start-ver=1.4
cd-journal=joma
no-vol=69
cd-vols=
no-issue=1
article-no=
start-page=17
end-page=27
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=201502
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Assessment of Melanoma-Initiating Cell Markers and Conventional Parameters in Sentinel Lymph Nodes of Malignant Melanoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sentinel lymph node (SLN) biopsies have widely been used for the detection of occult LN metastasis of malignant melanoma (MM). In addition to conventional biomarkers, we assessed the diagnostic and prognostic significance of melanoma-initiating cell (MIC) markers in SLNs of MM. We examined the expressions of gp100, MART-1 and tyrosinase mRNA for routine diagnosis and those of ABCB5, CD133, nestin, KDM5B, NGFR and RANK mRNA as MIC markers. The presence of micrometastasis was confirmed immunohistochemically using antibodies to S-100, HMB-45, MART-1, and tyrosinase. Discordance between immunohistochemical and molecular data was observed in 14 of 70 (20.0%) patients, among whom five (7.1%) were positive for only molecular markers;two of these five patients tested positive for micrometastasis by repeated immunohistochemical stainings. The quantitative expression levels of gp100, MART-1, and tyrosinase mRNA were significantly higher in the metastatic LNs;the cut-off values remain to be elucidated. ABCB5 mRNA expression was detected more frequently in the metastatic SLNs (p＜0.05) and in the group of patients with recurrence. To make a definite diagnosis of metastasis, we still need a combination of immunohistochemical and molecular probes. ABCB5 might be a suitable molecular marker for the detection of melanoma-initiating cells in SLNs.
en-copyright=
kn-copyright=

en-aut-name=SuzukiNorihiro
en-aut-sei=Suzuki
en-aut-mei=Norihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakataMinoru
en-aut-sei=Takata
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShirafujiYoshinori
en-aut-sei=Shirafuji
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OtsukaMasaki
en-aut-sei=Otsuka
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamasakiOsamu
en-aut-sei=Yamasaki
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AsagoeKenji
en-aut-sei=Asagoe
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HattaNaohito
en-aut-sei=Hatta
en-aut-mei=Naohito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

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

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

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

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

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

affil-num=6
en-affil=
kn-affil=Department of Dermatology, Okayama Medical Center

affil-num=7
en-affil=
kn-affil=Department of Dermatology, Toyama Prefectural Central Hospital

affil-num=8
en-affil=
kn-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=melanoma
kn-keyword=melanoma
en-keyword=cancer-initiating cell
kn-keyword=cancer-initiating cell
en-keyword=sentinel lymph node
kn-keyword=sentinel lymph node
en-keyword=ABCB5
kn-keyword=ABCB5
END

start-ver=1.4
cd-journal=joma
no-vol=44
cd-vols=
no-issue=4
article-no=
start-page=449
end-page=454
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2017
dt-pub=201704
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Usefulness of serum 5-S-cysteinyl-dopa as a biomarker for predicting prognosis and detecting relapse in patients with advanced stage malignant melanoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= With the recent development of novel molecular targeted drugs for advanced stage malignant melanoma (MM), including RAF and mitogen-activated protein kinase kinase inhibitors and immune checkpoint blockers, the early detection of relapse is important for managing patients with MM. In this study, we retrospectively analyzed two conventional serum biomarkers, 5-S-cysteinyl-dopa and lactate dehydrogenase, in patients with MM (n = 140) who were treated at a single Japanese institute from June 2007 to June 2015. At the initial hospital visit, serum 5-S-cysteinyl-dopa levels were significantly increased in patients with stages III (n = 38) and IV (n = 20) MM compared with patients with stages 0-II (n = 62) MM. In addition, in patients with stages III and IV MM, serum 5-S-cysteinyl-dopa levels of more than 15.0 nmol/L at initial hospital visit correlated with a poor prognosis. In 11 of 14 patients whose disease progressed during follow up (mostly from stages III-IV), serum 5-S-cysteinyl-dopa levels exceeded the normal limit of 10.0 nmol/L during the clinical detection of distant metastases. These results indicate the usefulness of measuring serum 5-S-cysteinyl-dopa levels at initial hospital visit and during follow up for early and effective therapeutic interventions using newly developed molecular targeted drugs.
en-copyright=
kn-copyright=

en-aut-name=HiroshiUmemura
en-aut-sei=Hiroshi
en-aut-mei=Umemura
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamasakiOsamu
en-aut-sei=Yamasaki
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KajiTatsuya
en-aut-sei=Kaji
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OtsukaMasaki
en-aut-sei=Otsuka
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AsagoeKenji
en-aut-sei=Asagoe
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakataMinoru
en-aut-sei=Takata
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=

