) and anti-CD28 Ab, but their CD30 induction was slower and weaker compared with PB CD4+ T cells of healthy controls (HC). Immunohistochemical analysis showed that only a small proportion of lymphocytes expressed CD30 in the ST (-1%). RA PB CD4+ T cells, after recovery from 6-day stimulation with anti-CD3 Ab and anti-CD28 Ab, showed in intracellular cytokine staining that CD30+ T cells could produce more interleukin-4 (IL-4) but less interferon-gamma. In the culture of RA PB CD4+ T Cells with anti-CD3 Ab and anti-CD28 Ab, blocking anti-CD30 Ab similarly inhibited the cell proliferation and activation of nuclear factor-kappaB on day 4 in RA and HC, but inhibited the apoptotic cell death on day 6 only in RA. These results indicate that despite high-level expression of sCD30, the anti-inflammatory activity of IL-4-producing CD30+ CD4+ T cells may be limited in the ST due to a poor induction of surface CD30 and a susceptibility to CD30-mediated cell death.</p>
en-copyright=
kn-copyright=

en-aut-name=OkamotoAkira
en-aut-sei=Okamoto
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamamuraMasahiro
en-aut-sei=Yamamura
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IwahashiMitsuhiro
en-aut-sei=Iwahashi
en-aut-mei=Mitsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AitaTetsushi
en-aut-sei=Aita
en-aut-mei=Tetsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UenoAkiko
en-aut-sei=Ueno
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KawashimaMasanori
en-aut-sei=Kawashima
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamanaJiro
en-aut-sei=Yamana
en-aut-mei=Jiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KagawaHidetoshi
en-aut-sei=Kagawa
en-aut-mei=Hidetoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University

affil-num=7
en-affil=
kn-affil=Okayama University

affil-num=8
en-affil=
kn-affil=Okayama University

affil-num=9
en-affil=
kn-affil=Okayama University
en-keyword=apoptosis
kn-keyword=apoptosis
en-keyword=CD4 Tcells
kn-keyword=CD4 Tcells
en-keyword=CD30
kn-keyword=CD30
en-keyword=interleukin-4(IL=4)
kn-keyword=interleukin-4(IL=4)
en-keyword=rheumatoid arthritis(RA)
kn-keyword=rheumatoid arthritis(RA)
END

start-ver=1.4
cd-journal=joma
no-vol=57
cd-vols=
no-issue=6
article-no=
start-page=285
end-page=292
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2003
dt-pub=200312
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effects of pulsing procedure of interleukin-12 in combination with interleukin-2 on the activation of peripheral blood lymphocytes derived from patients with hepatocellular carcinoma.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>In patients with hepatocellular carcinoma (HCC), natural killer (NK) cell activity decreases significantly, and the reduced activity may be associated with the progression of HCC. In this study we evaluated the effects of pulsing with interleukin (IL)-2 and/or IL-12 on the activation of freshly isolated peripheral blood lymphocytes (PBL) derived from patients with HCC. PBL obtained from 9 HCC patients, 4 liver cirrhosis patients, and 9 normal subjects were cultured in the presence of IL-2 and/or IL-12. After 24 h of incubation, the levels of interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha presented in the supernatants were determined by enzyme-linked immunosorbent assay (ELISA). The IFN-gamma and TNF-alpha production of PBL pulsed by a combination of IL-2 and IL-12 was significantly higher than those of PBL stimulated by either IL-2 or IL-12 alone. The mRNA encoding perforin, granzyme B, as well as IFN-gamma and TNF-alpha, were markedly enhanced in PBL stimulated with a combination of IL-12 and IL-2. The pulsing procedure of IL-12 in combination with IL-2 resulted in the increase of IFN-gamma and TNF-alpha, and the expression of perforin and granzyme B mRNA in PBL obtained from HCC patients, as well as in those obtained from normal subjects. These results indicate that adoptive immunotherapy based on PBL pulsed with a combination of IL-2 and IL-12 may be a promising adjunctive strategy for HCC treatment.</p>

en-copyright=
kn-copyright=

en-aut-name=SawayamaTomoyuki
en-aut-sei=Sawayama
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakaguchiKohsaku
en-aut-sei=Sakaguchi
en-aut-mei=Kohsaku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SenohTomonori
en-aut-sei=Senoh
en-aut-mei=Tomonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OhtaTakeyuki
en-aut-sei=Ohta
en-aut-mei=Takeyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NishimuraMamoru
en-aut-sei=Nishimura
en-aut-mei=Mamoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakakiAkinobu
en-aut-sei=Takaki
en-aut-mei=Akinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TsujiTakao
en-aut-sei=Tsuji
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ShiratoriYasushi
en-aut-sei=Shiratori
en-aut-mei=Yasushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University

affil-num=7
en-affil=
kn-affil=Okayama University

affil-num=8
en-affil=
kn-affil=Okayama University
en-keyword=hepatocellular carcinoma(HCC)
kn-keyword=hepatocellular carcinoma(HCC)
en-keyword=interleukin(IL)-2
kn-keyword=interleukin(IL)-2
en-keyword=interleukin(IL)-12
kn-keyword=interleukin(IL)-12
en-keyword=interferon(IFN)-r
kn-keyword=interferon(IFN)-r
en-keyword=granzyme B
kn-keyword=granzyme B
END

start-ver=1.4
cd-journal=joma
no-vol=46
cd-vols=
no-issue=1
article-no=
start-page=37
end-page=44
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=199202
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Difference of rejection between heart and heart-lung transplantation in rats: flowcytometric analysis of graft infiltrating lymphocyte subsets.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Reported clinical and experimental observations indicate that heart grafts in combined heart-lung transplantation are less frequently rejected than heart grafts transplanted alone. In order to elucidate the mechanism of this difference, twenty-eight inbred male Lewis rats receiving heterotopic allografts from inbred male Fisher rats were evaluated for surface markers of graft infiltrating lymphocytes (GIL) and peripheral blood lymphocytes (PBL) using flowcytometry. Monoclonal antibodies investigated in this study were W3/25 (anti-helper T lymphocyte), OX8 (anti-suppressor/cytotoxic T lymphocyte), OX39 (anti-interleukin 2 receptor), and OX6 (anti-MHC class II antigen). In the acute study, a heart transplanted group (n = 7) and a heart-lung transplanted group (n = 7) without immunosuppression were studied. In the chronic study, cyclosporine (10 mg/kg/day i.m.) were administered in the heart transplanted group (n = 7) and the heart-lung transplanted group (n = 7). Both in the acute and chronic studies, the proportion of W3/25 positive cells in GIL of heart grafts of the heart transplanted group was significantly higher than that of heart grafts and lung grafts of the heart-lung transplanted group. OX8 positive cell proportion in GIL of heart grafts and lung grafts of the heart-lung transplanted group were significantly higher than that of heart grafts of the heart transplanted group. These results lead us to speculate that suppressor T lymphocytes are an important distinguishing factor in the rejection processes of heart allografts and heart-lung allografts as observed in clinical experience.</p>

en-copyright=
kn-copyright=

en-aut-name=OkadaMasahiro
en-aut-sei=Okada
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SenooYoshimasa
en-aut-sei=Senoo
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TeramotoShigeru
en-aut-sei=Teramoto
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama  University

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama Univerisity
en-keyword=rejection
kn-keyword=rejection
en-keyword=heart transplantation
kn-keyword=heart transplantation
en-keyword=heart-lung transplantation
kn-keyword=heart-lung transplantation
en-keyword=lymphocyte subsets
kn-keyword=lymphocyte subsets
en-keyword=flowcytometry
kn-keyword=flowcytometry
END

start-ver=1.4
cd-journal=joma
no-vol=54
cd-vols=
no-issue=5
article-no=
start-page=201
end-page=209
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2000
dt-pub=200010
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Calcineurin antagonists inhibit interferon-gamma production by downregulation of interleukin-18 in human mixed lymphocyte reactions.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Tacrolimus (FK-506) and cyclosporin A (CsA) are calcineurin antagonists used widely as T-cell immunosuppressants; however, their relative efficacy on the production of interleukin-18 (IL-18) remains undefined. We have examined the effects of FK-506 and CsA on the cytokine generation of human peripheral blood mononuclear cells (PBMCs) in mixed lymphocyte reaction (MLR) with lipopolysaccharide (LPS). We studied the levels of interleukin-18 (IL-18), IL-12, IL-10, IL-6, IL-2 and interferon-gamma (IFN-gamma) in the supernatant in allo-MLR by ELISA assay. Supernatant levels of IFN-gamma, IL-2, IL-6, IL-10 and IL-12 were detected 12 h after MLR and markedly increased thereafter. In contrast, production of IL-18 was detected at 12 h, reached a near maximum level at 24 h and decreased at 72 h. These results suggested that IFN-gamma production depended on IL-18, IL-12 and IL-2 in the early phase of MLR and depended mainly on IL-12 and IL-2 in the late phase. Both calcineurin antagonists inhibit the generation of IL-18, which plays a large role in allogeneic cell interactions, in macrophages and they also promote an equivalent down-regulation of T helper 1 (Th1) and Th2 responses in a concentration-dependent manner. About 90% of IFN-gamma production induced by MLR was inhibited by an anti-IL-18 antibody, showing that IL-18 can trigger IFN-gamma production in MLR. These results suggest that dual signaling consisting of antigen-driven nuclear factor of activated T cells (NFAT) activation and LPS-mediated NF-kappaB activation is crucial for IL-18 production in macrophages, and that IL-18 can trigger IFN-gamma production in T-cells by MLR.</p>

en-copyright=
kn-copyright=

en-aut-name=KuinoseMasahiko
en-aut-sei=Kuinose
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IwagakiHiromi
en-aut-sei=Iwagaki
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MorimotoYoshinori
en-aut-sei=Morimoto
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KohkaHideo
en-aut-sei=Kohka
en-aut-mei=Hideo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KobashiKenta
en-aut-sei=Kobashi
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SadamoriHiroshi
en-aut-sei=Sadamori
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=InagakiMasaru
en-aut-sei=Inagaki
en-aut-mei=Masaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UrushiharaNaoto
en-aut-sei=Urushihara
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YagiTakahito
en-aut-sei=Yagi
en-aut-mei=Takahito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TanakaNoriaki
en-aut-sei=Tanaka
en-aut-mei=Noriaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University

affil-num=7
en-affil=
kn-affil=Okayama University

affil-num=8
en-affil=
kn-affil=Okayama University

affil-num=9
en-affil=
kn-affil=Okayama University

affil-num=10
en-affil=
kn-affil=Okayama University
en-keyword=tacrolimus
kn-keyword=tacrolimus
en-keyword=cyclosporin
kn-keyword=cyclosporin
en-keyword=calcineurin antagonist
kn-keyword=calcineurin antagonist
END

start-ver=1.4
cd-journal=joma
no-vol=58
cd-vols=
no-issue=3
article-no=
start-page=119
end-page=125
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2004
dt-pub=200406
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Rapid response of hepatocyte growth factor in pulmonary ischemia in a rat model.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Hepatocyte growth factor (HGF) is a multifunctional factor implicated in tissue regeneration, wound healing, and angiogenesis. HGF was initially thought to be liver-specific, but it has become clear that HGF acts on alveolar type II cells and bronchial epithelial cells. This study was conducted to determine the role of HGF in pulmonary ischemia in a rat model. The first increase of the plasma HGF level was noted 30 min after pulmonary ischemia, and reached a peak at 12 h. Real-time reverse transcription polymerase chain reaction (Real-time RT-PCR) revealed that the HGF messenger RNA (mRNA) expression in the injured left lung was markedly increased at 1, 6, and 12 h after pulmonary ischemia (P &#60; 0.05). The interleukin-1beta (IL-1beta) mRNA expression, one of the inflammatory cytokines which induces HGF expression, was markedly increased at 1 h in the injured left lung (P = 0.0007). Therefore, we considered that HGF might be mainly induced by paracrine mechanisms in pulmonary ischemia. In conclusion, we have shown that the expression of HGF was induced in pulmonary ischemia, and may be a useful biological marker for the early diagnosis.</p>

en-copyright=
kn-copyright=

en-aut-name=NagaiKazunobu
en-aut-sei=Nagai
en-aut-mei=Kazunobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AoeMotoi
en-aut-sei=Aoe
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShimizuNobuyoshi
en-aut-sei=Shimizu
en-aut-mei=Nobuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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
en-keyword=hepatocyte growth factor (HGF)
kn-keyword=hepatocyte growth factor (HGF)
en-keyword=  interleukin-1? (IL-1?)
kn-keyword=  interleukin-1? (IL-1?)
en-keyword=pulmonary ischemia
kn-keyword=pulmonary ischemia
en-keyword=  enzyme-linked im-munosorbent assay(ELISA)
kn-keyword=  enzyme-linked im-munosorbent assay(ELISA)
en-keyword=  real-time reverse transcription polymerase chain reaction (real-time RT-PCR)	 	 	 
kn-keyword=  real-time reverse transcription polymerase chain reaction (real-time RT-PCR)	 	 	 
END

start-ver=1.4
cd-journal=joma
no-vol=58
cd-vols=
no-issue=4
article-no=
start-page=169
end-page=180
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2004
dt-pub=200408
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A spectrum of clinical manifestations caused by host immune responses against Epstein-Barr virus infections.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Epstein-Barr virus (EBV), or human herpesvirus 4 (HHV-4), infects the vast majority of adults worldwide, and establishes both nonproductive (latent) and productive (lytic) infections. Host immune responses directed against both the lytic and latent cycle-associated EBV antigens induce a diversity of clinical symptoms in patients with chronic active EBV infections who usually contain an oligoclonal pool of EBV-infected lymphocyte subsets in their blood. Episomal EBV genes in the latent infection utilize an array of evasion strategies from host immune responses: the minimized expression of EBV antigens targeted by host cytotoxic T lymphocytes (CTLs), the down-regulation of cell adhesion molecule expression, and the release of virokines to inhibit the host CTLs. The oncogenic role of latent EBV infection is not yet fully understood, but latent membrane proteins (LMPs) expressed during the latency cycle have essential biological properties leading to cellular gene expression and immortalization, and EBV-encoded gene products such as viral interleukin-10 (vIL-10) and bcl-2 homologue function to survive the EBV-infected cells. The subsequent oncogenic DNA damage may lead to the development of neoplasms. EBV-associated NK/T cell lymphoproliferative disorders are prevalent in Asia, but quite rare in Western countries. The genetic immunological background, therefore, is closely linked to the development of EBV-associated neoplasms.</p>
en-copyright=
kn-copyright=

en-aut-name=IwatsukiKeiji
en-aut-sei=Iwatsuki
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamamotoTakenobu
en-aut-sei=Yamamoto
en-aut-mei=Takenobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TsujiKazuhide
en-aut-sei=Tsuji
en-aut-mei=Kazuhide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SuzukiDaisuke
en-aut-sei=Suzuki
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FujiiKazuyasu
en-aut-sei=Fujii
en-aut-mei=Kazuyasu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsuuraHironori
en-aut-sei=Matsuura
en-aut-mei=Hironori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OonoTakashi
en-aut-sei=Oono
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University

affil-num=7
en-affil=
kn-affil=Okayama University
en-keyword=latent infection
kn-keyword=latent infection
en-keyword=hydroa vacciniforme
kn-keyword=hydroa vacciniforme
en-keyword=mosquito allergy
kn-keyword=mosquito allergy
en-keyword=chronic active EB virus infection
kn-keyword=chronic active EB virus infection
en-keyword=hemophagocytic syndrome
kn-keyword=hemophagocytic syndrome
END

start-ver=1.4
cd-journal=joma
no-vol=55
cd-vols=
no-issue=1
article-no=
start-page=31
end-page=39
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2001
dt-pub=200102
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Analysis of the immune status in the recipients with long-term well-functioning kidneys allografts.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>The immune status of thirteen living and related kidney transplant recipients with stable allografts were examined. The immunological assays consisted of a mixed lymphocyte reaction (MLR), cell-mediated lympholysis (CML) assay, interleukin-2 (IL-2) production in mixed lymphocytes culture (MLC) and IL-2 receptor (IL-2 R) expression on MLC cells. The suppression rates of the monoclonal antibodies (mAbs) against IL-2 R were tested on MLRs. The stimulation indices (SI) of the MLR against both donor and third-party cells increased compared with those of pretransplantation. The MLC responder cells stimulated by donor cells produced detectable amounts of IL-2, these amounts were lower than those by third-party cells. The MLC cells against donor cells expressed IL-2 R alpha and beta chains to the same degree as those against third-party cells. Anti-IL-2 R mAbs equally inhibited the MLRs between recipient and donor or third-party cells. Cytotoxic T lymphocytes (CTL) against donor cells were not generated, even with the addition of recombinant IL-2 in any of recipients except one, while anti-donor CTL had been detected prior to transplantation and the CTL against third-party cells were induced in posttranspalnt CML </p>
<p>assays. These results indicate that the clonal anergy phenomenon might mediate the specific CTL unresponsiveness observed in kidney transplant recipients and the anergy phenomenon might serve in the long-term acceptance of allograft.</p>

