start-ver=1.4
cd-journal=joma
no-vol=4
cd-vols=
no-issue=2
article-no=
start-page=e70091
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=Olanzapine enabled rechallenge after lorlatinib-induced psychosis: A case report
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Lorlatinib is a third-generation tyrosine kinase inhibitor for anaplastic lymphoma kinase (ALK)-positive non-small cell lung cancer (NSCLC). While it has a high intracranial lesion control rate, it can also cause central nervous system complications, including psychotic symptoms. We present a case of lorlatinib-induced psychosis successfully managed with olanzapine, enabling lorlatinib rechallenge.<br>
Case Presentation: A 32-year-old woman with ALK-positive NSCLC and brain metastases was started on lorlatinib. After 18 months, she developed hallucinations and delusions. Despite treatment with risperidone, her psychotic symptoms persisted, leading to hospitalization. Her symptoms resolved upon lorlatinib discontinuation while risperidone was continued. Given the critical role of lorlatinib in controlling brain metastases, rechallenge was considered. To mitigate concerns regarding drug interactions, risperidone was replaced with olanzapine. Following lorlatinib rechallenge with olanzapine, no recurrence of psychiatric symptoms was observed, allowing continued lorlatinib treatment. Additionally, no progression of lung cancer was noted.<br>
Conclusion: Lorlatinib is an essential drug for controlling brain metastases in ALK-positive NSCLC. However, it can induce psychotic symptoms. When psychiatrists are involved in managing adverse effects during cancer treatment, close collaboration among oncologists, psychiatrists, and patients is essential.
en-copyright=
kn-copyright=

en-aut-name=YokodeAkiyoshi
en-aut-sei=Yokode
en-aut-mei=Akiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujiwaraMasaki
en-aut-sei=Fujiwara
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraYuko
en-aut-sei=Nakamura
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=SakamotoShinji
en-aut-sei=Sakamoto
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakakiManabu
en-aut-sei=Takaki
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

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

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

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

affil-num=4
en-affil=Department of Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Neuropsychiatry, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine,Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=psycho-oncology
kn-keyword=psycho-oncology
en-keyword=lorlatinib
kn-keyword=lorlatinib
en-keyword=lung cancer
kn-keyword=lung cancer
en-keyword=medication-induced psychosis
kn-keyword=medication-induced psychosis
END

start-ver=1.4
cd-journal=joma
no-vol=137
cd-vols=
no-issue=1
article-no=
start-page=4
end-page=6
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The 2023 Incentive Award of the Okayama Medical Association in General Medical Science (2023 Yuuki Prize)
kn-title=令和５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=SumiiYuichi
en-aut-sei=Sumii
en-aut-mei=Yuichi
kn-aut-name=住居優一
kn-aut-sei=住居
kn-aut-mei=優一
aut-affil-num=1
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=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=24
cd-vols=
no-issue=1
article-no=
start-page=116
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250416
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=ADAR1-high tumor-associated macrophages induce drug resistance and are therapeutic targets in colorectal cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Colorectal cancer (CRC) is considered the third most common type of cancer worldwide. Tumor-associated macrophages (TAMs) have been shown to promote drug resistance. Adenosine-to-inosine RNA-editing, as regulated by adenosine deaminase acting on RNA (ADAR), is a process that induces the posttranscriptional modification of critical oncogenes. The aim of this study is to determine whether the signals from cancer cells would induce RNA-editing in macrophages.<br>
Methods The effects of RNA-editing on phenotypes in macrophages were analyzed using clinical samples and in vitro and in vivo models.<br>
Results The intensity of the RNA-editing enzyme ADAR1 (Adenosine deaminase acting on RNA 1) in cancer and mononuclear cells indicated a strong positive correlation between the nucleus and cytoplasm. The ADAR1-positive mononuclear cells were positive for CD68 and CD163, a marker for M2 macrophages. Cancer cells transport pro-inflammatory cytokines or ADAR1 protein directly to macrophages via the exosomes, promoting RNA-editing in AZIN1 (Antizyme Inhibitor 1) and GLI1 (Glioma-Associated Oncogene Homolog 1) and resulting in M2 macrophage polarization. GLI1 RNA-editing in the macrophages induced by cancer cells promotes the secretion of SPP1, which is supplied to the cancer cells. This activates the NF kappa B pathway in cancer cells, promoting oxaliplatin resistance. When the JAK inhibitors were administered, oncogenic RNA-editing in the macrophages was suppressed. This altered the macrophage polarization from M2 to M1 and decreased oxaliplatin resistance in cancer cells.<br>
Conclusions This study revealed that ADAR1-high TAMs are crucial in regulating drug resistance in CRC and that targeting ADAR1 in TAMs could be a promising treatment approach for overcoming drug resistance in CRC.
en-copyright=
kn-copyright=

en-aut-name=UmedaHibiki
en-aut-sei=Umeda
en-aut-mei=Hibiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShigeyasuKunitoshi
en-aut-sei=Shigeyasu
en-aut-mei=Kunitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakahashiToshiaki
en-aut-sei=Takahashi
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MoriwakeKazuya
en-aut-sei=Moriwake
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KondoYoshitaka
en-aut-sei=Kondo
en-aut-mei=Yoshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

en-aut-name=TakedaSho
en-aut-sei=Takeda
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YanoShuya
en-aut-sei=Yano
en-aut-mei=Shuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MatsumiYuki
en-aut-sei=Matsumi
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KishimotoHiroyuki
en-aut-sei=Kishimoto
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
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=12
ORCID=

en-aut-name=YamamotoHideki
en-aut-sei=Yamamoto
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
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=14
ORCID=

en-aut-name=KayanoMasashi
en-aut-sei=Kayano
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
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=16
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=17
ORCID=

en-aut-name=MoriYoshiko
en-aut-sei=Mori
en-aut-mei=Yoshiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
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=19
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=20
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=21
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=22
ORCID=

en-aut-name=GoelAjay
en-aut-sei=Goel
en-aut-mei=Ajay
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
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=24
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=Department of Clinical Genomic Medicine, 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=

affil-num=16
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=17
en-affil=Department of Obstetrics and Gynecology, Okayama University Gradu?ate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=18
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=19
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=20
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=21
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=22
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=23
en-affil=Department of Molecular Diagnostics and Experimental Therapeutics, Beckman Research Institute, City of Hope Comprehensive Cancer Center
kn-affil=

affil-num=24
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=RNA-editing
kn-keyword=RNA-editing
en-keyword=Macrophage
kn-keyword=Macrophage
en-keyword=Chemoresistance
kn-keyword=Chemoresistance
en-keyword=Biomarker
kn-keyword=Biomarker
en-keyword=Colorectal cancer
kn-keyword=Colorectal cancer
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=8
article-no=
start-page=e70793
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250418
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Genomic Differences and Distinct TP53 Mutation Site-Linked Chemosensitivity in Early- and Late-Onset Gastric Cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Gastric cancer (GC) in younger patients often exhibits aggressive behavior and a poorer prognosis than that in older patients. Although the clinical differences may stem from oncogenic gene variations, it is unclear whether genetic differences exist between these groups. This study compared the genetic profiles of early- and late-onset GC and evaluated their impact on treatment outcomes.<br>
Methods: We analyzed genetic data from 1284 patients with GC in the Japanese nationwide Center for Cancer Genomics and Advanced Therapeutics (C-CAT) database, comparing early-onset (<= 39 years; n = 143) and late-onset (>= 65 years; n = 1141) groups. The influence of TP53 mutations on the time to treatment failure (TTF) with platinum-based chemotherapy and the sensitivity of cancer cells with different TP53 mutation sites to oxaliplatin were assessed in vitro.<br>
Results: Early- and late-onset GC showed distinct genetic profiles, with fewer neoantigen-associated genetic changes observed in early-onset cases. In particular, TP53 has distinct mutation sites; R175H and R273 mutations are more frequent in early- and late-onset GC, respectively. The R175H mutation showed higher sensitivity to oxaliplatin in vitro, consistent with the longer TTF in early-onset patients (17.3 vs. 7.0 months, p = 0.013) when focusing on the patients with TP53 mutations.<br>
Conclusion: Genomic differences, particularly in TP53 mutation sites, between early- and late-onset GC support the need for age-specific treatment strategies.
en-copyright=
kn-copyright=

en-aut-name=KamioTomohiro
en-aut-sei=Kamio
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=HirosunaKensuke
en-aut-sei=Hirosuna
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OzatoToshiki
en-aut-sei=Ozato
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamamotoHideki
en-aut-sei=Yamamoto
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HirasawaAkira
en-aut-sei=Hirasawa
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=

en-aut-name=TomidaShuta
en-aut-sei=Tomida
en-aut-mei=Shuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
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=10
ORCID=