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

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

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

affil-num=4
en-affil=Division of Dermatology, Shizuoka Cancer Center Hospital
kn-affil=

affil-num=5
en-affil=Department of Dermatology, National Hospital Organization Okayama Medical Center
kn-affil=

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

affil-num=7
en-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=5-S-cysteinyl-dopa
kn-keyword=5-S-cysteinyl-dopa
en-keyword=biomarker
kn-keyword=biomarker
en-keyword=lactate dehydrogenase
kn-keyword=lactate dehydrogenase
en-keyword=malignant melanoma
kn-keyword=malignant melanoma
en-keyword=serum 5-S-CD
kn-keyword=serum 5-S-CD
END

start-ver=1.4
cd-journal=joma
no-vol=167
cd-vols=
no-issue=2
article-no=
start-page=252
end-page=261
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=201208
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Detection of antibodies against the non-calcium-dependent epitopes of desmoglein 3 in pemphigus vulgaris and their pathogenic significance
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Antidesmoglein (anti-Dsg) 3 serum antibody titres are usually correlated with the disease activity of pemphigus vulgaris (PV), but some patients retain high titres even in remission. 

Objectives The aim of our study was to determine whether anti-Dsg3 antibodies in PV sera recognized calcium (Ca2+)-dependent or non-Ca2+-dependent epitopes, and to evaluate their pathogenicity. 

Methods Dsg3 baculoprotein-coated enzyme-linked immunosorbent assay (ELISA) plates were treated with 0.5 mmol L-1 ethylenediaminetetraacetic acid (EDTA). The binding ability of anti-Dsg3 monoclonal antibodies (mAbs) was analysed. Eight of the 83 patients with PV who were screened had elevated Dsg3 ELISA index values > 100 in remission. The binding ability of these PV sera was analysed. We evaluated the pathogenicity of anti-Dsg3 serum antibodies against the non-Ca2+-dependent epitopes using a dissociation assay. 

Results The reactivity of pathogenic anti-Dsg3 mAbs against the Ca2+-dependent epitopes diminished markedly in the EDTA-treated ELISA, whereas no such reduction was observed in mAbs against the non-Ca2+-dependent epitopes. The sera of all the patients contained antibodies against both Ca2+-dependent and non-Ca2+-dependent epitopes. In six out of the eight patients, the ratio of antibodies against Ca2+-dependent to non-Ca2+-dependent epitopes decreased in remission. EDTA-treated Dsg3 baculoproteins adsorbed anti-Dsg3 serum antibodies against the non-Ca2+-dependent epitopes, but the remnant PV antibodies retained the ability to induce acantholysis in the dissociation assay. 

Conclusions We have established an assay to measure indirectly the titres of anti-Dsg3 serum antibodies against the Ca2+-dependent epitopes, based on the differences between EDTA-untreated and EDTA-treated ELISA index values, as a routine laboratory test to reflect the pathogenic anti-Dsg3 serum antibody titres more accurately.
en-copyright=
kn-copyright=

en-aut-name=KamiyaK
en-aut-sei=Kamiya
en-aut-mei=K
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AoyamaY
en-aut-sei=Aoyama
en-aut-mei=Y
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShirafujiY
en-aut-sei=Shirafuji
en-aut-mei=Y
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HamadaT
en-aut-sei=Hamada
en-aut-mei=T
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MorizaneS
en-aut-sei=Morizane
en-aut-mei=S
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FujiiK
en-aut-sei=Fujii
en-aut-mei=K
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HisataK
en-aut-sei=Hisata
en-aut-mei=K
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IwatsukiK
en-aut-sei=Iwatsuki
en-aut-mei=K
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