en-copyright=
kn-copyright=

en-aut-name=NakagawaKazuhiko
en-aut-sei=Nakagawa
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsunoTsuyoshi
en-aut-sei=Matsuno
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IwagakiHiromi
en-aut-sei=Iwagaki
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FujiwaraTakuzo
en-aut-sei=Fujiwara
en-aut-mei=Takuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TanakaNoriaki
en-aut-sei=Tanaka
en-aut-mei=Noriaki
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=Kurashiki Medical Center

affil-num=5
en-affil=
kn-affil=Okayama University
en-keyword=renal transplantation
kn-keyword=renal transplantation
en-keyword=long-term stable recipients
kn-keyword=long-term stable recipients
en-keyword=specific CTL nuresponsiveness
kn-keyword=specific CTL nuresponsiveness
en-keyword=interleckin-2
kn-keyword=interleckin-2
en-keyword=interleukin-2 receptors
kn-keyword=interleukin-2 receptors
END

start-ver=1.4
cd-journal=joma
no-vol=56
cd-vols=
no-issue=6
article-no=
start-page=309
end-page=315
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=200212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Suppressive effects of transforming growth factor-beta1 produced by hepatocellular carcinoma cell lines on interferon-gamma production by peripheral blood mononuclear cells.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Transforming growth factor-beta1 (TGF-beta1) exerts potent immunosuppressive effects. In this study, we investigated the potential role of TGF-beta1 produced by hepatocellular carcinoma (HCC) cell lines in immunosuppression mechanisms. Using the Mv1Lu cell-growth inhibition assay and an enzyme-linked immunosorbent assay (ELISA), we detected optimal levels of TGF-beta1 in the culture supernatants conditioned by the HCC cell lines PLC/PRF/5, Hep3B, and HepG2. To determine the biological activity of TGF-beta1 in the supernatants, we examined the effects of the culture supernatants on the production of interferon (IFN)-gamma induced during the culture of peripheral blood mononuclear cells (PBMCs) stimulated with interleukin (IL)-12. IFN-gamma production of IL-12-stimulated PBMCs in the 1:1 dilution of the acid-activated conditioned medium of PLC/PRF/5, Hep3B, and HepG2 reduced to 14.7 +/- 0.8, 17.3 +/- 9.0, and 35.9 +/- 14.6%, respectively, compared with the value in the culture with control medium (complete culture medium). These results suggest that HCC cells producing TGF-beta1 may reduce the generation or activation of cytotoxic T lymphocytes (CTL) and natural killer (NK) cells, and thus could enhance their ability to escape immune-mediated surveillance.</p>

en-copyright=
kn-copyright=

en-aut-name=MouriHirokazu
en-aut-sei=Mouri
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakaguchiKohsaku
en-aut-sei=Sakaguchi
en-aut-mei=Kohsaku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SawayamaTomoyuki
en-aut-sei=Sawayama
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SenohTomonori
en-aut-sei=Senoh
en-aut-mei=Tomonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OhtaTakeyuki
en-aut-sei=Ohta
en-aut-mei=Takeyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NishimuraMamoru
en-aut-sei=Nishimura
en-aut-mei=Mamoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FujiwaraAkiko
en-aut-sei=Fujiwara
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TeraoMasako
en-aut-sei=Terao
en-aut-mei=Masako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShiratoriYasushi
en-aut-sei=Shiratori
en-aut-mei=Yasushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TsujiTakao
en-aut-sei=Tsuji
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University

affil-num=7
en-affil=
kn-affil=Okayama University

affil-num=8
en-affil=
kn-affil=Okayama University

affil-num=9
en-affil=
kn-affil=Okayama University

affil-num=10
en-affil=
kn-affil=Okayama University
en-keyword=hepatocellular carcinoma
kn-keyword=hepatocellular carcinoma
en-keyword=immunosuppression
kn-keyword=immunosuppression
en-keyword=   transforming growth factor-?1 (TGF-?1)
kn-keyword=   transforming growth factor-?1 (TGF-?1)
en-keyword=interleukin-12
kn-keyword=interleukin-12
en-keyword= interferon-? (IFN-?)
kn-keyword= interferon-? (IFN-?)
END

start-ver=1.4
cd-journal=joma
no-vol=53
cd-vols=
no-issue=1
article-no=
start-page=55
end-page=59
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1999
dt-pub=199902
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Hydrocortisone Sodium Succinate Suppressed Production of Interleukin-10 by Human Peripheral Blood Mononuclear Cells: Clinical Significance
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Corticoids are well known for their immunosuppressive properties. Interleukin-10 (IL-10) is an intrinsic antiinflammatory peptide in immune diseases, originally identified as cytokine synthesis inhibitory factor. We examined the effect of hydrocortisone sodium succinate (HSS) on the production of IL-10 by human peripheral blood mononuclear cells (PBMCs). PBMCs from healthy volunteers and cancer-burden patients were preincubated separately with or without HSS for 1 h, then stimulated with 5 microg/ml lipopolysaccharide (LPS). Production of IL-10 by human PBMCs was detected with LPS stimulation and its production was higher in cancer-burden patients than in normal volunteers, although this was not statistically significant. HSS suppressed production of IL-10 by LPS-stimulated PBMCs in a dose-dependent manner both in normal volunteers and in cancer-burden patients. These results indicate that, in addition to their antiinflammatory properties, corticoids act to restore the immunosuppressive states even in cancer-burden states</p>

en-copyright=
kn-copyright=

en-aut-name=KohkaHideo
en-aut-sei=Kohka
en-aut-mei=Hideo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IwagakiHiromi
en-aut-sei=Iwagaki
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YoshinoTadashi
en-aut-sei=Yoshino
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KobashiKenta
en-aut-sei=Kobashi
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SaitoShinnya
en-aut-sei=Saito
en-aut-mei=Shinnya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IsozakiHiroshi
en-aut-sei=Isozaki
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakakuraNorihisa
en-aut-sei=Takakura
en-aut-mei=Norihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TanakaNoriaki
en-aut-sei=Tanaka
en-aut-mei=Noriaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University

affil-num=7
en-affil=
kn-affil=Okayama University

affil-num=8
en-affil=
kn-affil=Okayama University
en-keyword=steroid
kn-keyword=steroid
en-keyword=interleukin-10
kn-keyword=interleukin-10
en-keyword=cancer-burden state
kn-keyword=cancer-burden state
END

start-ver=1.4
cd-journal=joma
no-vol=53
cd-vols=
no-issue=5
article-no=
start-page=239
end-page=244
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1999
dt-pub=199910
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Modulatory effect of a serine protease inhibitor on surgical stress: its clinical implications.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>The relationship between endogenous cytokine antagonists and surgical stress is poorly understood. Surgical stress induces immunosuppression, and the reversed therapy of postoperative immunosuppression has been expected. The aim of the present study was to assess the effect of a serine protease inhibitor on postoperative immune reactivity. Twenty patients with colorectal cancer were randomly separated into experimental and control groups of 10 patients each. The experimental group received perioperative administration of a serine protease inhibitor while the control group did not. Plasma levels of cytokine antagonists, which suppress cell-mediated immunity, such as cortisol, interleukin-1 receptor antagonist, soluble interleukin-2 receptor (sIL-2R) and soluble tumor necrosis factors p55, p75 (sTNF-R55, -R75) were simultaneously measured. Significant reductions of plasma concentration of sIL-2R and sTNF-R55 were observed. Perioperative administration of a serine protease inhibitor may contribute to ameliorating immunosuppression after major surgery.</p>

en-copyright=
kn-copyright=

en-aut-name=IwagakiHiromi
en-aut-sei=Iwagaki
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YagiTakahito
en-aut-sei=Yagi
en-aut-mei=Takahito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UrushiharaNaoto
en-aut-sei=Urushihara
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KobashiKenta
en-aut-sei=Kobashi
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MorimotoYoshinori
en-aut-sei=Morimoto
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IsozakiHiroshi
en-aut-sei=Isozaki
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakakuraNorihisa
en-aut-sei=Takakura
en-aut-mei=Norihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TanakaNoriaki
en-aut-sei=Tanaka
en-aut-mei=Noriaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University

affil-num=7
en-affil=
kn-affil=Okayama University

affil-num=8
en-affil=
kn-affil=Okayama University
en-keyword=surgical stress
kn-keyword=surgical stress
en-keyword=cytokine antagonist
kn-keyword=cytokine antagonist
en-keyword=protease inhibitor
kn-keyword=protease inhibitor
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=6
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1993
dt-pub=199302
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Comparison of the Effects of Intra-Third Ventricular Administration of Interleukin-1 or Platelet Activating Factor on ACTH Secretion and the Sympathetic-AdrenomeduIIary System in Conscious Rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>The effects of centrally administered interleukin-1 beta (IL-1) or platelet activating factor (PAF) on adrenocorticotropin (ACTH) and catecholamine secretion, blood pressure and heart rate were examined to determine if these agents stimulate similarly the hypothalamic-pituitary-adrenal (HPA) axis or the sympathetic-adrenomedullary system. Intra-third ventricular administration of IL-1 (50, 200 ng) evoked significant ACTH secretion. Centrally administered IL-1 (50 ng) elevated plasma noradrenaline and adrenaline levels, systolic blood pressure and heart rate. Plasma ACTH, noradrenaline and adrenaline levels were also increased by the higher dose (200 ng) of IL-1 while systolic blood pressure and heart rate were not affected. Intra-third ventricular administration of 9 micrograms of PAF elevated the plasma ACTH level while 3 micrograms of PAF did not stimulate ACTH secretion. Neither dose of centrally administered PAF affected any plasma catecholamine level or systolic blood pressure. These results suggest that central IL-1 stimulates both the HPA axis and the sympathetic-adrenomedullary system, that a higher dose of IL-1 stimulates a mechanism to antagonize the elevation of blood pressure and heart rate and that central PAF is not involved in the control of the sympathetic-adrenomedullary system. Thus, IL-1 and PAF do not interact in the brain, although they interact peripherally.</p>

en-copyright=
kn-copyright=

en-aut-name=HashimotoKozo
en-aut-sei=Hashimoto
en-aut-mei=Kozo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HirasawaRyuto
en-aut-sei=Hirasawa
en-aut-mei=Ryuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MakinoShinya
en-aut-sei=Makino
en-aut-mei=Shinya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=Kochi Medical School

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University
en-keyword=interleukin-1
kn-keyword=interleukin-1
en-keyword=platelet activating factor
kn-keyword=platelet activating factor
en-keyword=ACTH
kn-keyword=ACTH
en-keyword=noradrenaline
kn-keyword=noradrenaline
en-keyword=adrenaline
kn-keyword=adrenaline
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=1
article-no=
start-page=21
end-page=28
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1993
dt-pub=199302
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Inhibition of Liver Regeneration in Mice Following Extended Hepatectomy by Transfusion of Lymphokine Activated Killer Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Lymphokine activated killer (LAK) cells can destroy not only tumor cells but also syngeneic liver cells. In this study, the effects of passive transfer of LAK cells on liver regeneration were examined by the 3H-thymidine uptake and bromodeoxyuridine (BrdU) labeling methods after resection of 70% of the volume of the liver. LAK cells were infused 12h after hepatectomy and the effects on regeneration of liver cells were examined 36 h later. The transfusion of LAK cells induced significant inhibition of liver regeneration at a dose of 5-10 x 10(7) cells. Neuraminidase treatment of lymphocytes is desirable to enhance the selective entrapment of LAK cells into the liver. When LAK cells were treated with neuraminidase (0.5 units/ml), and transfused into hepatectomized mice, more potent suppression of liver regeneration was induced in comparison with the same dose of LAK cells. The intraperitoneal injection of recombinant interleukin 2 (rIL-2) after partial hepatectomy also inhibited the regeneration of remnant liver. From these results, lymphocytes such as LAK cells appear to regulate liver regeneration.</p>
en-copyright=
kn-copyright=

en-aut-name=TanakaNoriaki
en-aut-sei=Tanaka
en-aut-mei=Noriaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TatemotoAkihiko
en-aut-sei=Tatemoto
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UrabeTakamitsu
en-aut-sei=Urabe
en-aut-mei=Takamitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OnoMinoru
en-aut-sei=Ono
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HizutaAkio
en-aut-sei=Hizuta
en-aut-mei=Akio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NaomotoYoshio
en-aut-sei=Naomoto
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=GotohKiyotoshi
en-aut-sei=Gotoh
en-aut-mei=Kiyotoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MoreiraLuis Fernando
en-aut-sei=Moreira
en-aut-mei=Luis Fernando
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OritaKunzo
en-aut-sei=Orita
en-aut-mei=Kunzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama  University

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama Univeristy

affil-num=4
en-affil=
kn-affil=Okayama  University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University

affil-num=7
en-affil=
kn-affil=Okayama University

affil-num=8
en-affil=
kn-affil=Okayama University

affil-num=9
en-affil=
kn-affil=Okayama University
en-keyword=liver regeneration
kn-keyword=liver regeneration
en-keyword=hepatectomy
kn-keyword=hepatectomy
en-keyword=lymphokine activated killer cell
kn-keyword=lymphokine activated killer cell
en-keyword=interleukin-2
kn-keyword=interleukin-2
en-keyword=neuraminidase
kn-keyword=neuraminidase
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=3
article-no=
start-page=145
end-page=150
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1993
dt-pub=199306
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Early detection of acute allograft rejection in rat heart transplantation: flowcytometric monitoring of interleukin 2 receptor expression on CD8 positive lymphocytes.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>To assess the usefulness of flowcytometric monitoring in the early detection of acute allograft rejection, we studied surface markers of graft infiltrating lymphocytes, coronary sinus blood lymphocytes and peripheral blood lymphocytes after rat heart transplantation. Fisher rats served as donors and Lewis rats as recipients. Among recipients that received no immunosuppression, grafts were removed 2 days after transplantation (Ongoing Rejection Group: n = 7) and on the day of terminal rejection (Rejection Group: n = 7). The Immunosuppression Group (n = 7) was treated with cyclosporine A at a dose of 3 mg/kg/day intramuscularly for 14 days. The following two color analyses were studied: OX8 (anti-CD8) with OX39 (anti-interleukin 2 receptor; IL2R), W3/25 (anti-CD4) with OX39, W3/25 with OX8. Histological grading demonstrated no significant difference between the Ongoing Rejection Group and the Immunosuppression Group, which showed mild rejection (1.29 +/- 0.27 versus 1.14 +/- 0.24). The proportion of CD8(+)IL2R(+) graft infiltrating lymphocytes showed a more significant increase in the Ongoing Rejection Group than in the Immunosuppression Group (32.1 +/- 3.05 versus 20.6 +/- 9.02; p &#60; 0.01). The proportion of CD8(+) IL2R(+) coronary sinus blood lymphocytes also showed significant increase in the Ongoing Rejection Group compared with the Immunosuppression Group (4.63 +/- 1.91 versus 2.52 +/- 1.60; p &#60; 0.05). These results suggest that this technique can detect acute allograft rejection earlier than endomyocardial biopsy, before the phase in which histological findings become evident.</p>

en-copyright=
kn-copyright=

en-aut-name=KohmotoTakushi
en-aut-sei=Kohmoto
en-aut-mei=Takushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AraiSadahiko
en-aut-sei=Arai
en-aut-mei=Sadahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SenooYoshimasa
en-aut-sei=Senoo
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TeramotoShigeru
en-aut-sei=Teramoto
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama  University