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

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

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

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

affil-num=5
en-affil=Department of Clinical Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Department of Clinical Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of Gastroenterology and Hepatology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=comprehensive genomic profiling
kn-keyword=comprehensive genomic profiling
en-keyword=early-onset gastric cancer
kn-keyword=early-onset gastric cancer
en-keyword=oxaliplatin
kn-keyword=oxaliplatin
en-keyword=TP53
kn-keyword=TP53
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=4
article-no=
start-page=e70151
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250416
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Frequency and Characteristics of Gastrointestinal Diseases in Patients With Neurofibromatosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background and Aim: Patients with neurofibromatosis (NF) frequently experience gastrointestinal symptoms, but the specific characteristics of these lesions are not well understood.<br>
Methods: To investigate the prevalence and nature of gastrointestinal diseases in this population, we analyzed the gastrointestinal lesions identified through endoscopic examinations in patients with NF.<br>
Results: We included 225 patients with NF type 1 (NF1) and 15 with NF type 2 (NF2). None of the NF2 patients underwent endoscopy. Among the NF1 patients, 27 received endoscopies, and 13 (59%) had gastrointestinal lesions. These 13 patients were predominantly male (10 males and three females), with a median age of 53 years (range: 19-76 years). The identified lesions included colorectal polyps (n = 6), gastrointestinal stromal tumors ([GIST], n = 4), subepithelial lesions (n = 3), gastric fundic gland polyps (n = 3), diffuse intestinal ganglioneuromatosis (n = 2), esophageal polyps (n = 2), a Schwann cell hamartoma (n = 1), esophageal cancer (n = 1), and a gastric hyperplastic polyp (n = 1). All GISTs and one case of diffuse intestinal ganglioneuromatosis were surgically resected. Interestingly, six out of 13 patients were asymptomatic. Additionally, all patients who required surgery were 40 years of age or older.<br>
Conclusions: These findings suggest that routine endoscopic examinations, along with imaging techniques like computed tomography and magnetic resonance imaging, could be beneficial for the early detection of gastrointestinal lesions in NF1 patients aged 40 and above.
en-copyright=
kn-copyright=

en-aut-name=HondaManami
en-aut-sei=Honda
en-aut-mei=Manami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=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=YamasakiYasushi
en-aut-sei=Yamasaki
en-aut-mei=Yasushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
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=6
ORCID=

en-aut-name=KawaharaYoshiro
en-aut-sei=Kawahara
en-aut-mei=Yoshiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
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 Pathology, 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 Practical Gastrointestinal Endoscopy,Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=colonoscopy
kn-keyword=colonoscopy
en-keyword=esophagogastroduodenoscopy
kn-keyword=esophagogastroduodenoscopy
en-keyword=gastrointestinal neoplasms
kn-keyword=gastrointestinal neoplasms
en-keyword=gastrointestinal stromal tumor
kn-keyword=gastrointestinal stromal tumor
en-keyword=neurofibromatosis
kn-keyword=neurofibromatosis
END

start-ver=1.4
cd-journal=joma
no-vol=79
cd-vols=
no-issue=2
article-no=
start-page=139
end-page=144
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Safe Resection of Esophageal Cancer with a Non-Recurrent Inferior Laryngeal Nerve Associated with an Aberrant Right Subclavian Artery Using Intraoperative Nerve Monitoring
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In thoracic esophageal cancer, lymph node dissection around the recurrent laryngeal nerve is crucial but poses a risk of nerve palsy, affecting postoperative quality of life. In cases with an aberrant right subclavian artery (ARSA), the right recurrent laryngeal nerve is absent, and the non-recurrent inferior laryngeal nerve (NRILN) enters the larynx directly from the vagus nerve in the cervical region. Identifying the course of the NRILN is vital to avoid injury. A case of esophageal cancer with an ARSA, in which the course of the NRILN was preserved using the Nerve Integrity Monitoring (NIM) system during surgery, is described.
en-copyright=
kn-copyright=

en-aut-name=TakedaYasushige
en-aut-sei=Takeda
en-aut-mei=Yasushige
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=MaedaNaoaki
en-aut-sei=Maeda
en-aut-mei=Naoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MizusawaYohei
en-aut-sei=Mizusawa
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MatsumotoHijiri
en-aut-sei=Matsumoto
en-aut-mei=Hijiri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KondoYuhei
en-aut-sei=Kondo
en-aut-mei=Yuhei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KunitomoTomoyoshi
en-aut-sei=Kunitomo
en-aut-mei=Tomoyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TanoueYukinori
en-aut-sei=Tanoue
en-aut-mei=Yukinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HashimotoMasashi
en-aut-sei=Hashimoto
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TanabeShunsuke
en-aut-sei=Tanabe
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
ORCID=

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

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

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

affil-num=4
en-affil=Department of Gastroenterological Surgery, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Gastroenterological Surgery, Okayama University Hospital
kn-affil=

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

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

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

affil-num=9
en-affil=Department of Gastroenterological Surgery, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of Gastroenterological Surgery, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of Gastroenterological Surgery, Okayama University Hospital
kn-affil=
en-keyword=esophageal cancer
kn-keyword=esophageal cancer
en-keyword=intraoperative nerve monitoring
kn-keyword=intraoperative nerve monitoring
en-keyword=aberrant right subclavian artery
kn-keyword=aberrant right subclavian artery
en-keyword=non-recurrent inferior laryngeal nerve
kn-keyword=non-recurrent inferior laryngeal nerve
en-keyword=thoracoscopic esophagectomy
kn-keyword=thoracoscopic esophagectomy
END

start-ver=1.4
cd-journal=joma
no-vol=79
cd-vols=
no-issue=2
article-no=
start-page=129
end-page=134
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Case of Retinitis Pigmentosa Diagnosed with Severe Anterior Capsule Contraction after Cataract Surgery
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A 66-year-old woman presented with significant anterior capsule contraction and intraocular lens dislocation in both eyes 4 months after cataract surgery. Postoperative examinations such as fluorescein angiography, Goldmann perimetry, and electroretinography revealed retinitis pigmentosa (RP). Patients with significant anterior capsule contraction after cataract surgery should be closely examined because RP may be a contributing factor.
en-copyright=
kn-copyright=

en-aut-name=TsujiAkihiro
en-aut-sei=Tsuji
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShiodeYusuke
en-aut-sei=Shiode
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KimuraShuhei
en-aut-sei=Kimura
en-aut-mei=Shuhei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HosokawaMio
en-aut-sei=Hosokawa
en-aut-mei=Mio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MatobaRyo
en-aut-sei=Matoba
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MoritaTetsuro
en-aut-sei=Morita
en-aut-mei=Tetsuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakahashiKosuke
en-aut-sei=Takahashi
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MorizaneYuki
en-aut-sei=Morizane
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

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

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

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

affil-num=7
en-affil=Fukuyama City Hospital, Fukuyama City
kn-affil=

affil-num=8
en-affil=Department of Ophthalmology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=retinitis pigmentosa
kn-keyword=retinitis pigmentosa
en-keyword=intraocular lens
kn-keyword=intraocular lens
en-keyword=anterior capsule contraction
kn-keyword=anterior capsule contraction
END

start-ver=1.4
cd-journal=joma
no-vol=79
cd-vols=
no-issue=2
article-no=
start-page=117
end-page=121
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=From a Congenital Defect to Cancer: A Case of Squamous Cell Carcinoma in a Neglected Myelomeningocele
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Neural tube defects are common congenital anomalies, typically presenting early due to visible swelling and/or neurological deficits. Rarely, cystic swellings are neglected until adulthood, with only 14 cases of malignancy developing in an untreated meningomyelocele reported to date. We describe the case details of a 26-year-old Indian woman with this rare complication. Magnetic resonance imaging revealed a low-lying spinal cord with spinal dysraphism, cord herniation, and a cystic lesion. The biopsy confirmed a well-differentiated squamous cell carcinoma. Malignant transformation in an untreated myelomeningocele is rare, with chronic irritation and infection as proposed causes. Early biopsy and treatment are crucial for its management.
en-copyright=
kn-copyright=

en-aut-name=GautamAbhishek
en-aut-sei=Gautam
en-aut-mei=Abhishek
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KenawadekarRahul
en-aut-sei=Kenawadekar
en-aut-mei=Rahul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HattiholiVirupaxi
en-aut-sei=Hattiholi
en-aut-mei=Virupaxi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MastePraful Suresh
en-aut-sei=Maste
en-aut-mei=Praful Suresh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Neurosurgery, Jawaharlal Nehru Medical College, KAHER
kn-affil=

affil-num=2
en-affil=Department of General Surgery, Jawaharlal Nehru Medical College, KAHER
kn-affil=

affil-num=3
en-affil=Department of Radiology, Jawaharlal Nehru Medical College, KAHER
kn-affil=

affil-num=4
en-affil=Department of Neurosurgery, Jawaharlal Nehru Medical College, KAHER
kn-affil=
en-keyword=squamous cell carcinoma
kn-keyword=squamous cell carcinoma
en-keyword=meningomyelocele
kn-keyword=meningomyelocele
en-keyword=occult spinal dysraphism
kn-keyword=occult spinal dysraphism
END