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

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

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

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

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

start-ver=1.4
cd-journal=joma
no-vol=122
cd-vols=
no-issue=2
article-no=
start-page=147
end-page=149
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20100802
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Cooperative Network for Intractable Skin Diseases in Okayama
kn-title=岡山皮膚難病支援ネットワーク
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=IwatsukiKeiji
en-aut-sei=Iwatsuki
en-aut-mei=Keiji
kn-aut-name=岩月啓氏
kn-aut-sei=岩月
kn-aut-mei=啓氏
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学病院　皮膚科
en-keyword=天疱瘡
kn-keyword=天疱瘡
en-keyword=表皮水疱症
kn-keyword=表皮水疱症
en-keyword=膿疱性乾癬
kn-keyword=膿疱性乾癬
en-keyword=魚鱗癬様紅皮症
kn-keyword=魚鱗癬様紅皮症
en-keyword=色素性乾皮症
kn-keyword=色素性乾皮症
END

start-ver=1.4
cd-journal=joma
no-vol=122
cd-vols=
no-issue=2
article-no=
start-page=135
end-page=137
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20100802
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Foreword
kn-title=緒言
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=IwatsukiKeiji
en-aut-sei=Iwatsuki
en-aut-mei=Keiji
kn-aut-name=岩月啓氏
kn-aut-sei=岩月
kn-aut-mei=啓氏
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学病院　皮膚科
END

start-ver=1.4
cd-journal=joma
no-vol=125
cd-vols=
no-issue=3
article-no=
start-page=217
end-page=220
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20131202
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Th2 cytokines increase kallikrein 7 expression and function in patients with atopic dermatitis
kn-title=Th２サイトカインはアトピー性皮膚炎患者における カリクレイン７の発現と機能を増強する
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MorizaneShin
en-aut-sei=Morizane
en-aut-mei=Shin
kn-aut-name=森実真
kn-aut-sei=森実
kn-aut-mei=真
aut-affil-num=1
ORCID=

en-aut-name=YamasakiKenshi
en-aut-sei=Yamasaki
en-aut-mei=Kenshi
kn-aut-name=山崎研志
kn-aut-sei=山崎
kn-aut-mei=研志
aut-affil-num=2
ORCID=

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=3
ORCID=

en-aut-name=IkedaKazuko
en-aut-sei=Ikeda
en-aut-mei=Kazuko
kn-aut-name=池田佳寿子
kn-aut-sei=池田
kn-aut-mei=佳寿子
aut-affil-num=4
ORCID=

en-aut-name=ZhanMaosheng
en-aut-sei=Zhan
en-aut-mei=Maosheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AoyamaYumi
en-aut-sei=Aoyama
en-aut-mei=Yumi
kn-aut-name=青山裕美
kn-aut-sei=青山
kn-aut-mei=裕美
aut-affil-num=6
ORCID=

en-aut-name=Richard L Gallo
en-aut-sei=Richard L Gallo
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IwatsukiKeiji
en-aut-sei=Iwatsuki
en-aut-mei=Keiji
kn-aut-name=岩月啓氏
kn-aut-sei=岩月
kn-aut-mei=啓氏
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　皮膚科学

affil-num=2
en-affil=
kn-affil=東北大学大学院医学系研究科　皮膚科学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　皮膚科学

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　皮膚科学

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　皮膚科学

affil-num=6
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　皮膚科学

affil-num=7
en-affil=
kn-affil=米国カリフォルニア大学サンディエゴ校医学部　皮膚科学

affil-num=8
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　皮膚科学
en-keyword=アトピー性皮膚炎
kn-keyword=アトピー性皮膚炎
en-keyword=Th２サイトカイン
kn-keyword=Th２サイトカイン
en-keyword=カリクレイン
kn-keyword=カリクレイン
en-keyword=表皮角化細胞
kn-keyword=表皮角化細胞
END