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama  University
en-keyword=acute rejection
kn-keyword=acute rejection
en-keyword=heart transplantation
kn-keyword=heart transplantation
en-keyword=flowcytometry
kn-keyword=flowcytometry
en-keyword=immunologic monitoring
kn-keyword=immunologic monitoring
en-keyword=interleukin 2 receptor
kn-keyword=interleukin 2 receptor
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=2
article-no=
start-page=73
end-page=78
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1993
dt-pub=199304
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Overexpression of Interleukin-2 Receptor α mRNA in Pulmonary Lymphocytes of Lung Cancer Patients Associated with Interstitial Pulmonary Shadow
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The activity of pulmonary lymphocytes was evaluated by the detection of interleukin-2 (IL-2) receptor alpha mRNA expression in lung cancer patients associated with diffuse interstitial shadow on roentgenograms of their lungs. Reverse transcription coupled with the polymerase chain reaction was used to detect mRNA expression. In 5 of 6 patients, IL-2R alpha mRNA expression was increased in pulmonary lymphocytes compared with 4 normal controls. The expression in this mRNA in peripheral blood lymphocytes was almost undetectable in either normal controls or these patients. These results suggest that pulmonary lymphocytes in patients with lung cancer associated with diffuse interstitial shadows are activated and may promote the inflammatory process generating pulmonary fibrosis.
en-copyright=
kn-copyright=

en-aut-name=ShinagawaKatsuji
en-aut-sei=Shinagawa
en-aut-mei=Katsuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ImajoKenji
en-aut-sei=Imajo
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TadaShinya
en-aut-sei=Tada
en-aut-mei=Shinya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TsubotaTeruhiko
en-aut-sei=Tsubota
en-aut-mei=Teruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KimuraIkuro
en-aut-sei=Kimura
en-aut-mei=Ikuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Second Department of Internal Medicine, Okayama University Medical School

affil-num=2
en-affil=
kn-affil=Second Department of Internal Medicine, Okayama University Medical School

affil-num=3
en-affil=
kn-affil=Second Department of Internal Medicine, Okayama University Medical School

affil-num=4
en-affil=
kn-affil=Second Department of Internal Medicine, Okayama University Medical School

affil-num=5
en-affil=
kn-affil=Second Department of Internal Medicine, Okayama University Medical School
en-keyword=pulmonary fibrosis
kn-keyword=pulmonary fibrosis
en-keyword=lung cancer
kn-keyword=lung cancer
en-keyword=pulmonary lymphocytes
kn-keyword=pulmonary lymphocytes
en-keyword=IL-2R α mRNA
kn-keyword=IL-2R α mRNA
en-keyword=RT-PCR
kn-keyword=RT-PCR
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=2
article-no=
start-page=79
end-page=84
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1993
dt-pub=199304
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Immunotherapy by a Slow Delivery System of Interleukin-2 in Mice Model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>A sustained release system for interleukin-2 (IL-2), and IL-2 mini-pellet (IL-2 mp), was developed by fusing IL-2 into a needle shaped collagen. Serum concentration of IL-2 after a single subcutaneous injection of the IL-2 mp into C57BL/6 mice remained elevated longer than after an injection of aqueous IL-2. IL-2 in the serum became undetectable by 6h after a subcutaneous injection of 1 x 10(6) unit of IL-2 in phosphate-buffered saline (PBS). In contrast, after a single subcutaneous injection of IL-2 mp containing the same amount of IL-2, the concentration of IL-2 increased to its maximum at 6h after injection, then began to decrease gradually. IL-2 was detected even on the third day after a single subcutaneous injection of one IL-2 mp. Augmentation of NK activity and generation of IL-2 activated killer cells were observed in the spleen from day 1--day 3 after a single subcutaneous injection of IL-2 mp into C57BL/6 mice. This activation was not observed following a single subcutaneous injection of the same amount of IL-2 in PBS. Adoptive immunotherapy by a single subcutaneous injection of IL-2 mp followed by intravenous injections of in vitro cultured IL-2 activated killer cells showed better results in decreasing the number of metastases of Lewis lung carcinoma in C57BL/6 mice than immunotherapy using IL-2 solution.(ABSTRACT TRUNCATED AT 250 WORDS)</p>

en-copyright=
kn-copyright=

en-aut-name=MatsuokaJunji
en-aut-sei=Matsuoka
en-aut-mei=Junji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakagamiKenichi
en-aut-sei=Sakagami
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FujiwaraToshiyoshi
en-aut-sei=Fujiwara
en-aut-mei=Toshiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OnodaTadashi
en-aut-sei=Onoda
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IdaniHitoshi
en-aut-sei=Idani
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=GochiAkira
en-aut-sei=Gochi
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OritaKunzo
en-aut-sei=Orita
en-aut-mei=Kunzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Central Hospital

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama Univeristy

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University

affil-num=7
en-affil=
kn-affil=Okayama University
en-keyword=IL-2
kn-keyword=IL-2
en-keyword=drug delivery system
kn-keyword=drug delivery system
en-keyword=immunotherapy
kn-keyword=immunotherapy
en-keyword=mouse
kn-keyword=mouse
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=6
article-no=
start-page=399
end-page=406
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1993
dt-pub=199312
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Diagnosis of Rejection in the Allografted Rat Lung: Using Monoclonal Antibodies to T Cell Subsets for Immunologic Monitoring
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Early diagnosis of rejection and timely immunosuppression are absolutely important in clinical lung transplantation. We studied surface markers of peripheral blood lymphocytes (PBL), graft infiltrating lymphocytes (GIF) and bronchoalveolar lavage fluid (BALF) in a rat using flow cytometric monitoring to diagnose rejection. Left lung transplantation was performed on Brown Norway (BN) rats and Lewis (LEW) rats in the following groups; Group 1: LEW-LEW (isograft), Group 2: BN-LEW (allograft; no immunosuppression), Group 3: BN-LEW (allograft; treated with Cyclosporine A at a dose of 15 mg/kg/day i.m.). In each group, rats were killed 3, 5, 7 days postoperatively (n = 6 on each day). Monoclonal antibodies investigated in this study were W3/25 (anti-helper T lymphocyte), OX8 (anti-suppressor/cytotoxic T lymphocyte), and OX39 (anti-interleukin 2 receptor). Histological classification of rejection in Group 2 showed vascular phase at 3 days, alveolar phase at 5 days, and destructive phase at 7 days, respectively. No evidence of rejection was found in Group 1 or 3. In Group 2, W3/25 positive cell proportion in GIL and BALF significantly decreased as the rejection progressed, but OX8 positive and OX39 positive cell proportion increases were significantly greater than in Groups 1 and 3 as the rejection progressed. These results lead us to speculate that the studies of T cell subsets in GIL and BALF lymphocytes are useful for diagnosis of rejection in lung transplantation.</p>
en-copyright=
kn-copyright=

en-aut-name=MaruyamaShuichirou
en-aut-sei=Maruyama
en-aut-mei=Shuichirou
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SanoYoshifumi
en-aut-sei=Sano
en-aut-mei=Yoshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=DateHiroshi
en-aut-sei=Date
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShimizuNobuyuki
en-aut-sei=Shimizu
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TeramotoShigeru
en-aut-sei=Teramoto
en-aut-mei=Shigeru
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 Univerisity

affil-num=4
en-affil=
kn-affil=Okayama  University

affil-num=5
en-affil=
kn-affil=Okayama University
en-keyword=lung transplantation
kn-keyword=lung transplantation
en-keyword=rejection
kn-keyword=rejection
en-keyword=lymphocyte subsets
kn-keyword=lymphocyte subsets
en-keyword=flow cytometry
kn-keyword=flow cytometry
en-keyword=BALF
kn-keyword=BALF
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=6
article-no=
start-page=391
end-page=397
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1993
dt-pub=199312
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Stimulation by interleukin-7 of mononuclear cells in peripheral blood, synovial fluid and synovial tissue from patients with rheumatoid arthritis.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>To determine how interleukin-7 (IL-7) affects the proliferation of T cells in patients with rheumatoid arthritis (RA), we evaluated the response of mononuclear cells (MNC) obtained from their peripheral blood (PB), synovial fluid (SF) and synovial tissue (ST) to stimulation by recombinant IL-7 and interleukin-2 (IL-2). Each cytokine was administered alone or combined with phytohemagglutinin (PHA). Cellular DNA synthesis was assayed by the [3H]-thymidine incorporation method. The stimulatory effect of 500 u/ml IL-7 on PBMNC obtained from 19 patients with RA was significantly lower than on PBMNC from 19 healthy controls. However, the same degree of stimulatory activity of 500 u/ml IL-2 was observed on the PBMNC from both RA patients and control subjects. The response of PBMNC to a suboptimal dose of PHA (0.2 micrograms/ml) was enhanced by adding either IL-7 or IL-2 (100 or 500 u/ml) to the cultures. The enhanced synthesis of DNA by both RA and control PBMNC on exposure to IL-7 following stimulation by a suboptimal dose of PHA was higher than that of IL-2. The effect of IL-7 on RA PBMNC was significantly greater than that of IL-2 at the concentration of 100 u/ml on PBMNC from the same RA patients. The stimulatory activity of IL-2 at the concentrations of 100 and 500 u/ml on SF MNC and ST MNC exceeded that of IL-7. In particular, an IL-2 dose of 500 u/ml had a marked effect on SF MNC. The PHA response of SF MNC was the lowest seen among the MNC from three different compartments.(ABSTRACT TRUNCATED AT 250 WORDS)</p>

en-copyright=
kn-copyright=

en-aut-name=NatsumedaMasamitsu
en-aut-sei=Natsumeda
en-aut-mei=Masamitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishiyaKoji
en-aut-sei=Nishiya
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OtaZensuke
en-aut-sei=Ota
en-aut-mei=Zensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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
en-keyword=interleukin-1
kn-keyword=interleukin-1
en-keyword=interleukin-2
kn-keyword=interleukin-2
en-keyword=rheumatoid arthritis
kn-keyword=rheumatoid arthritis
en-keyword=lymphocyte proliferation
kn-keyword=lymphocyte proliferation
en-keyword=phytohemagglutinin
kn-keyword=phytohemagglutinin
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=4
article-no=
start-page=273
end-page=280
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1993
dt-pub=199308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cellular immunocompetence in aortitis syndrome.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Cellular immunocompetence was investigated in 17 cases of aortitis syndrome (3 active, 14 inactive stage). Both the active and inactive groups demonstrated significantly lower interleukin-2 (IL-2) production than healthy volunteers. The active aortitis syndrome group produced significantly more interleukin-1 beta (IL-1 beta) than the inactive group. The proportion of CD11b+ CD8+ cells was significantly lower in the active aortitis syndrome group. Further, the proportions of CD11b- CD8+ cells and CD57+ CD16- cells in the aortitis syndrome patients were significantly higher than the healthy volunteers. These results suggest that there are intrinsic qualitative abnormalities in the T cells that produce IL-2 in aortitis syndrome. Pathogenesis of aortitis syndrome is considered as follows: during the active stage, diminished IL-2 production impairs differentiation and proliferation of suppressor T cells, thus creating abnormalities in the inhibitory functions of immunoregulation and promoting the proliferation of cytotoxic T and natural killer (NK) cells. This presumably initiates inflammation of the aorta and/or artery.</p>
en-copyright=
kn-copyright=

en-aut-name=HosotaniAkihiro
en-aut-sei=Hosotani
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UchidaHatsuzo
en-aut-sei=Uchida
en-aut-mei=Hatsuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TeramotoShigeru
en-aut-sei=Teramoto
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama  University

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama Univerisity
en-keyword=aortitis syndrome
kn-keyword=aortitis syndrome
en-keyword=immunocompetence
kn-keyword=immunocompetence
en-keyword=interleukin-2
kn-keyword=interleukin-2
en-keyword=interleukin-1?
kn-keyword=interleukin-1?
en-keyword=lymphocyte subsets
kn-keyword=lymphocyte subsets
END

start-ver=1.4
cd-journal=joma
no-vol=39
cd-vols=
no-issue=2
article-no=
start-page=131
end-page=141
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1985
dt-pub=198504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Augmentation of anti-tumor activity by immunization with Mycobacterium tuberculosis (Tbc) and tuberculin-coupled tumor cells.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>The anti-tumor effect of immunization with heat-killed Mycobacterium tuberculosis (Tbc) and Tuberculin (PPD)-coupled syngeneic tumor cells was examined in vivo. Three tumor cell lines were employed. Immunization of Tbc-primed BALB/c mice with PPD-coupled syngeneic Meth-A tumor cells displayed a potent anti-tumor effect on viable Meth-A cells inoculated subcutaneously. Neither PPD-coupled LLC (Lewis Lung Carcinoma) cells nor sonicated PPD-coupled Meth-A cells were capable of immunizing these mice. PPD-coupled syngeneic whole tumor cells were indispensable for induction of this tumor-specific resistance. Immunization of Tbc-primed C3H/He mice with PPD-coupled syngeneic MH134 tumor cells did not elicit anti-tumor activity against MH134, but additional pretreatment of mice with cyclophosphamide brought on an anti-tumor effect. Antimetastatic reactivity was investigated in C57BL/6 mice bearing LLC, with a reduction in metastases noted. This antimetastatic effect was observed even when the mice were immunized with PPD-coupled LLC cells three days after removal of the initial tumor. Immunization with Tbc and PPD-coupled Meth-A cells together with intraperitoneal administration of murine or rat interleukin 2 (IL 2) further augmented anti-Meth-A resistance. Murine IL 2 further inhibited tumor growth during the early stage, while rat IL 2 showed an anti-tumor effect throughout the course of tumor growth.</p>

en-copyright=
kn-copyright=

en-aut-name=YadaYoshihiko
en-aut-sei=Yada
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanakaNoriaki
en-aut-sei=Tanaka
en-aut-mei=Noriaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OritaKunzo
en-aut-sei=Orita
en-aut-mei=Kunzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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
en-keyword=mycobacterium
kn-keyword=mycobacterium
en-keyword=Tuberculin
kn-keyword=Tuberculin
en-keyword=interleukin 2
kn-keyword=interleukin 2
en-keyword=coupling
kn-keyword=coupling
END

start-ver=1.4
cd-journal=joma
no-vol=48
cd-vols=
no-issue=1
article-no=
start-page=17
end-page=23
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1994
dt-pub=199402
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Regulatory Effect of Lymphokine-Activated Killer Cells on Epidermal Proliferation Induced by Cholera Toxin in Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>We investigated the effects of lymphokine-activated killer (LAK) cells on epidermal hyperplasia induced by cholera toxin (CT). LAK cells showed cytotoxic activity against both tumor cell lines and proliferating normal cells including skin epidermal cells. When 1 x 10(7) LAK cells were injected intradermally together with 1.0 ng of CT, epidermal hyperplasia was markedly suppressed. The LAK effectors inhibiting epidermal hyperplasia showed surface phenotypes of asialo-GM1+, Thy-1+, Lyt-2- and L3T4-, that were different from those of LAK cells killing tumor cells in vitro. Epidermal hyperplasia induced by CT was not suppressed by topical administration of cytokines such as interleukin-2, interferon and tumor necrosis factor. Therefore, the antiproliferative effect of LAK cells might be attributed to their direct action on the epidermal cells.</p>

en-copyright=
kn-copyright=

en-aut-name=OkamotoYasuhisa
en-aut-sei=Okamoto
en-aut-mei=Yasuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanakaNoriaki
en-aut-sei=Tanaka
en-aut-mei=Noriaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OritaKunzo
en-aut-sei=Orita
en-aut-mei=Kunzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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
en-keyword=lymphokine-activated killer cell
kn-keyword=lymphokine-activated killer cell
en-keyword=cholera toxin
kn-keyword=cholera toxin
en-keyword=epidermal proliferation
kn-keyword=epidermal proliferation
en-keyword=cytokine
kn-keyword=cytokine
END

start-ver=1.4
cd-journal=joma
no-vol=48
cd-vols=
no-issue=1
article-no=
start-page=63
end-page=65
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1994
dt-pub=199402
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Unresponsiveness of antidonor cytotoxic T cells in a long-term stable renal transplant recipient.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>The antidonor immune response was examined in a one haplotype-mismatched renal transplant recipient with an allograft that had been well-functioning for more than 10 years. Although the relative response of the mixed lymphocyte reaction (MLR) was (45.8)% and the MLR responder cells stimulated by donor cells produced measurable amounts of interleukin-2 (IL-2) (11.6 U/ml), the cytotoxic T lymphocytes (CTL) could not be generated against donor cells, even with exogenous IL-2. These results indicate that antidonor CTL precursors were either deleted or inactivated in this recipient.</p>

en-copyright=
kn-copyright=

en-aut-name=FujiwaraTakuzo
en-aut-sei=Fujiwara
en-aut-mei=Takuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakagamiKenichi
en-aut-sei=Sakagami
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SaitoShinya
en-aut-sei=Saito
en-aut-mei=Shinya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=UdaMasashi
en-aut-sei=Uda
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OritaKunzo
en-aut-sei=Orita
en-aut-mei=Kunzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Center for Adult Diseases

affil-num=2
en-affil=
kn-affil=Center for Adult Diseases

affil-num=3
en-affil=
kn-affil=Center for Adult Diseases

affil-num=4
en-affil=
kn-affil=Okayama  University

affil-num=5
en-affil=
kn-affil=Okayama University
en-keyword=renal transplantation
kn-keyword=renal transplantation
en-keyword=long-term stable recipient
kn-keyword=long-term stable recipient
en-keyword=cytotoxic T lymphocytes
kn-keyword=cytotoxic T lymphocytes
END

start-ver=1.4
cd-journal=joma
no-vol=48
cd-vols=
no-issue=2
article-no=
start-page=67
end-page=72
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1994
dt-pub=199404
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Partial Purification and Chraracterization of Dendritic Cell Differentiation Factor
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Previously, we reported that interleukin-2 (IL-2)-stimulated helper T cells produced an unknown soluble factor which induced dendritic cell-like differentiation in primary cultures of monocytic leukemia cells and we referred to this factor as dendritic cell differentiation factor (DCDF). In this study, we attempted to purify and characterize DCDF and investigated its biological effect on normal human monocytes. Gel filtration chromatography indicated that the molecular weight of DCDF is approximately 30-35 kDa. Chromatofocusing indicated that the isoelectric point of DCDF is approximately 5.0. DCDF, partially purified by subsequent gel filtration, chromatofocusing, and hydrophobic chromatography, significantly enhanced the HLA-DR expression of normal human monocytes and a human monocytic leukemia cell line, THP-1. This biological activity was not neutralized by any known antibodies to human cytokines. DCDF significantly amplified the T-cell stimulatory activity of monocytes in the allogeneic mixed leukocyte reaction (MLR). Moreover, DCDF significantly enhanced IL-1 beta and IL-6 production by monocytes in a dose-dependent manner. These results suggest that DCDF is a novel human cytokine which stimulates the accessory cell function of monocytes.</p>