start-ver=1.4
cd-journal=joma
no-vol=79
cd-vols=
no-issue=2
article-no=
start-page=81
end-page=92
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical Outcomes of Neoadjuvant Paclitaxel/Cisplatin/Gemcitabine Compared with Gemcitabine/Cisplatin for Muscle-Invasive Bladder Cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We retrospectively evaluated the oncologic outcomes of paclitaxel, cisplatin, and gemcitabine (PCG) with those of gemcitabine and cisplatin (GC) as neoadjuvant chemotherapy in muscle-invasive bladder cancer (MIBC) patients. The primary outcome was efficacy: pathological complete response (pCR), ypT0N0; and pathological objective response (pOR), ypT0N0, ? ypT1N0, or ypT0N1. Secondary outcomes included overall survival (OS), recurrence-free survival (RFS), predictive factors for pOR, OS, and RFS, and hematologic adverse events (AEs). Among 113 patients treated (PCG, n=28; GC, n=85), similar pOR and pCR rates were achieved by the groups (pOR: PCG, 57.1% vs. GC, 49. 4%; p=0.52; pCR: PCG, 39.3% vs. GC, 29.4%; p=0.36). No significant differences were observed in OS (p=1.0) or RFS (p=0.20). Multivariate logistic regression analysis showed that hydronephrosis (odds ratio [OR] 0.32, 95%CI: 0.11-0.92) and clinical node-positive status (cN+) (OR 0.22, 95%CI: 0.050-0.99) were significantly associated with a decreased probability of pOR. On multivariate Cox regression analyses, pOR achievement was associated with improved OS (hazard ratio [HR] 0.23, 95%CI: 0.10-0.56) and RFS (HR 0.30, 95%CI: 0.13-0.67). There were no significant between-group differences in the incidence of grade ? 3 hematologic AEs or dose-reduction required, but the PCG group had a higher incidence of grade 4 neutropenia.
en-copyright=
kn-copyright=

en-aut-name=KawadaTatsushi
en-aut-sei=Kawada
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KobayashiYasuyuki
en-aut-sei=Kobayashi
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TsugawaTakuji
en-aut-sei=Tsugawa
en-aut-mei=Takuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TsuboiKazuma
en-aut-sei=Tsuboi
en-aut-mei=Kazuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KatayamaSatoshi
en-aut-sei=Katayama
en-aut-mei=Satoshi
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=BekkuKensuke
en-aut-sei=Bekku
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KobayashiTomoko
en-aut-sei=Kobayashi
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=EdamuraKohei
en-aut-sei=Edamura
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=EbaraShin
en-aut-sei=Ebara
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=ArakiMotoo
en-aut-sei=Araki
en-aut-mei=Motoo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

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

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

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

affil-num=4
en-affil=Department of Urology, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

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

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

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

affil-num=10
en-affil=Department of Urology, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=11
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=urothelial carcinoma
kn-keyword=urothelial carcinoma
en-keyword=paclitaxel
kn-keyword=paclitaxel
en-keyword=cisplatin
kn-keyword=cisplatin
en-keyword=gemcitabine
kn-keyword=gemcitabine
en-keyword=neoadjuvant
kn-keyword=neoadjuvant
END

start-ver=1.4
cd-journal=joma
no-vol=79
cd-vols=
no-issue=2
article-no=
start-page=65
end-page=73
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Association between the Pretreatment Body Mass Index and Anamorelin’s Efficacy in Patients with Cancer Cachexia: A Retrospective Cohort Study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Anamorelin (ANAM) is used to treat cancer-associated cachexia, a syndrome involving muscle loss and anorexia. The timing of the initiation of ANAM treatment is crucial to its efficacy. Although the body mass index (BMI) is a diagnostic criterion for cancer cachexia, no studies have explored its association with ANAM efficacy. We conducted a single-center, retrospective cohort study to investigate the association between the pre-treatment BMI and ANAM efficacy in patients with cancer-associated cachexia (n=47). The ANAM treatment was considered effective if the patient’s appetite improved within 30 days of treatment initiation. We calculated a BMI cutoff value (19.5 kg/m2) and used it to divide the patients into high- and low-BMI groups. Their background, clinical laboratory values, cancer types, and treatment lines were investigated. Twenty (42.6%) had a high BMI (? 19.5 kg/m2) and 27 (57.4%) had a low BMI (< 19.5 kg/m2). High BMI was significantly associated with ANAM effectiveness (odds ratio 7.86, 95% confidence interval 1.99-31.00, p=0.003). Together these results indicate that it is beneficial to initiate ANAM treatment before a patient’s BMI drops below 19.5 kg/m2. Our findings will help advance cancer cachexia treatment and serve as a reference for clinicians to predict ANAM’s efficacy.
en-copyright=
kn-copyright=

en-aut-name=MakiMasatoshi
en-aut-sei=Maki
en-aut-mei=Masatoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakadaRyo
en-aut-sei=Takada
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IshigoTomoyuki
en-aut-sei=Ishigo
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FujiwaraMiki
en-aut-sei=Fujiwara
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakahashiYoko
en-aut-sei=Takahashi
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OtsukaShinya
en-aut-sei=Otsuka
en-aut-mei=Shinya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TamuraKoji
en-aut-sei=Tamura
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HamaokaTerutaka
en-aut-sei=Hamaoka
en-aut-mei=Terutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Hospital Pharmacy, NHO Fukuyama Medical Center
kn-affil=

affil-num=2
en-affil=Department of Hospital Pharmacy, NHO Fukuyama Medical Center
kn-affil=

affil-num=3
en-affil=Department of Pharmacy, Sapporo Medical University Hospital
kn-affil=

affil-num=4
en-affil=Department of Hospital Pharmacy, NHO Fukuyama Medical Center
kn-affil=

affil-num=5
en-affil=Department of Hospital Pharmacy, NHO Fukuyama Medical Center
kn-affil=

affil-num=6
en-affil=Department of Surgery, NHO Fukuyama Medical Center
kn-affil=

affil-num=7
en-affil=Department of Hospital Pharmacy, NHO Fukuyama Medical Center
kn-affil=

affil-num=8
en-affil=Department of Hospital Pharmacy, NHO Fukuyama Medical Center
kn-affil=
en-keyword=anamorelin
kn-keyword=anamorelin
en-keyword=cancer-associated cachexia
kn-keyword=cancer-associated cachexia
en-keyword=body mass index
kn-keyword=body mass index
en-keyword=albumin
kn-keyword=albumin
en-keyword=efficacy rate
kn-keyword=efficacy rate
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=20250410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Enterobacterial common antigen repeat-unit flippase WzxE is required for Escherichia coli growth under acidic conditions, low temperature, and high osmotic stress conditions
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Colanic acid and enterobacterial common antigen (ECA) are cell-surface polysaccharides that are produced by many Escherichia coli isolates. Colanic acid is induced under acidic, low temperature, and high-salt conditions and is important for E. coli resistance to these stresses; however, the role of ECA in these stresses is less clear. Here, we observed that knockout of flippase wzxE, which translocates lipid-linked ECA repeat units from the cytoplasmic side of the inner membrane to the periplasmic side, resulted in the sensitivity of E. coli BW25113 to acidic conditions. The wzxE-knockout mutant showed reduced growth potential and viable counts in vegetable extracts with acidic environments, including cherry tomatoes, carrots, celery, lettuce, and spinach. A double-knockout strain of wzxE and wecF (glycosyltransferase that adds the third-and-final sugar of the lipid-linked ECA repeat unit) was not sensitive to acidic conditions, with similar results obtained for a double-knockout strain of wzxE and wcaJ (glycosyltransferase that initiates colanic acid lipid-linked repeat-unit biosynthesis). The wzxE-knockout mutant was sensitive to low temperatures or high-salt conditions, which induced colanic acid synthesis, and these sensitivities were abolished by the additional knockout of wcaJ. These results suggest that lipid-linked ECA repeat units confer E. coli susceptibility to acidic, low temperatures, and high-salt conditions in a colanic acid-dependent manner and that wzxE suppresses this negative effect.
en-copyright=
kn-copyright=

en-aut-name=YamaguchiSaki
en-aut-sei=Yamaguchi
en-aut-mei=Saki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IshikawaKazuya
en-aut-sei=Ishikawa
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FurutaKazuyuki
en-aut-sei=Furuta
en-aut-mei=Kazuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KaitoChikara
en-aut-sei=Kaito
en-aut-mei=Chikara
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