start-ver=1.4
cd-journal=joma
no-vol=126
cd-vols=
no-issue=1
article-no=
start-page=65
end-page=67
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=SFTS : Severe fever with thrombocytopenia syndrome
kn-title=重症熱性血小板減少症候群
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=WatanabeTokiko
en-aut-sei=Watanabe
en-aut-mei=Tokiko
kn-aut-name=渡邉都貴子
kn-aut-sei=渡邉
kn-aut-mei=都貴子
aut-affil-num=1
ORCID=

en-aut-name=KusanoNobuchika
en-aut-sei=Kusano
en-aut-mei=Nobuchika
kn-aut-name=草野展周
kn-aut-sei=草野
kn-aut-mei=展周
aut-affil-num=2
ORCID=

en-aut-name=IwatsukiKeiji
en-aut-sei=Iwatsuki
en-aut-mei=Keiji
kn-aut-name=岩月啓氏
kn-aut-sei=岩月
kn-aut-mei=啓氏
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学病院　感染制御部

affil-num=2
en-affil=
kn-affil=岡山大学病院　感染制御部

affil-num=3
en-affil=
kn-affil=岡山大学病院　感染制御部
END

start-ver=1.4
cd-journal=joma
no-vol=120
cd-vols=
no-issue=2
article-no=
start-page=201
end-page=206
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Diagnoses and standard treatments for skin cancers
kn-title=XII 皮膚がんの診断と標準的治療
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=OtsukaMasaki
en-aut-sei=Otsuka
en-aut-mei=Masaki
kn-aut-name=大塚正樹
kn-aut-sei=大塚
kn-aut-mei=正樹
aut-affil-num=1
ORCID=

en-aut-name=AsagoeKenji
en-aut-sei=Asagoe
en-aut-mei=Kenji
kn-aut-name=浅越健治
kn-aut-sei=浅越
kn-aut-mei=健治
aut-affil-num=2
ORCID=

en-aut-name=IwatsukiKeiji
en-aut-sei=Iwatsuki
en-aut-mei=Keiji
kn-aut-name=岩月啓氏
kn-aut-sei=岩月
kn-aut-mei=啓氏
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　皮膚科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　皮膚科学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　皮膚科学
en-keyword=メラノーマ
kn-keyword=メラノーマ
en-keyword=有棘細胞癌
kn-keyword=有棘細胞癌
en-keyword=基底細胞癌
kn-keyword=基底細胞癌
en-keyword=乳房外 Paget 病
kn-keyword=乳房外 Paget 病
END

start-ver=1.4
cd-journal=joma
no-vol=113
cd-vols=
no-issue=1
article-no=
start-page=79
end-page=86
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2001
dt-pub=20010428
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=薬剤耐性菌について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=秋山尚範
kn-aut-sei=秋山
kn-aut-mei=尚範
aut-affil-num=1
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=荒田次郎
kn-aut-sei=荒田
kn-aut-mei=次郎
aut-affil-num=2
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=岩月啓氏
kn-aut-sei=岩月
kn-aut-mei=啓氏
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部皮膚科学講座

affil-num=2
en-affil=
kn-affil=岡山大学医学部皮膚科学講座

affil-num=3
en-affil=
kn-affil=岡山大学医学部皮膚科学講座
en-keyword=MRSA
kn-keyword=MRSA
en-keyword=VRE
kn-keyword=VRE
en-keyword=PRSP
kn-keyword=PRSP
en-keyword=緑膿菌
kn-keyword=緑膿菌
en-keyword=ESBL
kn-keyword=ESBL
en-keyword=BLNAR
kn-keyword=BLNAR
en-keyword=多剤耐性結核菌
kn-keyword=多剤耐性結核菌
en-keyword=バイオフィルム
kn-keyword=バイオフィルム
END