en-copyright=
kn-copyright=

en-aut-name=MiyataniKatsuya
en-aut-sei=Miyatani
en-aut-mei=Katsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakahashiKiyoshi
en-aut-sei=Takahashi
en-aut-mei=Kiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YanaiHiroyuki
en-aut-sei=Yanai
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YoshinoTadashi
en-aut-sei=Yoshino
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AkagiTadaatsu
en-aut-sei=Akagi
en-aut-mei=Tadaatsu
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 Univeristy

affil-num=4
en-affil=
kn-affil=Okayama  University

affil-num=5
en-affil=
kn-affil=Okayama University
en-keyword=dendritic cell
kn-keyword=dendritic cell
en-keyword=differentiation
kn-keyword=differentiation
en-keyword=protein purification
kn-keyword=protein purification
en-keyword=cytokine
kn-keyword=cytokine
END

start-ver=1.4
cd-journal=joma
no-vol=48
cd-vols=
no-issue=4
article-no=
start-page=225
end-page=226
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1994
dt-pub=199408
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical value of soluble interleukin-2 receptor in infectious complications.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>In this study, we investigated serum-soluble interleukin-2 receptor (sIL-2r) and neopterin (NPT) levels in five patients with severe postoperative infections. A total of 25 synchronous determinations of sIL-2r and NPT were performed. A marked increase in sIL-2r and NPT levels was observed, and the increase in sIL-2r was significantly correlated to that of NPT which is a marker of macrophage activity. These results suggest that macrophages are involved in the stimulation of sIL-2r release, representing a potentially negative biological effect. The results indicate that sIL-2r may be a useful indicator of the efficacy of antibiotics and of prognosis.</p>

en-copyright=
kn-copyright=

en-aut-name=IwagakiHiromi
en-aut-sei=Iwagaki
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HizutaAkio
en-aut-sei=Hizuta
en-aut-mei=Akio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IwadouHironori
en-aut-sei=Iwadou
en-aut-mei=Hironori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=PerdomoJose Antonio
en-aut-sei=Perdomo
en-aut-mei=Jose Antonio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TanakaNoriaki
en-aut-sei=Tanaka
en-aut-mei=Noriaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OritaKunzo
en-aut-sei=Orita
en-aut-mei=Kunzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University 

affil-num=4
en-affil=
kn-affil=Okayama University 

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University
en-keyword=soluble interleukin-2 receptor
kn-keyword=soluble interleukin-2 receptor
en-keyword=neopterin
kn-keyword=neopterin
en-keyword=intection
kn-keyword=intection
END

start-ver=1.4
cd-journal=joma
no-vol=48
cd-vols=
no-issue=4
article-no=
start-page=181
end-page=187
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1994
dt-pub=199408
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Impaired Interleukin-8-Dependent Chemotaxis by Synovial Fluid Polymorphonuclear Leukocytes in Rheumatoid Arthritis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>The accumulation of polymorphonuclear leukocytes (PMN) in synovial fluid is a common feature of rheumatoid arthritis (RA). We studied the chemotactic response of PMN obtained from the synovial fluid and from the peripheral blood of patients with RA using a modified Boyden's method, in which interleukin-8 (IL-8) or N-formyl-methionyl-leucyl-phenylalanine (FMLP) was used as a chemotactic agent. The IL-8-induced response of peripheral blood PMN from 15 patients with RA did not differ from that of 15 healthy controls. A decreased chemotactic response to IL-8 was, however, observed in PMN from the synovial fluid of 12 patients with RA compared with peripheral blood cells of the same individual. This defective chemotactic ability of PMN was inversely correlated with the number of infiltrating cells in the synovial fluid. We also obtained similar results with FMLP. These results indicate that the chemotactic ability of PMN may be reduced after migrating to the synovial fluid.</p>
en-copyright=
kn-copyright=

en-aut-name=HashimotoHiroo
en-aut-sei=Hashimoto
en-aut-mei=Hiroo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamamuraMasahiro
en-aut-sei=Yamamura
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NishiyaKoji
en-aut-sei=Nishiya
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OtaZensuke
en-aut-sei=Ota
en-aut-mei=Zensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Kochi Medical School

affil-num=4
en-affil=
kn-affil=Okayama  University
en-keyword=Interleukin-8
kn-keyword=Interleukin-8
en-keyword=chemotaxis
kn-keyword=chemotaxis
en-keyword=rheumatoid arthritis
kn-keyword=rheumatoid arthritis
en-keyword=synovial fluid PMN
kn-keyword=synovial fluid PMN
END

start-ver=1.4
cd-journal=joma
no-vol=42
cd-vols=
no-issue=2
article-no=
start-page=77
end-page=81
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1988
dt-pub=198804
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Prolongation of Cardiac Allograft Survival in Rats by Treatment with Anti-Interleukin 2 Antiserum
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Interleukin-2 (IL2) is the obligatory signal for both T cell mitogenesis and in vitro generation of alloreactive cytotoxic T lymphocytes (CTL). An investigation was made to determine whether an antibody directed against IL2 would suppress the rejection reaction of rat cardiac allografts. Rabbit anti-interleukin 2 (anti-IL2) antiserum was obtained by immunizing at 2 week intervals over a period of 8 weeks with 10(6) U of recombinant human IL2 along with complete Freund's adjuvant. The bioassay for inhibition of IL2 activity by anti-IL2 antiserum was carried out in conjunction with the IL2-dependent cytotoxic T cell (CTLL cell) assay. Cardiac allografts of F344 rats were heterotopically transplanted into ACI rats. Seven daily doses of 1 ml of anti-IL2 antiserum were administered intravenously following transplantation. IL2-driven [3H]thymidine incorporation in CTLL cells was significantly inhibited by rabbit anti-IL2 antiserum. Graft survival in the anti-IL2 serum-treated group was significantly prolonged in a dose-dependent fashion compared to control groups. In conclusion, these results indicate that rabbit anti-IL2 antiserum may prove to be of significant value as an immunosuppressive agent in clinical organ transplantation.</p>

en-copyright=
kn-copyright=

en-aut-name=OsakiToshihide
en-aut-sei=Osaki
en-aut-mei=Toshihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakagamiKenichi
en-aut-sei=Sakagami
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OritaKunzo
en-aut-sei=Orita
en-aut-mei=Kunzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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
en-keyword=anti-interleukin 2 antiserum
kn-keyword=anti-interleukin 2 antiserum
en-keyword=rat cardiac allograft
kn-keyword=rat cardiac allograft
en-keyword=immunosuppressive agent
kn-keyword=immunosuppressive agent
END

start-ver=1.4
cd-journal=joma
no-vol=62
cd-vols=
no-issue=2
article-no=
start-page=119
end-page=126
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=200804
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Interleukin-4 downregulates the cyclic tensile stress-induced matrix metalloproteinases-13 and cathepsin b expression by rat normal chondrocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Mechanical stress plays a key role in the pathogenesis of cartilage destruction seen in osteoarthritis (OA). We investigated the effect of cyclic tensile stress (CTS) on the anabolic and catabolic gene expression of rat cultured normal chondrocytes using the Flexercell strain unit. The effects of interleukin (IL)-4, a chondroprotective cytokine, on the changes in gene expression induced by CTS were also investigated. CTS (7% elongation at 0.5 Hz) for 24 h did not affect the expression of aggrecan and type II collagen, whereas CTS significantly upregulated matrix metalloproteinase (MMP)-13 and cathepsin B mRNA expression by chondrocytes. IL-1beta expression was also signifi cantly upregulated by CTS up to 12 h. The upregulation of MMP-13 was observed at 3 h, which was earlier than that of IL-1beta. Furthermore, pre-treatment with IL-4 (10 ng/ml) suppressed both MMP-13 and cathepsin B induction by mechanical stress, as well as CTS-induced IL-1beta expression. Our results suggest that IL-4 might have a therapeutic value in the treatment of OA by downregulation of mechanical stress-induced MMP-13 and cathepsin B expression by chondrocytes.</p>
en-copyright=
kn-copyright=

en-aut-name=DoiHideyuki
en-aut-sei=Doi
en-aut-mei=Hideyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishidaKeiichiro
en-aut-sei=Nishida
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YorimitsuMasanori
en-aut-sei=Yorimitsu
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KomiyamaTakamitsu
en-aut-sei=Komiyama
en-aut-mei=Takamitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KadotaYasutaka
en-aut-sei=Kadota
en-aut-mei=Yasutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TetsunagaTomonori
en-aut-sei=Tetsunaga
en-aut-mei=Tomonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshidaAki
en-aut-sei=Yoshida
en-aut-mei=Aki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KubotaSatoshi
en-aut-sei=Kubota
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TakigawaMasaharu
en-aut-sei=Takigawa
en-aut-mei=Masaharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OzakiToshifumi
en-aut-sei=Ozaki
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

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

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

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

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

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

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

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

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

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

affil-num=10
en-affil=
kn-affil=Departments of Orthopaedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=IL-4
kn-keyword=IL-4
en-keyword=MMP
kn-keyword=MMP
en-keyword=cathepsin B
kn-keyword=cathepsin B
en-keyword=mechanical stress
kn-keyword=mechanical stress
en-keyword=aggrecanase
kn-keyword=aggrecanase
END

start-ver=1.4
cd-journal=joma
no-vol=43
cd-vols=
no-issue=3
article-no=
start-page=143
end-page=151
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198906
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Immortalization of rat spleen and thymus T cells by human T-cell leukemia virus type I.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Co-cultivation of thymus and spleen cells of Fisher and Lewis rats with lethally irradiated MT-2 cells harboring human T-cell leukemia virus type I (HTLV-I) resulted in the establishment of lymphoid cell lines, FIRT-1, FIRS-1, LERT-1, and LERS-1, respectively. Cells of these cell lines had rat T-cell characters as demonstrated by the positive reaction to monoclonal antibodies (MAbs) to rat T cell antigens (Thy 1 and pan T). They lacked surface immunoglobulins and strongly expressed rat interleukin-2 receptor antigen (Tac) and Ia antigen. Karyotypic analysis revealed that they had the normal rat karyotype in early cultures, but showed marked aneuploidy after long cultivation. None of them expressed HTLV gag proteins (p19 and p24) or virus particles, but they contained HTLV-I proviral DNA monoclonally and weakly expressed pX gene products (p40x). They were not transplantable into syngeneic newborn rats.</p>

en-copyright=
kn-copyright=

en-aut-name=AkagiTadaatsu
en-aut-sei=Akagi
en-aut-mei=Tadaatsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakataHiroshi
en-aut-sei=Takata
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YoshinoTadashi
en-aut-sei=Yoshino
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TeramotoNorihiro
en-aut-sei=Teramoto
en-aut-mei=Norihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YanoShoki
en-aut-sei=Yano
en-aut-mei=Shoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OkaTakashi
en-aut-sei=Oka
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama  University

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama  University

affil-num=4
en-affil=
kn-affil=Okayama  University

affil-num=5
en-affil=
kn-affil=Kochi Medical School

affil-num=6
en-affil=
kn-affil=Kochi Medical School
en-keyword=human T-cell leukemia virus
kn-keyword=human T-cell leukemia virus
en-keyword=rat T cell
kn-keyword=rat T cell
en-keyword=immortalization
kn-keyword=immortalization
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=3
article-no=
start-page=149
end-page=157
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2006
dt-pub=200606
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Selective recruitment of CXCR3+ and CCR5+ CCR4+ T cells into synovial tissue in patients with rheumatoid arthritis.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>The inflamed synovial tissue (ST) of rheumatoid arthritis (RA) is characterized by the selective accumulation of interferon gamma-producing Th1-type CD4+ T cells. In this study, we investigated whether the predominance of Th1-type CD4+ cells in the ST lesion is mediated by their selective recruitment through Th1 cell-associated chemokine receptors CXCR3 and CCR5. The lymphocyte aggregates in the ST of RA contained a large number of CD4+ T cells, which mostly expressed both CXCR3 and CCR5, but not CCR4. In contrast, the frequencies of CD4+ and CD8+ T cells expressing CXCR3 and CCR5 in the blood were significantly decreased in RA patients, compared with healthy controls (HC), although there was no difference in the frequencies of CCR4-expressing CD4+ and CD8+ T cells between RA and HC. CXCR3, CCR5, and CCR4 expression in blood CD4 + T cells and CXCR3 expression in CD8+ T cells were increased after interleukin-15 (IL-15) stimulation. Therefore, the distribution of Th1-type CD4+ T cells into the ST from the blood in RA may be associated with the local expression of chemokines, both CXCR3 and CCR5 ligands, and IL-15 may play a role in enhancing these chemokine receptors on CD4+ T cell infiltrates.</p>
en-copyright=
kn-copyright=

en-aut-name=NoriiMika
en-aut-sei=Norii
en-aut-mei=Mika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamamuraMasahiro
en-aut-sei=Yamamura
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IwahashiMitsuhiro
en-aut-sei=Iwahashi
en-aut-mei=Mitsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=UenoAkiko
en-aut-sei=Ueno
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamanaJiro
en-aut-sei=Yamana
en-aut-mei=Jiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Aichi Medical University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University
en-keyword=CXCR3
kn-keyword=CXCR3
en-keyword=CCR5
kn-keyword=CCR5
en-keyword=CD4+ T cells
kn-keyword=CD4+ T cells
en-keyword=interleukin-15
kn-keyword=interleukin-15
en-keyword=rheumatoid arthritis
kn-keyword=rheumatoid arthritis
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=6
article-no=
start-page=325
end-page=330
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2006
dt-pub=200612
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Study of interleukin-6 in the spread of colorectal cancer: the diagnostic significance of IL-6.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We investigated the diagnostic significance of IL-6 for lymph node metastasis and/or hepatic metastasis from colorectal cancer in 65 patients and evaluated the contributions of 8 factors (IL-6, HGF, IL-1beta, TNF-alpha, TGF-beta1, ELAM-1, ICAM-1, VCAM-1) toward Dukes.s classification of 53 patients. We also examined IL-6 expression in tumor tissue. From the receiver operating characteristic (ROC) curve analysis, an optimal cutoff value of 5.8 pg/ml was determined to classify lymph node and/or hepatic metastasis, and that of 6.3 pg/ml was determined to classify hepatic metastasis. These values indicated sensitivities of 55.0% and 71.4%, and specifi cities of 100% and 88.6%, respectively. IL-6, HGF, and ELAM-1 were very useful for distinguishing among Dukes.s A/B group, C group, and D group. In all cases with high IL-6 values (more than 25.0 pg/ml), immunohistochemical staining was positive for IL-6 in the cytoplasm of cancer cells. IL-6 is strongly suspected to be involved in lymph node and/or hepatic metastasis by promoting it through HGF, and serum IL-6 value (pg/ml) would be useful diagnostically to estimate whether or not there is a high risk of lymph node and/or hepatic metastasis.
en-copyright=
kn-copyright=

en-aut-name=AshizawaTatsuto
en-aut-sei=Ashizawa
en-aut-mei=Tatsuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OkadaRyosuke
en-aut-sei=Okada
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SuzukiYoshiaki
en-aut-sei=Suzuki
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakagiMakoto
en-aut-sei=Takagi
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamazakiTatsuyuki
en-aut-sei=Yamazaki
en-aut-mei=Tatsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SumiTetsuo
en-aut-sei=Sumi
en-aut-mei=Tetsuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AokiToshiaki
en-aut-sei=Aoki
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AokiTatsuya
en-aut-sei=Aoki
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=Tokyo Medical University Hachioji Medical Center, Tokyo

affil-num=2
en-affil=
kn-affil=Tokyo Medical University Hachioji Medical Center, Tokyo

affil-num=3
en-affil=
kn-affil=Tokyo Medical University Hachioji Medical Center, Tokyo

affil-num=4
en-affil=
kn-affil=Tokyo Medical University Hachioji Medical Center, Tokyo

affil-num=5
en-affil=
kn-affil=Tokyo Medical University Hachioji Medical Center, Tokyo

affil-num=6
en-affil=
kn-affil=Tokyo Medical University Hachioji Medical Center, Tokyo

affil-num=7
en-affil=
kn-affil=Tokyo Medical University Hachioji Medical Center, Tokyo

affil-num=8
en-affil=
kn-affil=Tokyo Medical University Hachioji Medical Center, Tokyo
en-keyword=IL-6
kn-keyword=IL-6
en-keyword=colorectal cancer
kn-keyword=colorectal cancer
en-keyword=lymph node metastasis
kn-keyword=lymph node metastasis
en-keyword=hepatic metastasis
kn-keyword=hepatic metastasis
en-keyword=diagnostic signifi cance
kn-keyword=diagnostic signifi cance
END

start-ver=1.4
cd-journal=joma
no-vol=50
cd-vols=
no-issue=1
article-no=
start-page=11
end-page=16
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1996
dt-pub=199602
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Enhancement of experimental metastasis by gamma-interferon in a murine adenocarcinoma.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>This study was conducted to examine the effect of gamma-interferon (IFN-gamma) on experimental metastasis formation by murine colon 26 adenocarcinoma in BALB/c mice. We found that the number of experimental lung metastases was increased after colon 26 cells were pretreated for 1 h with as little as 1 OIU/ml of IFN-gamma. 5-[125I] iodo-2'-deoxyuridine-radiolabeled colon 26 cells pretreated with IFN-gamma remained at higher level in the lung at 24h after intravenous injection than when the cells were not pretreated. In vivo elimination of asialo GM1-positive cells increased the number of lung metastases and, in such mice, there was no longer a difference in metastatic ability between control and IFN-gamma-treated cells. Colon 26 cells were completely resistant to lysis by isolated splenocytes. Splenocytes incubated in vitro with interleukin 2 exhibited moderate cytotoxicity against colon 26 cells, but there were no significant differences between control and IFN-gamma-treated cells. Colon 26 cells pretreated with IFN-gamma demonstrated resistance to tumor necrosis factor alpha-mediated growth inhibition. The enhancement of metastases by IFN-gamma was dependent on de novo protein synthesis since the enhancement was abolished by cycloheximide. Taken together, the data suggest that the metastatic ability of colon 26 cells pretreated with IFN-gamma is significantly higher due to the resistance to asialo GM1-positive cells accompanied with de novo protein synthesis.</p>

en-copyright=
kn-copyright=

en-aut-name=HiranoTetsuo
en-aut-sei=Hirano
en-aut-mei=Tetsuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HizutaAkio
en-aut-sei=Hizuta
en-aut-mei=Akio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TanakaNoriaki
en-aut-sei=Tanaka
en-aut-mei=Noriaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OritaKunzo
en-aut-sei=Orita
en-aut-mei=Kunzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Universitry