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

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

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

affil-num=4
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=wzxE flippase
kn-keyword=wzxE flippase
en-keyword=enterobacterial common antigen
kn-keyword=enterobacterial common antigen
en-keyword=low pH
kn-keyword=low pH
en-keyword=low temperature
kn-keyword=low temperature
en-keyword=hyperosmotic stress
kn-keyword=hyperosmotic stress
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=2
article-no=
start-page=100016
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202507
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Changes in adrenoceptor expression level contribute to the cellular plasticity of glioblastoma cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Glioblastoma cells are known to regulate their cellular plasticity in response to their surrounding microenvironment, but it is not fully understood what factors contribute to the cells' changing plasticity. Here, we found that glioblastoma cells alter the expression level of adrenoreceptors depending on their differentiation stage. Catecholamines are abundant in the central nervous system, and we found that noradrenaline, in particular, enhances the stemness of glioblastoma cells and promotes the dedifferentiation potential of already differentiated glioblastoma cells. Antagonist and RNAi experiments revealed that signaling through alpha 1D-adrenoreceptor is important for noradrenaline action on glioblastoma cells. We also found that high alpha 1Dadrenoreceptor expression was associated with poor prognosis in patients with gliomas. These data suggest that glioblastoma cells increase the expression level of their own adrenoreceptors to alter the surrounding tumor microenvironment favorably for survival. We believe that our findings will contribute to the development of new therapeutic strategies for glioblastoma.
en-copyright=
kn-copyright=

en-aut-name=AsakaYutaro
en-aut-sei=Asaka
en-aut-mei=Yutaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MasumotoToshio
en-aut-sei=Masumoto
en-aut-mei=Toshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UnedaAtsuhito
en-aut-sei=Uneda
en-aut-mei=Atsuhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ChinVanessa D.
en-aut-sei=Chin
en-aut-mei=Vanessa D.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OtaniYusuke
en-aut-sei=Otani
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=PenaTirso
en-aut-sei=Pena
en-aut-mei=Tirso
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KatayamaHaruyoshi
en-aut-sei=Katayama
en-aut-mei=Haruyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ItanoTakuto
en-aut-sei=Itano
en-aut-mei=Takuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=AndoTeruhiko
en-aut-sei=Ando
en-aut-mei=Teruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HuangRongsheng
en-aut-sei=Huang
en-aut-mei=Rongsheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=FujimuraAtsushi
en-aut-sei=Fujimura
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

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

affil-num=2
en-affil=Division of Health Administration and Promotion, Department of Social Medicine, Faculty of Medicine, Tottori University
kn-affil=

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

affil-num=4
en-affil=UMass Chan Medical School, UMass Memorial Medical Center
kn-affil=

affil-num=5
en-affil=Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School
kn-affil=

affil-num=6
en-affil=Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School
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=Department of Orthopaedic Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Trauma Orthopedics, The Second Hospital of Dalian Medical University
kn-affil=

affil-num=11
en-affil=Department of Cellular Physiology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=Adrenoceptors
kn-keyword=Adrenoceptors
en-keyword=Glioma stem-like cells
kn-keyword=Glioma stem-like cells
en-keyword=Differentiated glioma cells
kn-keyword=Differentiated glioma cells
en-keyword=Noradrenaline
kn-keyword=Noradrenaline
en-keyword=Cellular plasticity
kn-keyword=Cellular plasticity
END

start-ver=1.4
cd-journal=joma
no-vol=213
cd-vols=
no-issue=
article-no=
start-page=128
end-page=137
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The potential mechanism maintaining transactive response DNA binding protein 43?kDa in the mouse stroke model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The disruption of transactive response DNA binding protein 43?kDa (TDP-43) shuttling leads to the depletion of nuclear localization and the cytoplasmic accumulation of TDP-43. We aimed to evaluate the mechanism underlying the behavior of TDP-43 in ischemic stroke. Adult male C57BL/6?J mice were subjected to 30 or 60?min of transient middle cerebral artery occlusion (tMCAO), and examined at 1, 6, and 24?h post reperfusion. Immunostaining was used to evaluate the expression of TDP-43, G3BP1, HDAC6, and RAD23B. The total and cytoplasmic number of TDP-43?positive cells increased compared with sham operation group and peaked at 6?h post reperfusion after tMCAO. The elevated expression of G3BP1 protein peaked at 6?h after reperfusion and decreased at 24?h after reperfusion in ischemic mice brains. We also observed an increase of expression level of HDAC6 and the number of RAD23B-positive cells increased after tMCAO. RAD23B was colocalized with TDP-43 24?h after tMCAO. We proposed that the formation of stress granules might be involved in the mislocalization of TDP-43, based on an evaluation of G3BP1 and HDAC6. Subsequently, RAD23B, may also contribute to the downstream degradation of mislocalized TDP-43 in mice tMCAO model.
en-copyright=
kn-copyright=

en-aut-name=BianYuting
en-aut-sei=Bian
en-aut-mei=Yuting
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FukuiYusuke
en-aut-sei=Fukui
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Ota-ElliottRicardo Satoshi
en-aut-sei=Ota-Elliott
en-aut-mei=Ricardo Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HuXinran
en-aut-sei=Hu
en-aut-mei=Xinran
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SunHongming
en-aut-sei=Sun
en-aut-mei=Hongming
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=BianZhihong
en-aut-sei=Bian
en-aut-mei=Zhihong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ZhaiYun
en-aut-sei=Zhai
en-aut-mei=Yun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YuHaibo
en-aut-sei=Yu
en-aut-mei=Haibo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HuXiao
en-aut-sei=Hu
en-aut-mei=Xiao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AnHangping
en-aut-sei=An
en-aut-mei=Hangping
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=LiuHongzhi
en-aut-sei=Liu
en-aut-mei=Hongzhi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
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=12
ORCID=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

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

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

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

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

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

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

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

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

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

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

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

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

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

affil-num=14
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=TDP-43
kn-keyword=TDP-43
en-keyword=ALS
kn-keyword=ALS
en-keyword=RNA-binding protein
kn-keyword=RNA-binding protein
en-keyword=Mislocalization
kn-keyword=Mislocalization
en-keyword=G3BP1
kn-keyword=G3BP1
en-keyword=HDAC6
kn-keyword=HDAC6
en-keyword=RAD23B
kn-keyword=RAD23B
en-keyword=tMCAO
kn-keyword=tMCAO
END

start-ver=1.4
cd-journal=joma
no-vol=17
cd-vols=
no-issue=4
article-no=
start-page=e82348
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250416
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Bilateral Scleritis and Neutrophilic Dermatosis With Cytogenetic Chromosomal Aberrancy Related to Pyoderma Gangrenosum: A Case Report of a 20-Year Follow-Up
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pyoderma gangrenosum is a non-infectious autoimmune disease with skin plaques and ulcers in the entity of neutrophilic dermatosis and may have a background of myelodysplastic syndromes. This study reported a 20-year follow-up of a patient with pyoderma gangrenosum and scleritis who showed chromosomal aberrancy from the initial phase and later in the course developed thrombocythemia. A 51-year-old man presented with widespread indurated erythematous plaques with scaling and pustules on the forehead, bilateral eyelids, and nasal bridge, in addition to nodular scleritis in the left eye and ulcer formation of the plaques in the lower legs. Skin biopsy revealed massive dermal infiltration mainly with neutrophils in the absence of neutrophilic vasculitis. Suspected of myelodysplastic syndromes, bone marrow biopsy was normal, while chromosomal aberrancy, 46, XY, del (20) (q11q13.3), was detected. In the diagnosis of neutrophilic dermatosis, probably of pyoderma gangrenosum, he began to have oral prednisolone 20 mg daily and colchicine 1 mg daily, leading to the subsidence of skin lesions. Four months later, he developed nodular scleritis in the right eye and began to use topical 0.1% betamethasone in both eyes. He was stable with only prednisolone 12.5 mg daily until the age of 55.5 years, when he showed an increase of serum lactate dehydrogenase. The bone marrow aspirate disclosed neither blast cell increase nor atypical cells. The same chromosomal aberrancy was repeatedly detected. One year later, he developed breathing difficulty and underwent tracheostomy. Laryngeal lesion biopsy disclosed squamous cell papilloma with human papillomavirus-6. At 60 years old, he showed marginal corneal infiltration in the left eye, and at 61 years old, hypopyon in the right eye. Platelets tended to increase up to 1000 × 103/?L, and bone marrow examinations were recommended but refused by the patient. At the latest follow-up at 71 years old, he was ambulatory in health and stable with a tracheostomy cannula. In conclusion, pyoderma gangrenosum with scleritis occurred in an undetermined hematological malignancy with chromosomal aberrancy.
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=AsadaNoboru
en-aut-sei=Asada
en-aut-mei=Noboru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ObikaMikako
en-aut-sei=Obika
en-aut-mei=Mikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OmichiRyotaro
en-aut-sei=Omichi
en-aut-mei=Ryotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
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 Hematology and Oncology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