start-ver=1.4
cd-journal=joma
no-vol=41
cd-vols=
no-issue=1
article-no=
start-page=3
end-page=10
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=201401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cutaneous lymphoma in Japan: A nationwide study of 1733 patients
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Types of cutaneous lymphoma (CL) and their incidences may vary among geographic areas or ethnic groups. The present study aimed to investigate the incidences of various CL in Japan, using epidemiological data from a nationwide registration system for CL. Between 2007 and 2011, 1733 new patients with CL were registered from over 600 dermatological institutes in Japan. The 1733 patients registered included 1485 (85.7%) patients with mature T- and natural killer (NK)-cell neoplasms, 224 (12.9%) with B-cell neoplasms and 24 (1.4%) with blastic plasmacytoid dendritic cell neoplasm. Mycosis fungoides (MF) is the most common CL subtype in the present study (750 patients, 43.3%). The proportion of MF patients with early-stage disease was 73%, similar to that of previous studies from other cohorts. The incidence rates of adult T-cell leukemia/lymphoma and extranodal NK/T-cell lymphoma, nasal type were 16.7% and 2.0%, respectively, which may account for the higher incidence of mature T- and NK-cell neoplasms in Japan, as compared with that in the USA and Europe. A male predominance was observed in most types of CL, except for several CL subtypes such as subcutaneous panniculitis-like T-cell lymphoma.
en-copyright=
kn-copyright=

en-aut-name=HamadaToshihisa
en-aut-sei=Hamada
en-aut-mei=Toshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

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

affil-num=2
en-affil=
kn-affil=Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci
en-keyword=adult T-cell leukemia
kn-keyword=adult T-cell leukemia
en-keyword=lymphoma
kn-keyword=lymphoma
en-keyword=cutaneous lymphoma
kn-keyword=cutaneous lymphoma
en-keyword=extranodal natural killer
kn-keyword=extranodal natural killer
en-keyword=T-cell lymphoma
kn-keyword=T-cell lymphoma
en-keyword=mycosis fungoides
kn-keyword=mycosis fungoides
en-keyword=nasal type
kn-keyword=nasal type
en-keyword=subcutaneous panniculitis-like T-cell lymphoma
kn-keyword=subcutaneous panniculitis-like T-cell lymphoma
END

start-ver=1.4
cd-journal=joma
no-vol=126
cd-vols=
no-issue=3
article-no=
start-page=255
end-page=257
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20141201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The 113th Annual Meeting of the Japanese Dermatological Association
kn-title=第113回日本皮膚科学会総会学会報告
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=IwatsukiKeiji
en-aut-sei=Iwatsuki
en-aut-mei=Keiji
kn-aut-name=岩月啓氏
kn-aut-sei=岩月
kn-aut-mei=啓氏
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　皮膚科学
END

start-ver=1.4
cd-journal=joma
no-vol=171
cd-vols=
no-issue=3
article-no=
start-page=492
end-page=498
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=201409
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cathelicidin antimicrobial peptide LL-37 augments interferon-beta expression and antiviral activity induced by double-stranded RNA in keratinocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Cathelicidin antimicrobial peptide LL-37 has the capacity to kill a wide range of microbes and to modify host immunity. Recently, our group observed that the activation of keratinocytes by LL-37 and DNA greatly increases interferon (IFN)-beta through Toll-like receptor (TLR) 9. However, the effect of LL-37 on the induction of IFN-beta through TLR3, a sensor of double-stranded (ds) RNA, in keratinocytes is not well known. 

Objectives To investigate whether LL-37 could affect TLR3 signalling and antiviral activity in normal human epidermal keratinocytes (NHEKs). 

Methods We investigated the production of IFN-beta in NHEKs stimulated with a TLR3 ligand, poly (I:C), in the presence of LL-37. To examine the effect of LL-37 and poly (I:C) on antiviral activity, a virus plaque assay using herpes simplex (HS) virus type-1 was carried out. The uptake of poly (I:C) conjugated with fluorescein isothiocyanate (FITC) into the keratinocytes was observed in the presence of LL-37. Immunostaining for TLR3 and LL-37 was performed using skin samples from HS. 

Results LL-37 and poly (I:C) synergistically induced the expression of IFN-beta in NHEKs. Furthermore, co-stimulation with LL-37 and poly (I:C) significantly decreased the viral plaque numbers compared with poly (I:C) or LL-37 alone. LL-37 enhanced the uptake of FITC-conjugated poly (I:C) into cells. Immunohistochemical analysis demonstrated that the expression of TLR3 and LL-37 is up-regulated in HS lesions. 