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama Univeristy

affil-num=4
en-affil=
kn-affil=Okayama  University
en-keyword=?-interferon
kn-keyword=?-interferon
en-keyword=colon 26 murine adenocarcinoma
kn-keyword=colon 26 murine adenocarcinoma
en-keyword=lung metastasis
kn-keyword=lung metastasis
END

start-ver=1.4
cd-journal=joma
no-vol=50
cd-vols=
no-issue=3
article-no=
start-page=145
end-page=150
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1996
dt-pub=199606
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Regulation of Interleukin-2 Receptor y Chain mRNA Expression in Human Monocytic Cell Line THP-1
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Circulating hepatitis C virus (HCV) particles can be fractionated by means of differential flotation centrifugation. It is reported that in the bottom fraction HCV is in the form immune complexes, whereas in the top, it is free of antibodies. We evaluated the significance of circulating complex and free HCV in chronic hepatitis C, and assessed the relationship in terms of the response to interferon (IFN) therapy. We examined sera before, just after, and 1 year after administering IFN to 18 patients with chronic hepatitis C, 10 of whom responded (group CR), and 8 did not (group NR). The amounts of virus were similar between both groups before therapy. After differential flotation centrifugation with 1.063 g/ml of NaCl, the top and bottom fractions were assayed for HCV RNA. Before therapy, HCV RNA was detected in the top fraction in 1 of 10 in group CR, and in 6 of 8 in group NR (P &#60; 0.05, chi-square test). HCV RNA was positive in the bottom fraction of all samples. In a follow-up study of group NR, HCV RNA was detected in the top fraction in 3 of 8 just after IFN therapy, and in 7 of 8 after 1 year. This study suggests that the presence of HCV in the top fraction can predict a poor response to IFN therapy.</p>

en-copyright=
kn-copyright=

en-aut-name=YanaiHiroyuki
en-aut-sei=Yanai
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YoshinoTadashi
en-aut-sei=Yoshino
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakahashiKiyoshi
en-aut-sei=Takahashi
en-aut-mei=Kiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NinomiyaYoshifumi
en-aut-sei=Ninomiya
en-aut-mei=Yoshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AkagiTadaatsu
en-aut-sei=Akagi
en-aut-mei=Tadaatsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama  University

affil-num=5
en-affil=
kn-affil=Okayama University
en-keyword=IL-2R ??chain
kn-keyword=IL-2R ??chain
en-keyword=phorbol ester
kn-keyword=phorbol ester
en-keyword=monocyte
kn-keyword=monocyte
en-keyword=differentiation
kn-keyword=differentiation
en-keyword=protein kinase
kn-keyword=protein kinase
END

start-ver=1.4
cd-journal=joma
no-vol=44
cd-vols=
no-issue=1
article-no=
start-page=13
end-page=20
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199002
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Role of endogenous prostaglandin E2 in interleukin 1 production by peripheral blood monocytes from patients with rheumatoid arthritis.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>We studied the effect of endogenous prostaglandin E2 (PGE2) on interleukin 1 (IL-1) production by peripheral blood monocytes from patients with rheumatoid arthritis (RA). IL-1 production by RA monocytes was not different from that of monocytes from normal controls, when the cells were either unstimulated or stimulated with lipopolysaccharide (LPS, 20 micrograms/ml), as measured by two different bioassays (thymocyte or fibroblast proliferation assay) and enzyme-linked immunosorbent assay. However, IL-1 production by LPS-stimulated monocytes from RA patients cultured in medium containing indomethacin, an inhibitor of PGE2 synthesis, was significantly greater than that of monocytes from normal controls. In addition, the levels of PGE2 in culture supernatants of unstimulated or LPS-stimulated monocytes from RA patients were higher than in culture supernatants of monocytes from normal controls. Moreover, the increase of in vitro IL-2 production by RA T cells stimulated by phytohemagglutinin (PHA) was observed when monocytes were removed from peripheral blood mononuclear cells. These results indicated that peripheral blood monocytes from RA patients could produce IL-1 in excess in vitro, but that in vivo IL-1 production by RA monocytes and IL-2 induction by RA T cells might be negatively regulated by endogenous PGE2.</p>

en-copyright=
kn-copyright=

en-aut-name=YamamuraMasahiro
en-aut-sei=Yamamura
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishiyaKoji
en-aut-sei=Nishiya
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OtaZensuke
en-aut-sei=Ota
en-aut-mei=Zensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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 Univresity
en-keyword=rheumatoid arthritis
kn-keyword=rheumatoid arthritis
en-keyword=monocytes
kn-keyword=monocytes
en-keyword=interleulin 1
kn-keyword=interleulin 1
en-keyword=prostaglandin E2
kn-keyword=prostaglandin E2
en-keyword=interleukin 2
kn-keyword=interleukin 2
END

start-ver=1.4
cd-journal=joma
no-vol=44
cd-vols=
no-issue=6
article-no=
start-page=301
end-page=308
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199012
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Increased ability of peripheral blood B cells from patients with rheumatoid arthritis to produce interleukin 1 in vitro.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Twenty-four patients with rheumatoid arthritis (RA) and 20 normal controls were examined for the ability of their peripheral blood B cells to produce interleukin 1 (IL-1) with or without lipopolysaccharide (LPS). B cells were purified from peripheral blood by negative selection methods (i.e., removal of adherent cells and sheep red blood cell rosette-forming cells, followed by treatment with monoclonal antibodies (OKT3 and OKM1) and complement). The amount of IL-1 in B cell culture supernatants (SN) was measured by thymocyte and fibroblast proliferation assays and an enzyme-linked immunosorbent assay for IL-1 alpha and beta. As a group, cultured B cells from patients with RA, both spontaneously and when stimulated with LPS, produced higher levels of IL-1 than those from normal controls. IL-1 production by RA B cells with LPS had a weak but positive correlation with disease activity. Moreover, RA B cell culture SN with elevated levels of IL-1 had a synergistic effect on the growth of anti-human IgM (anti-mu) stimulated B cells. In separate experiments, the growth of RA B cells was significantly promoted by IL-1 beta both with and without anti-mu stimulation. These results suggest that B cell-derived IL-1 may be involved in the B cell clonal expansion of RA through its own activity as a B cell stimulatory factor.</p>

en-copyright=
kn-copyright=

en-aut-name=YamamuraMasahiro
en-aut-sei=Yamamura
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishiyaNoji
en-aut-sei=Nishiya
en-aut-mei=Noji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OtaZensuke
en-aut-sei=Ota
en-aut-mei=Zensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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 
en-keyword=rheumatoid arthritis
kn-keyword=rheumatoid arthritis
en-keyword=B cells
kn-keyword=B cells
en-keyword=interleukin 1
kn-keyword=interleukin 1
en-keyword=B cell stimulatory factor
kn-keyword=B cell stimulatory factor
END

start-ver=1.4
cd-journal=joma
no-vol=49
cd-vols=
no-issue=5
article-no=
start-page=241
end-page=245
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1995
dt-pub=199510
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Combined therapy with interleukin 2 and indomethacin in mice inoculated with MH134 hepatoma.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>The antitumor effects of indomethacin and interleukin 2 (IL-2) were studied in C3H/HeJ mice inoculated with MH134 hepatoma cells. Combined treatment with indomethacin and IL-2 augmented natural killer (NK) cells in mice with MH134-induced peritoneal carcinomatosis, and the survival of the treated mice was significantly longer than the non-treated mice. In animals with subcutaneous MH134 tumors, the combined therapy with indomethacin and IL-2 significantly suppressed tumor growth and induced complete regression of the tumor in three out of five mice. These results suggest that indomethacin and IL-2 therapy could be effective on human gastrointestinal cancer cells as well.</p>

en-copyright=
kn-copyright=

en-aut-name=TanakaNoriaki
en-aut-sei=Tanaka
en-aut-mei=Noriaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OkamotoYasuhisa
en-aut-sei=Okamoto
en-aut-mei=Yasuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=GotohKiyotoshi
en-aut-sei=Gotoh
en-aut-mei=Kiyotoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HizutaAkio
en-aut-sei=Hizuta
en-aut-mei=Akio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YunokiShigeru
en-aut-sei=Yunoki
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OritaKunzo
en-aut-sei=Orita
en-aut-mei=Kunzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama  University

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama  University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University
en-keyword=indomethacin
kn-keyword=indomethacin
en-keyword=interleukin-2
kn-keyword=interleukin-2
en-keyword=mouse
kn-keyword=mouse
en-keyword=hepatoma
kn-keyword=hepatoma
END

start-ver=1.4
cd-journal=joma
no-vol=38
cd-vols=
no-issue=2
article-no=
start-page=207
end-page=213
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1984
dt-pub=198404
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Activation of NK activity and auto-reactive cytotoxicity after hepatectomy.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Spleen cells serially sampled from normal mice following partial hepatectomy were tested for antibody-dependent cellular cytotoxicity (ADCC) and natural killer (NK) activity. There was a marked augmentation of these activities of spleen cells from the hepatectomized animals, compared to cells from controls with a simple laparotomy. The augmentation of ADCC in the hepatectomized mice was largely attributable to the activity of T lymphocytes. When cultured with interleukin-2 (IL-2), the spleen cells from hepatectomized mice exhibited cytotoxicity to syngeneic lymphoblasts, which was found to be effected by T cells.</p>

en-copyright=
kn-copyright=

en-aut-name=OnoMinoru
en-aut-sei=Ono
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanakaNoriaki
en-aut-sei=Tanaka
en-aut-mei=Noriaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OritaKunzo
en-aut-sei=Orita
en-aut-mei=Kunzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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
en-keyword=antibody-dependent cellular cytotoxicity (ADCC)
kn-keyword=antibody-dependent cellular cytotoxicity (ADCC)
en-keyword=natural killer(NK) activity
kn-keyword=natural killer(NK) activity
en-keyword=auto-reactive cytotoxicity
kn-keyword=auto-reactive cytotoxicity
en-keyword= interleukin-2(IL-2)
kn-keyword= interleukin-2(IL-2)
en-keyword=hepatectomy
kn-keyword=hepatectomy
END

start-ver=1.4
cd-journal=joma
no-vol=22
cd-vols=
no-issue=
article-no=
start-page=20
end-page=23
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2005
dt-pub=200512
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Expression of interleukin-18 gene in the mouse uterus
kn-title=マウス子宮におけるインターロイキン-18遺伝子の発現
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MurakamiYousuke
en-aut-sei=Murakami
en-aut-mei=Yousuke
kn-aut-name=村上要介
kn-aut-sei=村上
kn-aut-mei=要介
aut-affil-num=1
ORCID=

en-aut-name=KusumotoKenji
en-aut-sei=Kusumoto
en-aut-mei=Kenji
kn-aut-name=楠本憲司
kn-aut-sei=楠本
kn-aut-mei=憲司
aut-affil-num=2
ORCID=

en-aut-name=OtsukiMariko
en-aut-sei=Otsuki
en-aut-mei=Mariko
kn-aut-name=大月真理子
kn-aut-sei=大月
kn-aut-mei=真理子
aut-affil-num=3
ORCID=

en-aut-name=TakeuchiSakae
en-aut-sei=Takeuchi
en-aut-mei=Sakae
kn-aut-name=竹内栄
kn-aut-sei=竹内
kn-aut-mei=栄
aut-affil-num=4
ORCID=

en-aut-name=TakahashiSumio
en-aut-sei=Takahashi
en-aut-mei=Sumio
kn-aut-name=高橋純夫
kn-aut-sei=高橋
kn-aut-mei=純夫
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院自然科学研究科高次生物科学講座･生体統御学分野

affil-num=2
en-affil=
kn-affil=岡山大学大学院自然科学研究科高次生物科学講座･生体統御学分野

affil-num=3
en-affil=
kn-affil=岡山大学大学院自然科学研究科高次生物科学講座･生体統御学分野

affil-num=4
en-affil=
kn-affil=岡山大学大学院自然科学研究科高次生物科学講座･生体統御学分野

affil-num=5
en-affil=
kn-affil=岡山大学大学院自然科学研究科高次生物科学講座･生体統御学分野
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=20090930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=可溶性IL-2レセプターの測定と層別化はびまん性大細胞型B細胞性リンパ腫患者の予後予測に有用である
kn-title=Serum soluble interleukin-2 receptor level and immunophenotype are prognostic factors for patients with diffuse large B-cell lymphoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MoritoToshiaki
en-aut-sei=Morito
en-aut-mei=Toshiaki
kn-aut-name=守都敏晃
kn-aut-sei=守都
kn-aut-mei=敏晃
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=20090325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=OUMS-27軟骨肉腫細胞およびヒト軟骨細胞におけるNFATc1経由インターロイキン1βによるADAMTS9の活性化
kn-title=ADAMTS9 activation by interleukin 1β via NFATc1 in OUMS-27 chondrosarcoma cells and in human chondrocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=YaykasliKursat Oguz
kn-aut-sei=Yaykasli
kn-aut-mei=Kursat Oguz
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=96
cd-vols=
no-issue=7-8
article-no=
start-page=665
end-page=674
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1984
dt-pub=19840830
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Establishment of a T cell hybridoma continuously producing Interleukin 2 (IL2) and functional analysis of secreted IL2
kn-title=IL2産生性T細胞ハイブリドーマの樹立とその免疫学的諸性質
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The AKR-derived T lymphoma cell line BW5147 was fused with a Mycobacterium tuberculosis-primed and boosted BALB/c T cell to produce a T cell hybridoma (A55-24) which continuously produces Interleukin 2 (IL2). A55-24 cells produce IL2 without stimulation by lectin or antigen. The hybridoma culture supernatant did not contain other lymphokine-activities, T cell-replacing factor (TRF), B cell growth factor (BCGF), or macrophage activating factor (MAF). The secreted IL2 possessed the following characteristics: 1) IL2 activity was precipitated at an ammonium sulphate saturation of 50-85% . 2) a molecular weight of 30 Kd 3) an isoelectric point of pH 5.3±0.2 4) IL2 activity was destroyed only partially by pH 2 treatment and heating (56℃, 30min), but eliminated by boiling (100℃, 10min). 5) IL2 activity was absorbed by an IL2-dependent cytotoxic T cell line. 6) Addition of IL1 and this IL2 could not generate any significant CTL responses from PNA(+)-thymocytes, whereas further addition of PPD-CFS obtained from PPD-stimulated Mycobacterium-primed T cells induced noticiable responses.
en-copyright=
kn-copyright=

en-aut-name=KanataniTomohisa
en-aut-sei=Kanatani
en-aut-mei=Tomohisa
kn-aut-name=金谷誠久
kn-aut-sei=金谷
kn-aut-mei=誠久
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部細菌学教室
en-keyword=interleukin 2
kn-keyword=interleukin 2
en-keyword=T cell hybridoma
kn-keyword=T cell hybridoma
en-keyword=lymphokine
kn-keyword=lymphokine
en-keyword=cytotoxic T lymphocyte
kn-keyword=cytotoxic T lymphocyte
END

start-ver=1.4
cd-journal=joma
no-vol=99
cd-vols=
no-issue=11-12
article-no=
start-page=1403
end-page=1410
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1987
dt-pub=19871230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Anti-tumor activity and production of cytotoxic factor by Lymphokine-activated killer cells
kn-title=Lymphokine-activated killer細胞の抗腫瘍効果とそのcytotoxic factor産生能の検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Lymphokine-activated killer (LAK) cells can be generated by incubating peripheral blood lymphocytes in recombinant Interleukin―2. LAK cells kill fresh autologous and allogeneic human tumor cells in vitro. The adoptive transfer of these LAK cells into tumor-bearing hosts can mediate the cure of disseminated cancer in a variety of animal model systems. But the mechanism of target cell killing by LAK cells is as yet undefined. We have postulated that such killing may involve some soluble cytotoxic factors produced and secreted by LAK cells. LAK cells were induced by mitogens and tumor cells to secrete cytotoxic factors against L929 cells. LAK cells produced cytotoxic factors within 2 hr after induction and maximal production was observed 6 hr after induction. There was a good correlation between in vitro LAK cell activity and production of cytotoxic factors. We have identified one of these cytotoxic factors as tumor necrosis factor (TNF). LAK cells lost their in vitro cytotoxic activity and TNF producibility after treatment with OKT-8 antibody. These findings suggest that TNF may be a mediator of in vitro LAK cell activity.
en-copyright=
kn-copyright=