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

affil-num=5
en-affil=Department of Otolaryngology, Head and Neck Surgery, 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=corneal infiltration
kn-keyword=corneal infiltration
en-keyword=hypopyon
kn-keyword=hypopyon
en-keyword=myelodysplastic syndromes
kn-keyword=myelodysplastic syndromes
en-keyword=neutrophilic dermatosis
kn-keyword=neutrophilic dermatosis
en-keyword=peripheral keratitis
kn-keyword=peripheral keratitis
en-keyword=pyoderma gangrenosum
kn-keyword=pyoderma gangrenosum
en-keyword=scleritis
kn-keyword=scleritis
en-keyword=sweet syndrome
kn-keyword=sweet syndrome
END

start-ver=1.4
cd-journal=joma
no-vol=50
cd-vols=
no-issue=1
article-no=
start-page=100
end-page=107
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=Investigating the Effects of Reconstruction Conditions on Image Quality and Radiomic Analysis in Photon-counting Computed Tomography
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction:Photon-counting computed tomography (CT) is equipped with an adaptive iterative reconstruction method called quantum iterative reconstruction (QIR), which allows the intensity to be changed during image reconstruction. It is known that the reconstruction conditions of CT images affect the analysis results when performing radiomic analysis. The aim of this study is to investigate the effect of QIR intensity on image quality and radiomic analysis of renal cell carcinoma (RCC).<br>
Materials and Methods:The QIR intensities were selected as off, 2 and 4. The image quality evaluation items considered were task-based transfer function (TTF), noise power spectrum (NPS), and low-contrast object specific contrast-to-noise ratio (CNRLO). The influence on radiomic analysis was assessed using the discrimination accuracy of clear cell RCC.<br>
Results:For image quality evaluation, TTF and NPS values were lower and CNRLO values were higher with increasing QIR intensity; for radiomic analysis, sensitivity, specificity, and accuracy were higher with increasing QIR intensity. Principal component analysis and receiver operating characteristics analysis also showed higher values with increasing QIR intensity.<br>
Conclusion:It was confirmed that the intensity of the QIR intensity affects both the image quality and the radiomic analysis.
en-copyright=
kn-copyright=

en-aut-name=OhataMiyu
en-aut-sei=Ohata
en-aut-mei=Miyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FukuiRyohei
en-aut-sei=Fukui
en-aut-mei=Ryohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MorimitsuYusuke
en-aut-sei=Morimitsu
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KobayashiDaichi
en-aut-sei=Kobayashi
en-aut-mei=Daichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamauchiTakatsugu
en-aut-sei=Yamauchi
en-aut-mei=Takatsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AkagiNoriaki
en-aut-sei=Akagi
en-aut-mei=Noriaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HondaMitsugi
en-aut-sei=Honda
en-aut-mei=Mitsugi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HayashiAiko
en-aut-sei=Hayashi
en-aut-mei=Aiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HasegawaKoshi
en-aut-sei=Hasegawa
en-aut-mei=Koshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KidaKatsuhiro
en-aut-sei=Kida
en-aut-mei=Katsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=GotoSachiko
en-aut-sei=Goto
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=HirakiTakao
en-aut-sei=Hiraki
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

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

affil-num=2
en-affil=Department of Radiological Technology, Faculty of Health Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Division of Radiological Technology, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Division of Radiological Technology, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Division of Radiological Technology, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Division of Radiological Technology, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Division of Radiological Technology, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Radiology, Hiroshima University Hospital
kn-affil=

affil-num=9
en-affil=Department of Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Radiological Technology, Faculty of Health Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Radiological Technology, Faculty of Health Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Radiology, Faculty of Medicine, Dentistry and Pharmaceutical, Okayama University
kn-affil=
en-keyword=Image quality
kn-keyword=Image quality
en-keyword=photon-counting computed tomography
kn-keyword=photon-counting computed tomography
en-keyword=quantum iterative reconstruction
kn-keyword=quantum iterative reconstruction
en-keyword=radiomics
kn-keyword=radiomics
en-keyword=renal cell carcinoma
kn-keyword=renal cell carcinoma
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=10462
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250326
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Gingipain regulates isoform switches of PD-L1 in macrophages infected with Porphyromonas gingivalis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Periodontal pathogen Porphyromonas gingivalis (P. gingivalis) is believed to possess immune evasion capabilities, but it remains unclear whether this immune evasion is related to host gene alternative splicing (AS). In this study, RNA-sequencing revealed significant changes in both AS landscape and transcriptomic profile of macrophages following P. gingivalis infection with/without knockout of gingipain (a unique toxic protease of P. gingivalis). P. gingivalis infection increased the PD-L1 transcripts expression and selectively upregulated a specific coding isoform that more effectively binds to PD-1 on T cells, thereby inhibiting immune function. Biological experiments also detected AS switch of PD-L1 in P. gingivalis-infected or gingipain-treated macrophages. AlphaFold 3 predictions indicated that the protein docking compatibility between PD-1 and P. gingivalis-upregulated PD-L1 isoform was over 80% higher than another coding isoform. These findings suggest that P. gingivalis employs gingipain to modulate the AS of PD-L1, facilitating immune evasion.
en-copyright=
kn-copyright=

en-aut-name=ZhengYilin
en-aut-sei=Zheng
en-aut-mei=Yilin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=WengYao
en-aut-sei=Weng
en-aut-mei=Yao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SitosariHeriati
en-aut-sei=Sitosari
en-aut-mei=Heriati
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HeYuhan
en-aut-sei=He
en-aut-mei=Yuhan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ZhangXiu
en-aut-sei=Zhang
en-aut-mei=Xiu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ShiotsuNoriko
en-aut-sei=Shiotsu
en-aut-mei=Noriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FukuharaYoko
en-aut-sei=Fukuhara
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IkegameMika
en-aut-sei=Ikegame
en-aut-mei=Mika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
ORCID=

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

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

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

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

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

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

affil-num=7
en-affil=Comprehensive Dental Clinic, Okayama University Hospital, Okayama University
kn-affil=

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

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

affil-num=10
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University
kn-affil=
en-keyword=Porphyromonas gingivalis
kn-keyword=Porphyromonas gingivalis
en-keyword=Gingipain
kn-keyword=Gingipain
en-keyword=Macrophage
kn-keyword=Macrophage
en-keyword=Alternative splicing
kn-keyword=Alternative splicing
en-keyword=PD-L1
kn-keyword=PD-L1
en-keyword=Immune evasion
kn-keyword=Immune evasion
END

start-ver=1.4
cd-journal=joma
no-vol=96
cd-vols=
no-issue=3
article-no=
start-page=033907
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Development of density measurement at high pressure and high temperature using the x-ray absorption method combined with laser-heated diamond anvil cell
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The densities of liquid materials at high pressures and high temperatures are important information to understand the elastic behavior of liquids at extreme conditions, which is closely related to the formation and evolution processes of the Earth and planetary interiors. The x-ray absorption method is an effective method to measure the density of non-crystalline materials at high pressures. However, the temperature condition of the x-ray absorption method using a diamond anvil cell (DAC) has been limited to 720 K to date. To significantly expand the measurable temperature condition of this method, in this study, we developed a density measurement technique using the x-ray absorption method in combination with a laser-heated DAC. The density of solid Ni was measured up to 26 GPa and 1800 K using the x-ray absorption method and evaluated by comparison with the density obtained from the x-ray diffraction. The density of solid Ni with a thickness >17 μm was determined with an accuracy of 0.01%?2.2% (0.001?0.20 g/cm3) and a precision of 0.8%?1.8% (0.07?0.16 g/cm3) in the x-ray absorption method. The density of liquid Ni was also determined to be 8.70 ± 0.15?8.98 ± 0.38 g/cm3 at 16?23 GPa and 2230?2480 K. Consequently, the temperature limit of the x-ray absorption method can be expanded from 720 to 2480 K by combining it with a laser-heated DAC in this study.
en-copyright=
kn-copyright=

en-aut-name=TerasakiHidenori
en-aut-sei=Terasaki
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KaminaHiroyuki
en-aut-sei=Kamina
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KawaguchiSaori I.
en-aut-sei=Kawaguchi
en-aut-mei=Saori I.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoTadashi
en-aut-sei=Kondo
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MoriokaKo
en-aut-sei=Morioka
en-aut-mei=Ko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TsuruokaRyo
en-aut-sei=Tsuruoka
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakuraiMoe
en-aut-sei=Sakurai
en-aut-mei=Moe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YonedaAkira
en-aut-sei=Yoneda
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KamadaSeiji
en-aut-sei=Kamada
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HiraoNaohisa
en-aut-sei=Hirao
en-aut-mei=Naohisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Earth Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Earth Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Japan Synchrotron Radiation Research Institute, SPring-8
kn-affil=

affil-num=4
en-affil=Department of Earth and Space Science, Osaka University
kn-affil=

affil-num=5
en-affil=Department of Earth Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Earth and Space Science, Osaka University
kn-affil=

affil-num=7
en-affil=Department of Earth Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Earth and Space Science, Osaka University
kn-affil=