Conclusions Our findings suggest that LL-37 augments the antiviral activity induced by dsRNA in keratinocytes, which may contribute to the innate immune response to cutaneous viral infections such as HS.
en-copyright=
kn-copyright=

en-aut-name=TakiguchiT
en-aut-sei=Takiguchi
en-aut-mei=T
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MorizaneS
en-aut-sei=Morizane
en-aut-mei=S
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamamotoT
en-aut-sei=Yamamoto
en-aut-mei=T
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KajitaA
en-aut-sei=Kajita
en-aut-mei=A
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IkedaK
en-aut-sei=Ikeda
en-aut-mei=K
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IwatsukiK
en-aut-sei=Iwatsuki
en-aut-mei=K
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

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

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

affil-num=3
en-affil=
kn-affil=Kawasaki Med Univ, Dept Dermatol

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

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

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

start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=6
article-no=
start-page=670
end-page=675
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=201411
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Increase of DC-LAMP+ mature dendritic cell subsets in dermatopathic lymphadenitis of mycosis fungoides
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Little is known about the immunological milieu of the skin-draining lymph nodes (LNs) in mycosis fungoides (MF). Objectives: We studied dendritic cell (DC) subsets in the dermatopathic lymphadenitis of MF patients. Methods: We immunohistochemically examined DC subsets and their distribution in 16 LN samples from 14 patients with MF (N1 LN, eight patients; N2, four; and N3, four), and we compared them with non-metastatic sentinel LNs from eight patients with melanoma. Results: The number of S-100 protein+ DCs was markedly increased in the LNs from the MF patients and the major component was DC-LAMP+ mature DCs in the outer and paracortex areas, where DC-SIGN+ immature DCs were relatively decreased in proportion. In contrast, DC-SIGN+ cells were relatively increased in proportion compared to DC-LAMP+ cells in the medulla. Although no significant difference was observed in the proportions of CD1a+ or Langerin+ DCs among the N1, N2, and N3 nodes, CD163+ M2-type macrophages were increased in number in the N2 and N3 nodes. Conclusions: Our observations indicate that mature DCs accumulate in the outer and paracortex areas in dermatopathic lymphadenitis and M2-type macrophages might increase in number during disease progression.
en-copyright=
kn-copyright=

en-aut-name=TadaKotaro
en-aut-sei=Tada
en-aut-mei=Kotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HamadaToshihisa
en-aut-sei=Hamada
en-aut-mei=Toshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AsagoeKenji
en-aut-sei=Asagoe
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=UmemuraHiroshi
en-aut-sei=Umemura
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=Mizuno-IkedaKazuko
en-aut-sei=Mizuno-Ikeda
en-aut-mei=Kazuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AoyamaYumi
en-aut-sei=Aoyama
en-aut-mei=Yumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OtsukaMasaki
en-aut-sei=Otsuka
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamasakiOsamu
en-aut-sei=Yamasaki
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
ORCID=

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

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

affil-num=3
en-affil=
kn-affil=Department of Dermatology, Okayama Medical Center

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

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

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

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

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

affil-num=9
en-affil=
kn-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
en-keyword=Mycosis fungoides
kn-keyword=Mycosis fungoides
en-keyword=dendritic cell
kn-keyword=dendritic cell
en-keyword=dermatopathic lymphadenitis
kn-keyword=dermatopathic lymphadenitis
en-keyword=DC-LAMP
kn-keyword=DC-LAMP
en-keyword=DC-SIGN
kn-keyword=DC-SIGN
en-keyword=M2-type macrophage
kn-keyword=M2-type macrophage
END

start-ver=1.4
cd-journal=joma
no-vol=128
cd-vols=
no-issue=1
article-no=
start-page=71
end-page=72
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 40th Annual Meeting of the Japanese Society for Investigative Dermatology
kn-title=日本研究皮膚科学会第40回年次学術大会・総会 を終えて
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=IwatsukiKeiji
en-aut-sei=Iwatsuki
en-aut-mei=Keiji
kn-aut-name=岩月啓氏
kn-aut-sei=岩月
kn-aut-mei=啓氏
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　皮膚科学
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=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