en-aut-name=GangiJunichi
en-aut-sei=Gangi
en-aut-mei=Junichi
kn-aut-name=雁木淳一
kn-aut-sei=雁木
kn-aut-mei=淳一
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第一外科教室
en-keyword=LAK細胞
kn-keyword=LAK細胞
en-keyword=細胞障害活性
kn-keyword=細胞障害活性
en-keyword=細胞障害因子
kn-keyword=細胞障害因子
en-keyword=腫瘍壊死因子
kn-keyword=腫瘍壊死因子
END

start-ver=1.4
cd-journal=joma
no-vol=100
cd-vols=
no-issue=5-6
article-no=
start-page=565
end-page=575
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1988
dt-pub=1988
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on the role of cell mediated immunity in the pathogenesis of intractable asthma -Evaluation of interleukin 2 production in response to Candida antigen-
kn-title=重症難治性喘息における�W型アレルギー反応に関する研究 第1編 カンジダ抗原による末梢血中及びBALF中リンパ球のinterleukin 2（IL-2）産生能の検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Candida antigen is known to be the major causative agent of adult bronchial asthma, especially intractable asthma. High responsiveness of lymphocytes in bronchoalveolar lavage fluid (BALF) to Candida antigen has been reported in patients with intractable asthma. Therefore, IL-2 production of peripheral blood (PB) lymphocytes and BALF lymphocytes in patients with various types of bronchial asthma was evaluated to clarify the role of cellular immunity against Candida antigen in the pathogenesis of intractable asthma. IL-2 production of PB lymphocytes in intractable asthma patients was higher than in non-intractable asthma patients and normal controls (p<0.01). Patients with intractable asthma receiving prednisolone at a dose of over 10mg/day showed lower IL-2 production by PB lymphocytes than patients receiving prednisolone at a dose of under 10mg/day. The direct suppressive effect of prednisolone was also evaluated in a vitro study, which revealed that the suppression of IL-2 production was dose dependent in the range of therapeutic concentrations. IL-2 production by BALF lymphocytes against Candida antigen was also studied, and it was shown that IL-2 production was higher in intractable asthma patients than in non-intractable asthma patients (p<0.01). IL-2 production correlated significantly (p<0.05) with lymphocyte blastogenic responses against Candida antigen in patients with intractable asthma.
en-copyright=
kn-copyright=

en-aut-name=MiyagawaHidefumi
en-aut-sei=Miyagawa
en-aut-mei=Hidefumi
kn-aut-name=宮川秀文
kn-aut-sei=宮川
kn-aut-mei=秀文
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=intractable asthma
kn-keyword=intractable asthma
en-keyword=Candida antigen
kn-keyword=Candida antigen
en-keyword=interleukin 2 production
kn-keyword=interleukin 2 production
END

start-ver=1.4
cd-journal=joma
no-vol=100
cd-vols=
no-issue=5-6
article-no=
start-page=483
end-page=494
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1988
dt-pub=1988
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Interleukin l(IL-1) and interleukin 2(IL-2) production in patients with chronic renal failure
kn-title=慢性腎不全患者におけるインターロイキン1（IL-1）及びインターロイキン2（IL-2）産生能
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The mechanism of immune deficiency in patients with chronic renal failure(CRF) was investigated by testing both the ability of monocytes to produce IL-1 and the ability of T cells to produce IL-2.IL-1 production by lipopolysaccharide(LPS)-stimulated monocytes from CRF patients was not less than that of healthy controls. In fact, some patients showed higher values than the normal range(mean±2SD of normal value).IL-2 production by phytohemagglutinin(PHA)-stimulated peripheral blood mononuclear cells(PBMC) from patients on hemodialysis was significantly greater than that of healthy controls and non-hemodialysis patients. To exclude the influence of monocytes, the ability of T cells to produce IL-2 was also examined. IL-2 production by PHA-stimulated T cells was also increased in patients on hemodialysis. There was no correlation between IL-2 production by PHA-stimulated T cells and IL-1 production by LPS-stimulated monocytes. These results indicated that the enhanced IL-2 production by T cells was independent of monocytes.The mean IL-1 activity produced by non-stimulated monocytes was less than lU/ml in all groups. IL-2 production by unstimulated T cells was not observed in any subject. Both the expression of the IL-2 receptor(IL-2R) and that of the transferrin receptor on PBMC were less than 2% at the time cultures were started, or after incubations without stimulation.Thus, the possibility that monocytes and T cells were preactivated could be excluded.There was a significant correlation between IL-2 responsiveness and IL-2R expression on PHA-stimulated PBMC. Both were significantly lower in non-hemodialysis patients than in healthy controls, and gradually improved with the continuation of hemodialysis. One of the causes of immune deficiency, particularly in patients with non-hemodialysis renal failure, might be decreased IL-2 responsiveness based on defective expression of IL-2R.
en-copyright=
kn-copyright=

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=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第三内科学教室
en-keyword=慢性腎不全
kn-keyword=慢性腎不全
en-keyword=IL-1産生能
kn-keyword=IL-1産生能
en-keyword=IL-2産生能／反応性
kn-keyword=IL-2産生能／反応性
en-keyword=IL-2受容体
kn-keyword=IL-2受容体
en-keyword=transferrin受容体
kn-keyword=transferrin受容体
END

start-ver=1.4
cd-journal=joma
no-vol=121
cd-vols=
no-issue=2
article-no=
start-page=85
end-page=90
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=20090803
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=CRTH2 plays an essential role in the pathophysiology of Cry j 1 -induced pollinosis in mice
kn-title=マウススギ花粉症モデルにおける CRTH2の役割
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NomiyaRie
en-aut-sei=Nomiya
en-aut-mei=Rie
kn-aut-name=野宮理恵
kn-aut-sei=野宮
kn-aut-mei=理恵
aut-affil-num=1
ORCID=

en-aut-name=OkanoMitsuhiro
en-aut-sei=Okano
en-aut-mei=Mitsuhiro
kn-aut-name=岡野光博
kn-aut-sei=岡野
kn-aut-mei=光博
aut-affil-num=2
ORCID=

en-aut-name=FujiwaraTazuko
en-aut-sei=Fujiwara
en-aut-mei=Tazuko
kn-aut-name=藤原田鶴子
kn-aut-sei=藤原
kn-aut-mei=田鶴子
aut-affil-num=3
ORCID=

en-aut-name=NishizakiKazunori
en-aut-sei=Nishizaki
en-aut-mei=Kazunori
kn-aut-name=西�ｱ和則
kn-aut-sei=西�ｱ
kn-aut-mei=和則
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　耳鼻咽喉・頭頸部外科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　耳鼻咽喉・頭頸部外科学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　耳鼻咽喉・頭頸部外科学

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　耳鼻咽喉・頭頸部外科学
en-keyword=スギ花粉症
kn-keyword=スギ花粉症
en-keyword=モデルマウス
kn-keyword=モデルマウス
en-keyword=プロスタグランジンD(2)
kn-keyword=プロスタグランジンD(2)
en-keyword=CRTH(2)
kn-keyword=CRTH(2)
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=5-6
article-no=
start-page=505
end-page=515
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=1991
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Zinc metabolism in the endotoxin-treated rats
kn-title=エンドトキシンが体内亜鉛代謝に及ぼす影響に関する実験的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The effect of endotoxin administration on zinc metabolism was studied in rats. In the endotoxin-treated rats, serum zinc concentration was significantly reduced as compared to saline-treated rats (control group). On the other hand, hepatic zinc concentration was significantly increased after endotoxin administration as compared to the control group. However, the zinc concentrations of the liver cell components showed slightly dissimilarity. In the mitochondria and cytsol, the concentration increased significantly after endotoxin administration as compared to the control group, whereas no change was observed in the microsomes. Furthermore, we have examined whether the increase of the zinc level in the cytosol of the liver is associated with zinc-binding protein metallothioneins (MTs) or not. MTs also increased significantly after endotoxin administration. Furthermore hepatic MTs were analyzed for MT isoforms. In the endotoxin-treated MT-II was the major Iso-MT. Judging from these results and some other published reports, the role of zinc metabolism in endotoxemia is proposed to be as follows. In endotoxemia the serum zinc concentration is reduced and as a result the production of superoxide by polymorphonuclear leukocytes is increased as zinc has an inhibitory effect on it. This free radical helps the host against the organism. On the other hand zinc accumulation in the liver following endotoxin administration increases the activity of the zinc binding-enzyme and also stabilizes the plasma membrane. MTs induced by endotoxin protect the host from the harmful effects of the free radical in the host by its scavenging action.
en-copyright=
kn-copyright=

en-aut-name=MatsumiMasaki
en-aut-sei=Matsumi
en-aut-mei=Masaki
kn-aut-name=松三昌樹
kn-aut-sei=松三
kn-aut-mei=昌樹
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部麻酔・蘇生学教室
en-keyword=エンドトキシン
kn-keyword=エンドトキシン
en-keyword=亜鉛
kn-keyword=亜鉛
en-keyword=メタロチオネイン
kn-keyword=メタロチオネイン
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=4
article-no=
start-page=399
end-page=409
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=1991
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on the lymphocyte function of bronchial asthma Part 2. Examination of Concanavalin A induced suppressor cell function in patients with bronchial asthma
kn-title=気管支喘息におけるリンパ球機能に関する研究 第2編 気管支喘息における suppressor cell 機能の検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cellular immunity in bronchial asthma has become essential for the regulation of various allergic reactions in the asthmatic attack. The function of peripheral blood lymphocytes of asthmatic patients was examined by the concanavalin A (Con A) induced suppressor cell assay. The suppressor activity of lymphocytes in mitogen-induced blastogenesis was shown to be decreased in patints with atopic and intractable asthma in comparison with the normal control. The suppressor activity in mite antigen induced lymphocyte blastogenesis was also decreased in patients with atopic asthma. Furthermore, the decrease of ConA induced suppressor activity correlated with the increase of serum IgE level in patients with atopic asthma. These findings indicate that the decreased suppressor cell activity is part of the mechanism of attack and may play an important role in the pathogensis of bronchial asthma.
en-copyright=
kn-copyright=

en-aut-name=TakadaSho
en-aut-sei=Takada
en-aut-mei=Sho
kn-aut-name=武田昌
kn-aut-sei=武田
kn-aut-mei=昌
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=気管支喘息
kn-keyword=気管支喘息
en-keyword=ConA induced suppressor cell assay
kn-keyword=ConA induced suppressor cell assay
en-keyword=Candida
kn-keyword=Candida
en-keyword=mite
kn-keyword=mite
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=5-6
article-no=
start-page=701
end-page=711
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=1992
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on the pathogenesis of interstitial pneumonia of collagen vascular diseases Part 2. Examination of interleukin 2 receptor in interstitial pneumonia of collagen vascular diseases
kn-title=膠原病肺の病態に関する研究　第2編　膠原病肺における血清中および気管支肺胞洗浄液中 soluble IL-2 receptor の検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Abnormality of cellular immunity has been reported in the pathogenesis of collagen vascular diseases (CVD). IL-2 and IL-2 receptors play important roles as immunological regulation in CVD. In this study, the soluble forms of IL-2 receptor (sIL-2R) and IL-2 receptor positive lymphocytes (CD25) were analyzed to evaluate the role of IL-2R in the pathogenesis of interstitial pneumonia (IP) of CVD such as RA, SLE, polymyositis/dermatomyositis (PM/DM), and PSS and idiopathic interstitial pneumonia (IIP) as a disease control. High levels of sIL-2R were found in sera of patients with IP of CVD. The level of soluble IL-2R in sera of RA without IP correlated with the disease activity of the joints, while the level of sIL-2R in sera of RA with IP was higher than in that of RA without IP. Soluble IL-2R in bronchoalveolar lavage fluind (BALF) was also measured and the level was higher in IP with CVD. There were fewer IL-2R positive lymphocytes in the peripheral blood of CVD with IP than in the normal controls or IIP cases, although the serum level of sIL-2R was higher in CVD with IP and IIP than in the normal controls. These findings indicate that actibve immunological activities involving IL-2/IL-2R/sIL-2R systems play an important role in the pathogenesis of IP of CVD.
en-copyright=
kn-copyright=

en-aut-name=YokotaSatoshi
en-aut-sei=Yokota
en-aut-mei=Satoshi
kn-aut-name=横田聡
kn-aut-sei=横田
kn-aut-mei=聡
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=collagen vascular disease
kn-keyword=collagen vascular disease
en-keyword=interstitial pneumonia
kn-keyword=interstitial pneumonia
en-keyword=bronchoalveolar lavage
kn-keyword=bronchoalveolar lavage
en-keyword=soluble IL-2 receptor
kn-keyword=soluble IL-2 receptor
en-keyword=IL-2 receptor positive lymphocyte
kn-keyword=IL-2 receptor positive lymphocyte
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=5-6
article-no=
start-page=625
end-page=637
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=1992
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Metallothionein gene expression in rat liver following intraperitonal endotoxin administration
kn-title=エンドトキシン投与ラットにおける肝内メタロチオネイン遺伝子発現に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To clarify the functions of hepatic metallothioneins (MTs) after the administration of endotoxin (lipopolysaccharide : LPS), we investigated the expression on MT genes in the bacterial endoxin-treated rat liver by Norhern blot hybridization and in situ hybridization methol with riboprobes synthesized from mouse cDNA of MT-�U chronologically. Northern blot analysis revealed a rapid increase in the amount of MT gene transcripts in the liver 3 hours after the administration of LPS, with a maximum at 6 to 12 hours followed by a gradual decrease. In the in situ hybridization method, MT genes are expressed in the liver lobule for 3 hours after the adiminstration of LPS, and hepatocellular damage was observed at 6 hours after the LPS administration initially and expanded most extensively at 18 hours. During this peripd, MT genes are expressed in intact tissue intensely and specifically. At 24 hours after the administration, transcripts of the MT gene were detected in intact hepatocytes around the shrinking necrotic area. These findings suggest that MTs protect the liver cells by scavenging the free radicals, which probably cause liver cell damage due to LPS administration, and that MTs provide the zinc ions necessary for stabilizing the cell membrane and to heal the liver cell damge.
en-copyright=
kn-copyright=

en-aut-name=TagaNaoyuki
en-aut-sei=Taga
en-aut-mei=Naoyuki
kn-aut-name=多賀直行
kn-aut-sei=多賀
kn-aut-mei=直行
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部麻酔・蘇生学教室
en-keyword=エンドトキンショック
kn-keyword=エンドトキンショック
en-keyword=メタロチオネイン
kn-keyword=メタロチオネイン
en-keyword=in situ hybridization
kn-keyword=in situ hybridization
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=9-10
article-no=
start-page=1097
end-page=1102
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=1991
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on alveolar macrophage function in interstitial lung disease Part 2. Abnormalities of alveolar macrophages in sarcoidosis and the correlations with clinical findings
kn-title=間質性肺疾患における肺胞マクロファージに関する研究　第2編　サルコイドーシスにおける肺胞マクロファージ活性と疾患活動性との比較について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Several abnormalities of alveolar macrophage function were found in patients with sarcoidosis, and such abnormalities reflected the recruitment of immature macrophages to the local sites. In this study, alveolar macrophage function was compared with the disease activity in patients with sarcoidosis. The alveolar macrophage phagocytic index correlated closely with the spleen index obtained by ultrasonography, but not with serum angiotensin converting enzyme levels, lung function tests, or the cell differentiations of bronchoalveolar lavage fluid. The patients who had a positive uptake of 67-gallium scintigram showed a higher phagocytic index and a higher percentage of CD15-positive alveolar macrophages than those with negative scintigrams. Acid phosphatase activity and the percentage of CD15-positive alveolar macrophages were increased in patients with negative PPD skin tests compared to those with positive tests. We previously reported that alveolar lymphocytes in patients with sacroidosis are sensitized to Propionibacterium acnes (P. acnes), which may play a significant role in the induction of alveolitis in these patients. There was a significant correlation between the blastogenesis of alveolar lymphocytes induced by P. acnes and beta-galactosidase activity as well as the percentage of CD14-positive alveolar macrophages. These findings suggest that alveolar macrophages play an important role in the pathogenesis of sarcoidosis, in which the clinical abnormalities may reflect abnormal alveolar macrophage function.
en-copyright=
kn-copyright=