affil-num=9
en-affil=AD Science Incorporation
kn-affil=

affil-num=10
en-affil=Japan Synchrotron Radiation Research Institute, SPring-8
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=6
article-no=
start-page=2485
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=Vesicular Glutamate Transporter 3 Is Involved in Glutamatergic Signalling in Podocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Glomerular podocytes act as a part of the filtration barrier in the kidney. The activity of this filter is regulated by ionotropic and metabotropic glutamate receptors. Adjacent podocytes can potentially release glutamate into the intercellular space; however, little is known about how podocytes release glutamate. Here, we demonstrated vesicular glutamate transporter 3 (VGLUT3)-dependent glutamate release from podocytes. Immunofluorescence analysis revealed that rat glomerular podocytes and an immortal mouse podocyte cell line (MPC) express VGLUT1 and VGLUT3. Consistent with this finding, quantitative RT-PCR revealed the expression of VGLUT1 and VGLUT3 mRNA in undifferentiated and differentiated MPCs. In addition, the exocytotic proteins vesicle-associated membrane protein 2, synapsin 1, and synaptophysin 1 were present in punctate patterns and colocalized with VGLUT3 in MPCs. Interestingly, approximately 30% of VGLUT3 colocalized with VGLUT1. By immunoelectron microscopy, VGLUT3 was often observed around clear vesicle-like structures in differentiated MPCs. Differentiated MPCs released glutamate following depolarization with high potassium levels and after stimulation with the muscarinic agonist pilocarpine. The depletion of VGLUT3 in MPCs by RNA interference reduced depolarization-dependent glutamate release. These results strongly suggest that VGLUT3 is involved in glutamatergic signalling in podocytes and may be a new drug target for various kidney diseases.
en-copyright=
kn-copyright=

en-aut-name=NishiiNaoko
en-aut-sei=Nishii
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawaiTomoko
en-aut-sei=Kawai
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YasuokaHiroki
en-aut-sei=Yasuoka
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AbeTadashi
en-aut-sei=Abe
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TatsumiNanami
en-aut-sei=Tatsumi
en-aut-mei=Nanami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HaradaYuika
en-aut-sei=Harada
en-aut-mei=Yuika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MiyajiTakaaki
en-aut-sei=Miyaji
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=LiShunai
en-aut-sei=Li
en-aut-mei=Shunai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TsukanoMoemi
en-aut-sei=Tsukano
en-aut-mei=Moemi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
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=11
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=12
ORCID=

en-aut-name=TakeiKohji
en-aut-sei=Takei
en-aut-mei=Kohji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
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=14
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 Cell Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

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

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

affil-num=6
en-affil=Department of Genomics and Proteomics, Advanced Science Research Center, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Genomics and Proteomics, Advanced Science Research Center, Okayama University
kn-affil=

affil-num=8
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Central Research Laboratory, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

affil-num=14
en-affil=Department of Neuroscience, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=VGLUT3
kn-keyword=VGLUT3
en-keyword=glutamate
kn-keyword=glutamate
en-keyword=podocyte
kn-keyword=podocyte
en-keyword=glutamatergic transmission
kn-keyword=glutamatergic transmission
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=6
article-no=
start-page=2713
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250318
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Involvement of a Novel Variant of FGFR1 Detected in an Adult Patient with Kallmann Syndrome in Regulation of Gonadal Steroidogenesis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Fibroblast growth factor receptor 1 (FGFR1), also known as KAL2, is a tyrosine kinase receptor, and variants of FGFR1 have been detected in patients with Kallmann syndrome (KS), which is a congenital developmental disorder characterized by central hypogonadism and anosmia. Herein, we report an adult case of KS with a novel variant of FGFR1. A middle-aged male was referred for a compression fracture of a lumbar vertebra. It was shown that he had severe osteoporosis, anosmia, gynecomastia, and a past history of operations for cryptorchidism. Endocrine workup using pituitary and gonadal stimulation tests revealed the presence of both primary and central hypogonadism. Genetic testing revealed a novel variant of FGFR1 (c.2197_2199dup, p.Met733dup). To identify the pathogenicity of the novel variant and the clinical significance for the gonads, we investigated the effects of the FGFR1 variant on the downstream signaling of FGFR1 and gonadal steroidogenesis by using human steroidogenic granulosa cells. It was revealed that the transfection of the variant gene significantly impaired FGFR1 signaling, detected through the downregulation of SPRY2, compared with that of the case of the forced expression of wild-type FGFR1, and that the existence of the variant gene apparently altered the expression of key steroidogenic factors, including StAR and aromatase, in the gonad. The results suggested that the novel variant of FGFR1 detected in the patient with KS was linked to the impairment of FGFR1 signaling, as well as the alteration of gonadal steroidogenesis, leading to the pathogenesis of latent primary hypogonadism.
en-copyright=
kn-copyright=

en-aut-name=SoejimaYoshiaki
en-aut-sei=Soejima
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OtsukaYuki
en-aut-sei=Otsuka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KawaguchiMarina
en-aut-sei=Kawaguchi
en-aut-mei=Marina
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=YamamotoKoichiro
en-aut-sei=Yamamoto
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakanoYasuhiro
en-aut-sei=Nakano
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YasudaMiho
en-aut-sei=Yasuda
en-aut-mei=Miho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

en-aut-name=UedaKeigo
en-aut-sei=Ueda
en-aut-mei=Keigo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HasegawaKosei
en-aut-sei=Hasegawa
en-aut-mei=Kosei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=IwataNahoko
en-aut-sei=Iwata
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
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=12
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=

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

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

affil-num=10
en-affil=Department of Pediatrics, Okayama University Hospital
kn-affil=

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

affil-num=12
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=fibroblast growth factor receptor 1 (FGFR1)
kn-keyword=fibroblast growth factor receptor 1 (FGFR1)
en-keyword=gynecomastia
kn-keyword=gynecomastia
en-keyword=Kallmann syndrome (KS)
kn-keyword=Kallmann syndrome (KS)
en-keyword=osteoporosis and steroidogenesis
kn-keyword=osteoporosis and steroidogenesis
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=19
cd-vols=
no-issue=
article-no=
start-page=1551700
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250305
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Acetoacetate, a ketone body, attenuates neuronal bursts in acutely-induced epileptiform slices of the mouse hippocampus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The ketogenic diet increases ketone bodies (beta-hydroxybutyrate and acetoacetate) in the brain, and ameliorates epileptic seizures in vivo. However, ketone bodies exert weak or no effects on electrical activity in rodent hippocampal slices. Especially, it remains unclear what kinds of conditions are required to strengthen the actions of ketone bodies in hippocampal slices. In the present study, we examined the effects of acetoacetate on hippocampal pyramidal cells in normal slices and epileptiform slices of mice. By using patch-clamp recordings from CA1 pyramidal cells, we first confirmed that acetoacetate did not change the membrane potentials and intrinsic properties of pyramidal cells in normal slices. However, we found that acetoacetate weakened spontaneous epileptiform bursts in pyramidal cells of epileptiform slices, which were acutely induced by applying convulsants to normal slices. Interestingly, acetoacetate did not change the frequency of the epileptiform bursts, but attenuated individual epileptiform bursts. We finally examined the effects of acetoacetate on excitatory synaptic barrages during epileptiform activity, and found that acetoacetate weakened epileptiform bursts by reducing synchronous synaptic inputs. These results show that acetoacetate attenuated neuronal bursts in epileptiform slices, but did not affect neuronal activity in normal slices, which leads to seizure-selective actions of ketone bodies.
en-copyright=
kn-copyright=

en-aut-name=WenHao
en-aut-sei=Wen
en-aut-mei=Hao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SadaNagisa
en-aut-sei=Sada
en-aut-mei=Nagisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=InoueTsuyoshi
en-aut-sei=Inoue
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

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

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

affil-num=3
en-affil=Department of Biophysical Chemistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=epilepsy
kn-keyword=epilepsy
en-keyword=ketone body
kn-keyword=ketone body
en-keyword=ketogenic diet
kn-keyword=ketogenic diet
en-keyword=hippocampus
kn-keyword=hippocampus
en-keyword=slice physiology
kn-keyword=slice physiology
en-keyword=patch-clamp recording
kn-keyword=patch-clamp recording
END

start-ver=1.4
cd-journal=joma
no-vol=85
cd-vols=
no-issue=6
article-no=
start-page=1082
end-page=1096
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250314
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Myeloid Cells Induce Infiltration and Activation of B Cells and CD4+ T Follicular Helper Cells to Sensitize Brain Metastases to Combination Immunotherapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Brain metastasis is a poor prognostic factor in patients with cancer. Despite showing efficacy in many extracranial tumors, immunotherapy with anti?PD-1 mAb or anti?CTLA4 mAb seems to be less effective against intracranial tumors. Promisingly, recent clinical studies have reported that combination therapy with anti?PD-1 and anti?CTLA4 mAbs has a potent antitumor effect on brain metastasis, highlighting the need to elucidate the detailed mechanisms controlling the intracranial tumor microenvironment (TME) to develop effective immunotherapeutic strategies. In this study, we analyzed the tumor-infiltrating lymphocytes in murine models of brain metastasis that responded to anti?CTLA4 and anti?PD-1 mAbs. Activated CD4+ T follicular helper (TFH) cells with high CTLA4 expression characteristically infiltrated the intracranial TME, which were activated by combination anti?CTLA4 and anti?PD-1 treatment. The loss of TFH cells suppressed the additive effect of CTLA4 blockade on anti?PD-1 mAb. B-cell?activating factor belonging to the TNF family (BAFF) and a proliferation-inducing ligand (APRIL) produced by abundant myeloid cells, particularly CD80hiCD206lo proinflammatory M1-like macrophages, in the intracranial TME induced B-cell and TFH-cell infiltration and activation. Furthermore, the intracranial TME of patients with non?small cell lung cancer featured TFH- and B-cell infiltration as tertiary lymphoid structures. Together, these findings provide insights into the immune cell cross-talk in the intracranial TME that facilitates an additive antitumor effect of CTLA4 blockade with anti?PD-1 treatment, supporting the potential of a combination immunotherapeutic strategy for brain metastases.<br>
Significance: B-cell and CD4+ T follicular helper cell activation via BAFF/APRIL from abundant myeloid cells in the intracranial tumor microenvironment enables a combinatorial effect of CTLA4 and PD-1 blockade in brain metastases.
en-copyright=
kn-copyright=

en-aut-name=NinomiyaToshifumi
en-aut-sei=Ninomiya
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KemmotsuNaoya
en-aut-sei=Kemmotsu
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MukoharaFumiaki
en-aut-sei=Mukohara
en-aut-mei=Fumiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MagariMasaki
en-aut-sei=Magari
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyamotoAi
en-aut-sei=Miyamoto
en-aut-mei=Ai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UedaYouki
en-aut-sei=Ueda
en-aut-mei=Youki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IshinoTakamasa
en-aut-sei=Ishino
en-aut-mei=Takamasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NagasakiJoji
en-aut-sei=Nagasaki
en-aut-mei=Joji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=FujiwaraTomohiro
en-aut-sei=Fujiwara
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YamamotoHidetaka
en-aut-sei=Yamamoto
en-aut-mei=Hidetaka
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=TachibanaKota
en-aut-sei=Tachibana
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=13
ORCID=

en-aut-name=OtaniYoshihiro
en-aut-sei=Otani
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=TanakaShota
en-aut-sei=Tanaka
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
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=16
ORCID=

en-aut-name=OkamotoIsamu
en-aut-sei=Okamoto
en-aut-mei=Isamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=TogashiYosuke
en-aut-sei=Togashi
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

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

affil-num=2
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

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

affil-num=5
en-affil=Medical Protein Engineering, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

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

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

affil-num=11
en-affil=Department of Medical Oncology, Kindai University Faculty of Medicine
kn-affil=

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

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

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

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

affil-num=16
en-affil=Department of General Thoracic Surgery, Breast and Endocrinological Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Science, Okayama University
kn-affil=

affil-num=17
en-affil=Department of Respiratory Medicine, Graduate School of Medical Sciences, Kyushu University
kn-affil=

affil-num=18
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=1757
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=Keratinocyte-driven dermal collagen formation in the axolotl skin
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Type I collagen is a major component of the dermis and is formed by dermal fibroblasts. The development of dermal collagen structures has not been fully elucidated despite the major presence and importance of the dermis. This lack of understanding is due in part to the opacity of mammalian skin and it has been an obstacle to cosmetic and medical developments. We reveal the process of dermal collagen formation using the highly transparent skin of the axolotl and fluorescent collagen probes. We clarify that epidermal cells, not dermal fibroblasts, contribute to dermal collagen formation. Mesenchymal cells (fibroblasts) play a role in modifying the collagen fibers already built by keratinocytes. We confirm that collagen production by keratinocytes is a widely conserved mechanism in other model organisms. Our findings warrant a change in the current consensus about dermal collagen formation and could lead to innovations in cosmetology and skin medication.
en-copyright=
kn-copyright=

en-aut-name=OhashiAyaka
en-aut-sei=Ohashi
en-aut-mei=Ayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KurodaJunpei
en-aut-sei=Kuroda
en-aut-mei=Junpei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoYohei
en-aut-sei=Kondo
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KameiYasuhiro
en-aut-sei=Kamei
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NonakaShigenori
en-aut-sei=Nonaka
en-aut-mei=Shigenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FurukawaSaya
en-aut-sei=Furukawa
en-aut-mei=Saya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamamotoSakiya
en-aut-sei=Yamamoto
en-aut-mei=Sakiya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SatohAkira
en-aut-sei=Satoh
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Frontier Biosciences, Osaka University
kn-affil=

affil-num=4
en-affil=Center for One Medicine Innovative Translational Research (COMIT), Nagoya University
kn-affil=

affil-num=5
en-affil=Laboratory for Biothermology, National Institute for Basic Biology
kn-affil=

affil-num=6
en-affil=The Graduate University for Advanced Studies (SOKENDAI)
kn-affil=

affil-num=7
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=9
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=752
cd-vols=
no-issue=
article-no=
start-page=151481
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Discovery of myeloid zinc finger (MZF) 1 nuclear bodies
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Myeloid zinc finger 1 (MZF1) is a multifaceted transcription factor that can act either as a transcriptional activator or a gene repressor. We examined its production of nuclear bodies (NBs) and subcellular localization. Proteomic and protein?protein interaction analysis were used to identify its cofactors and interactions. These revealed the presence of MZF1-NBs (intranuclear oligomers containing MZF1). MZF-NBs are similar to some other nuclear bodies, notably promyelocytic leukemia (PML) -NBs in terms of size and morphology. However the two structures appear to be different. MZF-NBs and PML-NBs were found to associate in the nucleus. Both MZF1 and PML are SUMO1-SUMOylated in PC-3 cells. Sumoylated MZF1 can interact with proteins containing SUMO-interaction motifs (SIM) through SUMO-SIM interaction. Interactome analysis revealed that its NBs participate in the stress response (TPR and UBAP2L), protein folding (CALR and ANKRD40), transcription, post-translational modification (TRIM33, ACOT7, CAMK2D, and CAMK2G), and RNA binding (ALURBP and CPSF5).

en-copyright=
kn-copyright=

en-aut-name=EguchiTakanori
en-aut-sei=Eguchi
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=CalderwoodStuart K.
en-aut-sei=Calderwood
en-aut-mei=Stuart K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

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

affil-num=2
en-affil=Division of Molecular and Cellular Biology, Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School
kn-affil=
en-keyword=Myeloid zinc finger 1
kn-keyword=Myeloid zinc finger 1
en-keyword=MZF1
kn-keyword=MZF1
en-keyword=Nuclear body
kn-keyword=Nuclear body
en-keyword=PML
kn-keyword=PML
en-keyword=Sumoylation
kn-keyword=Sumoylation
en-keyword=SCAN domain protein
kn-keyword=SCAN domain protein
END

start-ver=1.4
cd-journal=joma
no-vol=2
cd-vols=
no-issue=9
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20160908
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=S-nitrosylation of laforin inhibits its phosphatase activity and is implicated in Lafora disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Recently, the relation between S-nitrosylation by nitric oxide (NO), which is over?produced under pathological conditions and neurodegenerative diseases, includingAlzheimer’s and Parkinson’s diseases, has become a focus of attention. Although mostcases of Parkinson’s disease are known to be caused by mutations in the Parkin gene, arecent finding has indicated that S-nitrosylation of Parkin affects its enzymatic activityand leads to the Parkinsonian phenotype. Therefore, it is important to understand thefunction of S-nitrosylated proteins in the pathogenesis of neurodegenerative diseases.Lafora disease (LD, OMIM 254780) is a neurodegenerative disease characterized by theaccumulation of insoluble glucans called Lafora bodies (LBs). LD is caused by mutationsin genes that encode the glucan phosphatase, Laforin, or the E3 ubiquitin ligase, Malin.In this study, we hypothesized that LD may be caused by S-nitrosylation of Laforin,which is similar to the finding that Parkinson’s disease is caused by S-nitrosylation ofParkin. To test this hypothesis, we first determined whether Laforin was S-nitrosylatedusing a biotin switch assay, and compared the three main functions of unmodified andS-nitrosylated Laforin, namely glucan- and Malin-binding activity and phosphataseactivity. Furthermore, we examined whether the numbers of LBs were changed byNO in the cells expressing wild-type Laforin. Here, we report for the first time thatS-nitrosylation of Laforin inhibited its phosphatase activity and that LB formation wasincreased by an NO donor. Our results suggest a possible hypothesis for LD pathogenesis; that is, the decrease in phosphatase activity of Laforin by S-nitrosylation leads toincreased LB formation. Therefore, LD may be caused not only by mutations in theLaforin or Malin genes, but also by the S-nitrosylation of Laforin.