en-aut-name=HosoyaShigee
en-aut-sei=Hosoya
en-aut-mei=Shigee
kn-aut-name=細谷茂衛
kn-aut-sei=細谷
kn-aut-mei=茂衛
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=alveolar macrophage
kn-keyword=alveolar macrophage
en-keyword=sarcoidosis
kn-keyword=sarcoidosis
en-keyword=Propionibacterium acnes
kn-keyword=Propionibacterium acnes
en-keyword=lymphocyte blastgenesis
kn-keyword=lymphocyte blastgenesis
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=9-10
article-no=
start-page=1089
end-page=1095
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=199110
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on alveolar macrophage function in interstitial lung disease Part 1. Abnormalities of alveolar macrophage functions
kn-title=間質性肺疾患における肺胞マクロファージに関する研究　第1編　肺胞マクロファージの機能，胞体内ライソゾーム酵素活性，膜表面抗原の検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Interstitial lung diseases comprise a heterogeneous group of disorders that are characterized by the chronic accumulation of inflammatory and immune effector cells within the alveoli, where they produce alveolitis, granulomas, or fibrosis. To investigate the pathogenesis of these diseases, the fucntions of alveolar macrophages recovered from bronchoalveolar lavage were evaluated in patients with interstitial lung disease in comparison to healthy controls. Thirty six patients were investigated : 18 with sarcoidosis, 6 with idiopathic interstitial pneumonia (IIP), 5 with interstitial pneumonia associated with collagen vascular disease (IP-CVD), and 7 with hypersensitivity pneumonitis (HP). Both the chemotactic and phagocytic indices were significantly higher in the patients with sarcoidosis, IIP, and HP than in the healthy subjects. However, the patients with IP-CVD had a lower phagocytic index than the normal subjects. Acid phosphatase activity was lower in patients with IIP, IP-CVD, and HP compared with the healthy subjects, while beta-galactosidase activity was lower in patients with sarcoidosis and IP-CVD compared with the normal controls. Analysis of surface markers showed that CD15-positive macrophages were increased in patients with sarcoidosis, IIP, and HP, but there were no differences in CD14- and HLA-DR-positive macrophages in these patients when compared to the healthy subjects. These findings indicate that the recruitment of peripheral blood monocytes to the lungs is increased in patients with sarcoidosis, IIP, and HP. Alveolar macrophages may play an important role in the pathogenesis of intersitial lung disease.
en-copyright=
kn-copyright=

en-aut-name=HosoyaShigee
en-aut-sei=Hosoya
en-aut-mei=Shigee
kn-aut-name=細谷茂衛
kn-aut-sei=細谷
kn-aut-mei=茂衛
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=alveolar macrophage
kn-keyword=alveolar macrophage
en-keyword=chemotaxis
kn-keyword=chemotaxis
en-keyword=phagocytosis
kn-keyword=phagocytosis
en-keyword=lysosomal enzyme
kn-keyword=lysosomal enzyme
en-keyword=intersitial lung disease
kn-keyword=intersitial lung disease
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=1-2
article-no=
start-page=117
end-page=127
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=1991
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Metallothionein gene expression in rat brain following intraperitoneal endotoxin administration
kn-title=エンドトキシンによるラット脳内メタロチオネイン遺伝子発現に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To clarify the acute-phase response in brain, we investigated the induction of metallothionein (MT) genes by administering an endotoxin (lipopolysaccharide) in rat intraperitoneum. We performed in situ hybridization on the serial brain sections to identify the cells expressing the MT genes in the acute-phase. After endotoxin administration, transcripts of MT genes were detected in the arachnoideal, ependymal cells and the Bergmann glia of the cerebellum, while no significant induction of the MT genes by zinc ion was observed in the brain. These results suggest that the acute-phase response occurs specifically in at least these three non-neuronal cells.
en-copyright=
kn-copyright=

en-aut-name=ItanoYoshitaro
en-aut-sei=Itano
en-aut-mei=Yoshitaro
kn-aut-name=板野義太郎
kn-aut-sei=板野
kn-aut-mei=義太郎
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部麻酔・蘇生学教室
en-keyword=メタロチオネイン
kn-keyword=メタロチオネイン
en-keyword=エンドトキシン
kn-keyword=エンドトキシン
en-keyword=脳
kn-keyword=脳
en-keyword=acute-phase
kn-keyword=acute-phase
en-keyword=in situ hybridization
kn-keyword=in situ hybridization
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=9-10
article-no=
start-page=1055
end-page=1063
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=1991
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Correlation between natural killer (NK) cell activity and graft-versus-host disease (GVHD) after small bowel transplantation of rat - especially for cutaneous GVHD -
kn-title=ラット小腸移植による Graft-Versus-Host Disease (GVHD) と Natural Killer (NK) 細胞活性の相関―特に cutaneous GVHD との関連について―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Using (LEW) parent to (LEW×WKA)F1 combination, heterotopic total small bowel transplantation was performed in rats. We divided this GVHD model into four groups (group 1 ; control, group 2 ; Cyclosporine A (CyA) 5mg/�s 0-2 pod, group 3 ; CyA 5mg/�s 0-6 pod, group 4 ; anti-ASGM1 antibody 50μ1 twice). All rats in group 1 developed cutaneous GVHD on 8 or 9 pod, and developed systemic GVHD and died within 19 pod (Mean Survival Times (MST)＝17.5±1.5). All rats in group 2 developed cutaneous GVHD on 11-14 pod and died in 20-25 pod due to systemic GVHD (MST＝22.7±1.6). However, 3 of the 7 rats in group 3 and none of those in group 4 developed cutaneous GVHD and survival times were elongated (MST≧107.6±106.9, 52.5±41.9). We also evaluated the cytotoxic activity of recipient spleen cells against three strains of rat skin cells (LEW, WKA, (LEW×WKA)F1) and K-562 cell line on 7 pod. In group 1 and 2, cytotoxic activity was augmented, compared with that in normal F1 rat, against all target cells. However, in group 3 and 4, cytotoxic activity was attenuated, compared with that in group 1 and 2, and lower than in normal F1 rat. We considered that this cytotoxic activity was due to MHC non-restricted NK cells, because there were no differences in any kind of target cells. We concluded that the NK cell might play a great role in GVHD, especially for skin lesions.
en-copyright=
kn-copyright=

en-aut-name=FujiokaMasahiro
en-aut-sei=Fujioka
en-aut-mei=Masahiro
kn-aut-name=藤岡正浩
kn-aut-sei=藤岡
kn-aut-mei=正浩
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第一外科学教室
en-keyword=小腸移植
kn-keyword=小腸移植
en-keyword=GVHD
kn-keyword=GVHD
en-keyword=NK 細胞
kn-keyword=NK 細胞
en-keyword=AsialoGM 1
kn-keyword=AsialoGM 1
en-keyword=Cyclosporine A
kn-keyword=Cyclosporine A
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=5-6
article-no=
start-page=457
end-page=469
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=1992
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Metallothionein induction in the rat kidneys by endotoxin and zinc administration
kn-title=エンドトキシンおよび亜鉛投与ラットにおける腎メタロチオネインの誘導に関する実験的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Metallothionein (MT) induction in the rat kidneys by endotoxin and zinc was investigated at the MT-protein level and the MT-mRNA level. The MT-mRNA level increased 3-6 hr after endotoxin administration, which suggested that MT was not transported from an other organ, but was de novo synthesized. Two MT-protein isoforms, MT-�T and MT-�U, were induced by administration of both endotoxin and zinc. The maximum levels of the proteins were seen 9 hr after administration of endotoxin and zinc. The span life of the renal MT induced by zinc was shorter than that of the liver MT induced by zinc. The MT-�U isoform was predominantly induced by both inducers, endotoxin and zinc, and the ratios of MT-�U to MT-�T were relatively constant. The finding that MT-�T and MT-�U were almost equally induced by zinc in the liver indicate that MT induction is controlled by an organ-specific system.
en-copyright=
kn-copyright=

en-aut-name=KanaiYoshizumi
en-aut-sei=Kanai
en-aut-mei=Yoshizumi
kn-aut-name=金居義純
kn-aut-sei=金居
kn-aut-mei=義純
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部麻酔・蘇生学教室
en-keyword=エンドトキシン
kn-keyword=エンドトキシン
en-keyword=亜鉛
kn-keyword=亜鉛
en-keyword=腎メタロチオネイン
kn-keyword=腎メタロチオネイン
en-keyword=高速液体クロマトグラフィー
kn-keyword=高速液体クロマトグラフィー
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=5-6
article-no=
start-page=425
end-page=431
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=1992
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Effect of splenectomy and immuno-potentiator on tumor-bearing mice
kn-title=担癌マウスにおける摘脾と免疫賦活剤の効果
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To determine the effect of splenectomy on tumor growth, the immunological role of the spleen was studied at various time intervals following subcutaneous implantation of MH-134 hepatoma cells into syngeneic C(3) H/He mice.
 Both tumor neutralizing activity and PHA-suppressor cell activity were generated. the former reached a maximum on the 28th day of implantation, and belonged to Lyt-1(+)2(-)T cells. The latter appeared on the 3rd day, decreased once, and increased again. Mainly, this suppres-sive activity was found in Lyt-1(+)2(-)T cells on the 3rd day and in nylon-wool-adherent cells after the 14th day. Splenectomy or sham splenectomy (sham ope) was performed on the 3rd day of implantation. There was no significant difference in tumor growth between the groups. Immunotherapy with lentinan effectively suppressed tumor grouth both in the tumor-bearing mice that had splenectomy and in those that had sham ope, with no significant difference in tumor growth between the two groups. Therefore, the effectiveness of splenectomy on tumor growth might be difficult to evaluate, since these opposite activities are simultaneously induced in the spleen of tumor-bearing mouse.
en-copyright=
kn-copyright=

en-aut-name=TakatsukaShojiro
en-aut-sei=Takatsuka
en-aut-mei=Shojiro
kn-aut-name=竹束正二郎
kn-aut-sei=竹束
kn-aut-mei=正二郎
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第一外科学教室
en-keyword=摘脾
kn-keyword=摘脾
en-keyword=中和活性
kn-keyword=中和活性
en-keyword=サプレッサー細胞活性
kn-keyword=サプレッサー細胞活性
en-keyword=Lyt-1(+)2(-)T 細胞
kn-keyword=Lyt-1(+)2(-)T 細胞
en-keyword=レンチナン
kn-keyword=レンチナン
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=3-4
article-no=
start-page=387
end-page=398
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=1992
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on transferrin receptor of macrophages in iron metabolism Part 2. Regulation of tranferrin receptors on alveolar macorophages in iron-overloaded and iron-deficient conditions
kn-title=鉄代謝におけるマクロファージのトランスフェリンレセプターに関する研究　第2編　鉄過剰及び鉄欠乏状態における肺胞マクロファージのトランスフェリンレセプターに関する検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Transferrin receptors (TfR) are involved in the first step of iron uptake into cells. To clarify the changes in TfR under various conditions, radiobinding assay of (125)I-labeled iron-saturated transferrin was performed in alveolar macrophages from 2 patients with idiopathic hemo-chromatosis and iron-overloaded or iron-deficient guinea pigs. Patients with idiopathic hemochromatosis showed a reduction in the Fe-TfR count on alveolar macrophages (5.0×10(4)/cell) as compared to that in healthy individuals (19.88±8.19×10(4)/cell). Concerning the Fe-TfR binding constant, no differnce was observed between patients with idiopathic hemochromatosis and healthy controls. The Fe-TfR count on alveolar macrophages was significantly lower in iron-overloaded guined pigs than in normal cntrols. The count was significantly elevated in iron-deficient guinea pigs. Concerning the Fe-TfR binding constant, none of the iron-overloaded and iron-deficient groups showed any significant difference from the normal controls. These findings suggest that experimentally-induced iron overload and iron deficiency may be autoregulated by intracellular iron levels.
en-copyright=
kn-copyright=

en-aut-name=InadaToshio
en-aut-sei=Inada
en-aut-mei=Toshio
kn-aut-name=稲田俊雄
kn-aut-sei=稲田
kn-aut-mei=俊雄
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=Transferrin receptor
kn-keyword=Transferrin receptor
en-keyword=Hemochromatotis
kn-keyword=Hemochromatotis
en-keyword=Iron overloaded
kn-keyword=Iron overloaded
en-keyword=Iron depleted Alveolar macrophage
kn-keyword=Iron depleted Alveolar macrophage
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=11-12
article-no=
start-page=1117
end-page=1125
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=199212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on the role of interferon gamma (IFN-γ) in the pathogenesis of bronchial asthma : Evaluation of IFN-γ production induced by Candida or mite antigen in comparison with other factors of lymphocytic function
kn-title=気管支喘息における interferon-γ (IFN-γ) 産生能に関する研究 第2編 気管支喘息における IFN-γ 産生能と各種リンパ球機能との比較検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=It is known that IFN-γ, T-cell lymphokine, has potent effects on immunoglobulin synthesis, leukotrienes synthesis and delayed-type hypersensitivity. These factors are thought to be closely related to allergic reactions in bronchial asthma. Therefore, IFN-γ production from peripheral blood mononuclear cells induced by Candida or mite antigen was examined in asthmatics, and relations with other lymphocytic functions were studied to eluciate the role of IFN-γ. The results were as follows : (1) There was a significant correlation between IFN-γ production and Candida specific serum IgG1 antibody. (2) There was a significant correlation between IFN-γ production and lymphocyte blastgenesis induced by Candida antigen. (3) High levels of IFN-γ production were observed in asthmatics with positive late phase or delayed phase skin reaction to Candida antigen compared to asthmatics with negative late phase or delayed phase skin reaction. (4) Asthmatics with positive Candida or mite specific IgE radioallergosorbent test(RAST) showed a low level of IFN-γ production compared to asthmatics with negative IgE RAST. These results indicate that asthmatics with low IgE antibody and activated lymphocytes show high levels of IFN-γ production, and in these low IgE asthmatics, IFN-γ may play an important role in the allergic reactions of bronchial asthma.
en-copyright=
kn-copyright=

en-aut-name=KimuraGoro
en-aut-sei=Kimura
en-aut-mei=Goro
kn-aut-name=木村五郎
kn-aut-sei=木村
kn-aut-mei=五郎
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=bronchial asthma
kn-keyword=bronchial asthma
en-keyword=delayed-type hypersensitivity
kn-keyword=delayed-type hypersensitivity
en-keyword=IFN-γ
kn-keyword=IFN-γ
en-keyword=IgE antibody
kn-keyword=IgE antibody
en-keyword=IgG1 antibody
kn-keyword=IgG1 antibody
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=11-12
article-no=
start-page=1107
end-page=1116
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=199212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on the role of interferon gamma (IFN-γ) in the pathogenesis of bronchial asthma : Evaluation of IFN-γ production induced by Candida or mite antigen in clinical types of bronchial asthma
kn-title=気管支喘息における interferon-γ (IFN-γ) 産生能に関する研究 第1編 気管支喘息の各種病態における IFN-γ 産生能の検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=It is known that IFN-γ, T-cell lymphokine, suppresses IgE synthesis and enhances leukotrienes synthesis, and plays an important role in the allergic reactions of a bronchial asthma attack. It is reported that IFN-γ production from peripheral blood mononuclear cells(PBMC) induced by phytohemagglutinin was decreased in atopic subjects compared with normal subjects. In fact, some bronchial asthmatics do not have atopic features, and sometimes they display severe symptoms. Therefore, IFN-γ production from PBMC induced by Candida or mite antigen was studied in bronchal asthmatics. The results were as follows : (1) There was no significant difference in IFN-γ production between asthmatics and normal subjects. Among asthmatics, non-atopic asthmatics showed higher levels of IFN-γ production compared with atopic asthmatics. (2) Severe asthmatics showed high levels of IFN-γ production compared with mild and moderate asthmatics and normal subjects in Candida antigen stimulation. (3) High levels of IFN-γ production was observed in asthmatics with late asthmatic response to Candida antigen inhalation compared to asthmatics with no airway response and healthy controls. These results indicate that IFN-γ plays an important role in non-atopic and severe asthma attack and late asthmatic response to Candida antigen inhalation.
en-copyright=
kn-copyright=

en-aut-name=KimuraGoro
en-aut-sei=Kimura
en-aut-mei=Goro
kn-aut-name=木村五郎
kn-aut-sei=木村
kn-aut-mei=五郎
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=IFN-γ
kn-keyword=IFN-γ
en-keyword=bronchial asthma
kn-keyword=bronchial asthma
en-keyword=T-cell
kn-keyword=T-cell
en-keyword=Candida
kn-keyword=Candida
en-keyword=mite
kn-keyword=mite
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=3-4
article-no=
start-page=241
end-page=246
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=1992
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The effect of cyclosporin A on liver regeneration
kn-title=肝再生に及ぼす Cyclosporin A の影響
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=When lymphokine activiated killer cells (LAK cell) induced by IL-2 are infused into the same strain C(3)H mice following 70% partial hepatectomy, they display an action to suppress liver regeneration. Therefore, when Cyclosporin A (CsA) which inhibits IL-2 production was administerd to mice following partial hepatectomy, we studied as our indicator the labeling index of hepatic parenchyma cells using Brdu. Our findings showed that proliferation of live cells at 36 hours following partial hepatectomy was promoted by CsA, and the streongest promotion occuring at a dose of 5mg/kg. Before anf after hepatectomy when CsA was administered at 10mg/kg for 3 dadys, a further strong proliferation increasing effect was observed, and under these conditions at 48 and 60 hours after hepatectomy a significant increase in liver weight was observed. Give the above results, CsA  it thought to have a promoting effect in liver regeneration following hepatectomy.
en-copyright=
kn-copyright=

en-aut-name=YamamotoHiroshi
en-aut-sei=Yamamoto
en-aut-mei=Hiroshi
kn-aut-name=山本浩史
kn-aut-sei=山本
kn-aut-mei=浩史
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第一外科学教室
en-keyword=Cyclosporin A
kn-keyword=Cyclosporin A
en-keyword=肝再生
kn-keyword=肝再生
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=1-2
article-no=
start-page=129
end-page=136
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=1992
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on pulmonary granuloma formation by Propionibacterium acnes in sarcoidosis Part 2. Interleukin-2 production and responsiveness to Interleukin-2 of alveolar lymphocytes stimulated in experimental pulmonary granulomatosis produced by Propionibacterium acnes
kn-title=サルコイドーシスの肺肉芽腫形成に対する Propionibacterium acens の関与に関する研究　第2編　Propionibacterium acens による実験的肺肉芽腫症における肺胞リンパ球の Interleukin-2 産生及び Interleukin-2　受容体発現のついて
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The role of Propionibacterium acnes (P. acnes) isolated from a high percentage of patients with sarcoidosis by Dr. Honnma, as a cause of sarcoidosis was examined. Interleukin-2 (IL-2) production and the responsiveness to IL-2 of alveolar lymphocytes stimulated by P. acnes were examined in vitro in a guinea pig model. The animals were divided into 4 groups, normal guinea pigs (group 1), guinea pigs intracutaneously presensitized with P. acnes and intratracheally challenged by saline (group 2), guinea pigs presensitized as above and intratracheally challenged with P. acnes (group 3), and guinea pigs presensitized as above and intratracheally challenged by P. acnes-pyridine extract residue (P. acnes-PER)(group 4). The production of IL-2 by alveolar lymphocytes stimulated by P. acnes-PER for 48 hours was determined using the method described by Gillis et al. The responsiveness of alveoloar lymphocytes to IL-2 was evaluated by 3H-TdR uptake in the presence and absence of P. acnes-PER. The amount of IL-2 produced by alveolar lymphocytes was 0.6±1.1, 0.7±1.1, 21.2±27.9 and 329.4±294.1 u/ml (M±SD), respectively, in groups 1, 2, 3 and 4. The value of IL-2 production in groups 3 and 4, the intratracheally challenged groups, was significantly higher htna that in groups 1 and 2, the control groups (p<0.02, p<0.01). By contrast, the IL-2 production of peripheral lymphocytes in groups 1, 2, 3 and 4 was 0, 7.4±10.3, 8.6±15.7 and 9.3±8.9 u/ml, respectively. The amount of IL-2 produced was about one-tenth thar of alveolar lymphocytes. In the intratracheally challenged groups, the responsiveness to IL-2 of alveolar lymphocytes in the presence and absence of P. acnes-PER was 12,514±12,766 and 6,611±7,066 for group 3, and 12,362±9,414 and 5,818±5,494 dpm, respectively, for group 4. The responsiveness to IL-2 of alveolar lymphoctyes in group 4 was signifincantly increased by stimulation with P. acnes-PER (p<0.05), but that in groups 1 and 2, control groups, was not different. Our findings indicate that P. acnes-PER stimulated IL-2 production from alveolar lymphocytes and induced a functionally active state of alveolar lymphocytes to IL-2 in this guinea pig model. In conclusion, the role of alveolar lymphocytes in an animal model stimulated by P. acnes appears to be consistent with that obtained on the sarcoidosis patients we previously reported.
en-copyright=
kn-copyright=

en-aut-name=MoriYoshihiro
en-aut-sei=Mori
en-aut-mei=Yoshihiro
kn-aut-name=森由弘
kn-aut-sei=森
kn-aut-mei=由弘
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=experimental pulmonary granulomatosis
kn-keyword=experimental pulmonary granulomatosis
en-keyword=guinea pig
kn-keyword=guinea pig
en-keyword=Propionibacterium acens
kn-keyword=Propionibacterium acens
en-keyword=Interleukin-2
kn-keyword=Interleukin-2
en-keyword=Interleukin-2 receptor
kn-keyword=Interleukin-2 receptor
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=1-2
article-no=
start-page=117
end-page=127
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=1992
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on pulmonary granuloma formation by Propionibacterium acnes in sarcoidosis Part 1. Interleukin-2 production and receptor expression of alveolar lymphocytes stimulated by Propionibacterium acnes in sarcoidosis
kn-title=サルコイドーシスの肺肉芽腫形成に対する Propionibacterium acens の関与に関する研究　第1編　サルコイドーシス肺胞リンパ球のPropionibacterium acens に対する Interleukin-2 産生及び Interleukin-2　受容体発現のついて
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We previously reported that alveolar lymophocytes in patients with active sarcoidosis are sensitized Propionibacterium acnes (P. acnes) which may play a significant role in the induction of alveolitis in these patients. We further investigated the production of Interleukin-2 (IL-2), and the responsiveness to IL-2 of alveolar lymphocytes obtained from sarcoidosis patients and stimulated by P. acnes in vitro. In 21 untreated  sarcoidosis patients, 7 treated patients and 13 control subjects, the mean IL-2 activity of fluid released from cultured alveoloar lymphocytes was 9.8±15.7 (M±SD), 1.9±4.7 and 0.2±0.8 u/ml respectively. The IL-2 activity of lymphocytes from untreated patients was significantly higher than that of control subjects (p<0.02). Neither perioheral lymphocytes in sarcoidosis patients nor in controls produced IL-2 stimulated by P. acnes. The responsiveness of alveloar lymphocytes to recombinant IL-2 was evaluated by 3H-thymidine uptake in the presence and absence of P. acnes. Lymphocytes stimulated by P. acnes showed a significantly increased uptake (3,766±3,929 dpm) compred to ustimulated lymphocytes (1,123±968 dpm) obtained from 11 untreated sarcoidosis patients (p<0.02). On the other hand, the responsiveness of lymphocytes obtained from 6 control subjects was low regardless of stimulation by P. acnes. There was a significant correlation (p<0.05) between the P. acnes-induced production of IL-2 by alveolar lymphocytes and the blastogenesis of alveloar lymphocytes in untreated sarcoidosis patietnes. Our findings indicate that P. acnes stimulated IL-2 production and IL-2 receptor induction in alveolar lymphocytes from patients with active sarcoidosis. This study supported our hypothesis that P. acnes could be an antigen causing sarcoidosis.
en-copyright=
kn-copyright=

en-aut-name=MoriYoshihiro
en-aut-sei=Mori
en-aut-mei=Yoshihiro
kn-aut-name=森由弘
kn-aut-sei=森
kn-aut-mei=由弘
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=sarcoidosis
kn-keyword=sarcoidosis
en-keyword=Propionibacterium acens
kn-keyword=Propionibacterium acens
en-keyword=Interleukin-2
kn-keyword=Interleukin-2
en-keyword=Interleukin-2 receptor
kn-keyword=Interleukin-2 receptor
en-keyword=alveolar lymphocyte
kn-keyword=alveolar lymphocyte
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=7-8
article-no=
start-page=863
end-page=870
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=199208
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on the mechanism of initial attack in intractable asthma Part 2. Lymphocyte subpopulations of asthmatics analyzed by two-color flow cytometry
kn-title=難治性喘息の発症に関する研究 第2編 フローサイトメトリーによる喘息患者抹梢血のリンパ球サブセット･表面抗原の検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To elucidate the role of lymphocytes in asthmatics, lymphocyte subpopulations were analyzed using monoclonal antibodies (CD2, CD3, CD4, CD8, CD16, CD19, CD25, and HLA-DR, all from Leu series) and flow cytometry (FACScan, Beckton-Dickinson). Blood samples were obtained when there was no attack unless otherwise stated. Patients were defined as intractable when they had been taking more than 5 mg of prednisolone for at least one year. (1) Non-intractable asthmatics had greater ％ of CD16＋NK cells as compared with agematched normal subjects. (2) No differences were observed between RAST or intradermal test-positive and negative patients, although the former had significantly higher serum IgE levels than the latter. (3) Intractable asthmatics showed an increased proportion of IL−2R＋lymphocytes as compared with normal subjects. (4) Patients on attack also had a higher ％ of IL−2R＋lymphocytes than patients without attack. These findings suggest that NK cells play an important role in bronchial asthma, and that activeted lymphocytes are involved in the pathogenesis of intractable asthma and asthmatic attack.
en-copyright=
kn-copyright=

en-aut-name=TakataMinoru
en-aut-sei=Takata
en-aut-mei=Minoru
kn-aut-name=高田穣
kn-aut-sei=高田
kn-aut-mei=穣
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=intractable asthma
kn-keyword=intractable asthma
en-keyword=lymphocyte subpopulation
kn-keyword=lymphocyte subpopulation
en-keyword=flow cytometry
kn-keyword=flow cytometry
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=7-8
article-no=
start-page=843
end-page=852
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=199208
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Analysis of suppressor T cells induced in long-term human allogeneic mixed lymphocyte culture
kn-title=長期リンパ球混合培養で誘導される抑制性T細胞の免疫学的解析
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Suppressor T cells (Ts) may play an important role in the regulation of immunological responses. Ts may play a role in the long-term acceptance of an allogeneic organ graft and the beneficial effects of donor-specific blood transfusions on subsequent transplant survival. The population of Ts induced in mixed lymphocyte culture (MLC) was analyzed, and the mechanism underlying the suppressor activity was examined. The Ts generated in 10-day MLC were found to belong to the OKT8(+) subset and inhibited both mixed lymphocyte reaction (MLR) and cell-mediated lympholysis. These Ts inhibited MLR in an antigen-specific manner, but failed to alter the kinetics of the MLR. Furthermore, these Ts inhibited the production of endogenous interleukin-2 and exerted a suppressive effect only when added early in the culture. In condition, the precise target of Ts generated in 10-day MLC might be the earliest responding T helper clone.
en-copyright=
kn-copyright=

en-aut-name=TsuboiKatsutoshi
en-aut-sei=Tsuboi
en-aut-mei=Katsutoshi
kn-aut-name=壺井克敏
kn-aut-sei=壺井
kn-aut-mei=克敏
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第一外科学教室
en-keyword=抑制性T細胞
kn-keyword=抑制性T細胞
en-keyword=リンパ球混合培養
kn-keyword=リンパ球混合培養
en-keyword=mixed lymphocyte reaction
kn-keyword=mixed lymphocyte reaction
en-keyword=cell-mediated lympholysis
kn-keyword=cell-mediated lympholysis
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=7-8
article-no=
start-page=797
end-page=807
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=199208
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on IgG subclass antibodies in asthmatics with late asthmatic responses Part 1. Serum antigen-specific IgG subclass antibodies in asthmatics with late asthmatic response
kn-title=遅発型気道反応におけるIgG サブクラス抗体に関する研究　第1編　血清中抗原特異的 IgG サブクラス抗体と遅発型気道反応の関連について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The immediate asthmatic response is mainly induced by IgE-dependent mechanisms. However, the late asthmatic response (LAR) is induced by inhalation of antigens without the participation of antigen-specific IgE antibodies in some asthmatics, especially in intractable asthma induced by Candida antigen. To elucidate the relationship between antibodies and those bronchial responses, the antigen-specific IgG subclass antibodies in sera from asthmatics were measureed and compared with IgE antibody. The avidin-biotin ELISA (enzyme-linked immunosorbent assay) method was established for the measurement of specific IgG and IgG subclass antibodies to mite or Candida antigen. Serum levels of IgG and IgG1 antibodies to mite and Candida antigen in bronchial asthmatics were significantly higher than those in healthy subjects (p<0.01). Bronchial asthmatics who were tested with inhalation of house dust or Candida antigen were divided into group A (higher levels of serum IgG1 antibody) and group B (lower levels of serum IgG1 antibody). The percentage of LAR including DAR after inhalation of house dust antigen in group A were significantly higher than those in group B (p<0.01). The percentages of LAR and LAR including DAR after inhalation of Candida antigen in group A were significantly higherSerum levels of house du than those in group B(p<0.01). Serum levels of antigen-specific IgG and IgG1 antibodies in asthmatics with LAR after inhalation of house dust or Candida antigen were significantly higher than those in asthmatics with IAR or non-responders (p<0.01). The serum level of specific IgE antibody to these antigens in asthmatics with LAR after inhalation of house dust or Candida antigen was slightly lower than that in the asthmatics without LAR, though the difference was not significant. These findings suggest that high serum levels of specific IgG and IgG1 antibodies to adequate antigens play a role in inducing an attack in asthmatics with LAR.
en-copyright=
kn-copyright=

en-aut-name=OgurusuKazuro
en-aut-sei=Ogurusu
en-aut-mei=Kazuro
kn-aut-name=小栗栖和郎
kn-aut-sei=小栗栖
kn-aut-mei=和郎
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=遅発型気道反応
kn-keyword=遅発型気道反応
en-keyword=IｇG サブクラス抗体
kn-keyword=IｇG サブクラス抗体
en-keyword=IgE 抗体
kn-keyword=IgE 抗体
en-keyword=抗原吸入誘発試験
kn-keyword=抗原吸入誘発試験
en-keyword=難治性喘息
kn-keyword=難治性喘息
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=7-8
article-no=
start-page=791
end-page=801
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=199108
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on the regulation of eosinophils in bronchial asthma Part 2. Migratory responses of eosinophils from asthmatics
kn-title=気管支喘息における好酸球動態の調節に関する研究　第2編　喘息患者末梢血好酸球の遊走能に関する検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Eosinophil infiltration in lung tissue is one of the characteristic features of bronchial asthma. Such cell infiltration seems to be induced by the eosinophil chemotactic factor (ECF). PAF and IL-5 are potent chemoattractants and activators for eosinophils. To evaluate the reactivity of eosinophils in asthmatics under various conditions, the migratory function of eosinophils to PAF and IL-5 was investigated by the modified Boyden chamber method. Eosinophils of asthmatics were highly purified using a flow cytometric method previously reported. The migratory response of the eosinophils of asthmatics was greater than that of healthy suljects. Eosinophils from atopic asthmatics showed a higher response to PAF than those from non-atopic asthmatics. Eosinophils in the attack stage showed a higher response than those in the non-attack stage. Hypodense eosinophils showed an increased migratory response. The migratory response was correlated to the serum concentration of ECP and blood eosinophil count. These findings suggest that the reactivity of eosinophils is heterogenous and relates to the degree of eosinophilia, and that IL-5 as well as PAF plays an important role in the pathogenesis of bronchial asthma.
en-copyright=
kn-copyright=

en-aut-name=TakahashiHisaho
en-aut-sei=Takahashi
en-aut-mei=Hisaho
kn-aut-name=高橋寿保
kn-aut-sei=高橋
kn-aut-mei=寿保
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=Bronchial asthma
kn-keyword=Bronchial asthma
en-keyword=Eosinophil migratory response
kn-keyword=Eosinophil migratory response
en-keyword=Platelet-activating factor
kn-keyword=Platelet-activating factor
en-keyword=Interleukin-5
kn-keyword=Interleukin-5
en-keyword=Eosinophil heterogeneity
kn-keyword=Eosinophil heterogeneity
END

start-ver=1.4
cd-journal=joma
no-vol=106
cd-vols=
no-issue=5-6
article-no=
start-page=641
end-page=654
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1994
dt-pub=1994
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The pathogenesis of interstitial pneumonia and the role of cytokines
kn-title=間質性肺疾患の病態に関する研究―気管支肺胞洗浄液中サイトカインの検討―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Various cytokines are known to participate in the pathogenesis of interstitial pneumonia follewed by lung fibrosis due to the proliferation of fibroblasts and production of collagen fibers. Patients with interstitial pneumonia including idiopathic interstitial pneumonia (IIP) and interstitial pneumonia with collagen vascular disease (IP with CVD) were examined by bronchoalveolar lavage (BAL). Cytokines such as IL-1α,　TGF-α, and TGF-β in BAL fluid were measured by enzyme linked immunosorbent assay (ELISA). The concentrations of TGF-α and TGF-β in BAL fluid of patients with IIP and IP with CVD were higher than those of normal control, while IL-1α, in BAL fluid was detected in few patoents. The level of TGF-β in BAL fluid was higher in patients with greater decreases in pulmonary function and overt fibrosis on chest X-ray film, although TGF-α was higher in patients with milder disorders. The concentrations of TGF-α and TGF-β showed positive correlation with soluble IL-2 receptor as well as procollagen type �V in BAL fluid. These results indicated that cytokines regulationg lung fibrosis play important roles in the pathogenesis of interstitial pneumonia.
en-copyright=
kn-copyright=

en-aut-name=SugimotoKeisuke
en-aut-sei=Sugimoto
en-aut-mei=Keisuke
kn-aut-name=杉本啓介
kn-aut-sei=杉本
kn-aut-mei=啓介
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第二内科学教室
en-keyword=間質性肺疾患
kn-keyword=間質性肺疾患
en-keyword=気管支肺胞洗浄法 (broncho alveolar lavage : BAL)
kn-keyword=気管支肺胞洗浄法 (broncho alveolar lavage : BAL)
en-keyword=Interleukin 1 (IL-1)
kn-keyword=Interleukin 1 (IL-1)
en-keyword=transforming growth factor α
kn-keyword=transforming growth factor α
en-keyword=transforming growth factor β
kn-keyword=transforming growth factor β
END