en-copyright=
kn-copyright=

en-aut-name=ToyotaRikako
en-aut-sei=Toyota
en-aut-mei=Rikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HonjoYasuko
en-aut-sei=Honjo
en-aut-mei=Yasuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ImajoRisa
en-aut-sei=Imajo
en-aut-mei=Risa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

affil-num=1
en-affil=
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University; Research Institute for Radiation Biology and Medicine, Hiroshima University
kn-affil=

affil-num=3
en-affil=Graduate School of Natural Science and Technology, Okayama University; Research Institute for Radiation Biology and Medicine, Hiroshima University
kn-affil=

affil-num=4
en-affil=Graduate School of Natural Science and Technology, Okayama University; Research Institute for Radiation Biology and Medicine, Hiroshima University
kn-affil=
en-keyword=S-Nitrosylation Of Laforin
kn-keyword=S-Nitrosylation Of Laforin
en-keyword=Post-Translational Modification 
kn-keyword=Post-Translational Modification 
en-keyword=Nitrosylation
kn-keyword=Nitrosylation
en-keyword=Phosphatase
kn-keyword=Phosphatase
en-keyword=Glucan-Binding
kn-keyword=Glucan-Binding
END

start-ver=1.4
cd-journal=joma
no-vol=33
cd-vols=
no-issue=4
article-no=
start-page=252
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250305
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Characteristics of oral mucositis in patients undergoing haploidentical stem cell transplantation with posttransplant cyclophosphamide: marked difference between busulfan and melphalan regimens
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose This study was performed to examine the effects of conditioning regimens on oral mucositis in haploidentical (haplo) donor hematopoietic stem cell transplantation (HSCT) with posttransplant cyclophosphamide (PTCy).<br>
Methods Thirty consecutive patients (male, 23; female, 7; 18?68 years, median, 59 years) undergoing haplo-HSCT with PTCy using one of three conditioning regimens?reduced intensity conditioning (RIC)-melphalan (Mel); RIC-Busulfan (Bu); and myeloablative conditioning (MAC)-Bu?were enrolled in this study. Data on the WHO grade of oral mucositis (day???7 to?+?20) were collected retrospectively. The incidences of ulcerative and severe mucositis (Grade 2?4 and Grade 3?4, respectively) were compared between the three groups.<br>
Results Ulcerative mucositis occurred in 0% (0/10) of patients in the RIC-Mel group, 57.1% (4/7) in the RIC-Bu group, and 100% (13/13) in the MAC-Bu group. The differences between the RIC-Mel and RIC-Bu groups and between the RIC-Bu and MAC-Bu groups were significant (all P?<?0.05). Severe mucositis occurred in 57.1% (4/7) of patients in the RIC-Bu group and 100% (13/13) of patients in the MAC-Bu group, and the difference was significant (P?<?0.05). The rates of ulcerative mucositis (??grade 2) and of severe mucositis (??grade 3) were significantly higher in the MAC-Bu group than the RIC-Bu group on days 10, 13, 15, and 16 and on days 10, 14, 15, and 16, respectively (all P?<?0.05).<br>
Conclusion The risk of oral mucositis in patients undergoing haplo-HSCT with PTCy is highest with the MAC-Bu conditioning regimen, followed by RIC-Bu, and lowest with RIC-Mel.
en-copyright=
kn-copyright=

en-aut-name=OguraSaki
en-aut-sei=Ogura
en-aut-mei=Saki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SogaYoshihiko
en-aut-sei=Soga
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
ORCID=

en-aut-name=MiuraRumi
en-aut-sei=Miura
en-aut-mei=Rumi
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=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=

affil-num=1
en-affil=Division of Dental Hygienist, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Division of Hospital Dentistry, 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=Division of Dental Hygienist, Okayama University Hospital
kn-affil=

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

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

affil-num=7
en-affil=Division of Dental Hygienist, Okayama University Hospital
kn-affil=
en-keyword=Oral mucositis
kn-keyword=Oral mucositis
en-keyword=Hematopoietic cell transplantation
kn-keyword=Hematopoietic cell transplantation
en-keyword=Posttransplant cyclophosphamide
kn-keyword=Posttransplant cyclophosphamide
en-keyword=Busulfan
kn-keyword=Busulfan
en-keyword=Melphalan
kn-keyword=Melphalan
END

start-ver=1.4
cd-journal=joma
no-vol=34
cd-vols=
no-issue=1
article-no=
start-page=35
end-page=40
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=2025
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Evaluation of CT Findings in Squamous and Non-Squamous Cell Carcinomas of the Maxillary Sinus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The aim of the present study was to compare CT images between squamous cell carcinoma (SCC) and non-SCC found in the maxillary sinus, and to identify features that could be used to differentiate between SCC and non-SCC. Patients who visited the Faculty of Dentistry, Okayama University Hospital, between April 2007 and March 2023, underwent head and neck CT, and had tumors extending into the maxillary sinus that were diagnosed histopathologically as malignancy, were enrolled. The main seat of the mass, bony changes in the maxillary sinus wall, and extension into the surrounding area were assessed. These imaging features were evaluated according to SCC or non-SCC, and the characteristics of the two classes were assessed. Comparisons between the two groups were made using the Fisher exact probability test. There were 11 cases each of SCC and non-SCC. In 11 SCC and 7 non-SCC cases, the main seat of the mass occupied the entire maxillary sinus. The frequency of mass occupying the whole sinus was significantly higher in SCC than in non-SCC (p<0.05). Bone-thickening type disease was found only in squamous cell carcinoma 4/11 (36.4%), with there being a significant difference between SCC and non-SCC (p<0.05). Occupancy of the entire maxillary sinus by the mass and bone thickening on CT images were useful for differentiating between SCC and non-SCC arising in the maxillary sinus.
en-copyright=
kn-copyright=

en-aut-name=AsaumiYuka
en-aut-sei=Asaumi
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujikuraMamiko
en-aut-sei=Fujikura
en-aut-mei=Mamiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HisatomiMiki
en-aut-sei=Hisatomi
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=E. Al-HammadWlla
en-aut-sei=E. Al-Hammad
en-aut-mei=Wlla
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakeshitaYohei
en-aut-sei=Takeshita
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OkadaShunsuke
en-aut-sei=Okada
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KawazuToshiyuki
en-aut-sei=Kawazu
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YanagiYoshinobu
en-aut-sei=Yanagi
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=AsaumiJunichi
en-aut-sei=Asaumi
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

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

affil-num=2
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Hospital
kn-affil=

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

affil-num=5
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Dental Informatics, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Maxillary sinus
kn-keyword=Maxillary sinus
en-keyword=Squamous cell carcinoma
kn-keyword=Squamous cell carcinoma
en-keyword=Non-squamous cell carcinoma
kn-keyword=Non-squamous cell carcinoma
en-keyword=CT
kn-keyword=CT
END

start-ver=1.4
cd-journal=joma
no-vol=106
cd-vols=
no-issue=
article-no=
start-page=106690
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=EGF-induced P-gp expression in tumor vasculature contributes to therapeutic resistance to doxorubicin-PEG-liposomes in mice bearing doxorubicin-resistant B16-BL6 tumors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We previously indicated that doxorubicin (DOX)-loaded polyethylene glycol (PEG)-modified liposomes (DOX-PEG-liposomes) were therapeutically effective in mice bearing DOX-resistant colon-26 (C26/DOX) tumors, and the efficacy was comparable in mice bearing DOX-sensitive C26 tumors. However, in the current study, DOX-PEG-liposomes exerted no therapeutic activity in DOX-resistant B16-BL6 melanoma (B16/DOX)-bearing mice, although they significantly suppressed DOX-sensitive B16 tumor growth in mice. Although we previously reported that the anti-tumor effects in C26/DOX-bearing mice were derived from the cytotoxic effects of DOX on vascular endothelial cells (VECs) in tumors, the B16/DOX tumor vasculature was not substantially damaged after administration of DOX-PEG-liposomes. In B16/DOX tumors, P-gp expression was significantly induced in the VECs, but not in the C26/DOX tumors, indicating that the high expression of P-gp in the tumor vasculature would be responsible for the lack of therapeutic effect of DOX-PEG-liposomes in B16/DOX-bearing mice. Epidermal growth factor (EGF), a possible induction factor for P-gp expression, was highly expressed in B16/DOX cells and tumor tissues, and significantly induced P-gp expression in human umbilical vein endothelial cells (HUVEC). The EGF receptor (EGFR) was also highly expressed in B16/DOX tumor VECs, suggesting that the activation of EGF/EGFR signaling may induce P-gp expression in VECs in B16/DOX tumors.
en-copyright=
kn-copyright=

en-aut-name=MaruyamaMasato
en-aut-sei=Maruyama
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UedaTomoki
en-aut-sei=Ueda
en-aut-mei=Tomoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IenakaYusuke
en-aut-sei=Ienaka
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TojoHaruka
en-aut-sei=Tojo
en-aut-mei=Haruka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HyodoKenji
en-aut-sei=Hyodo
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OgawaraKen-ichi
en-aut-sei=Ogawara
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HigakiKazutaka
en-aut-sei=Higaki
en-aut-mei=Kazutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Eisai Co., Ltd.
kn-affil=

affil-num=6
en-affil=Laboratory of Pharmaceutics, Kobe Pharmaceutical University
kn-affil=

affil-num=7
en-affil=Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Drug resistance
kn-keyword=Drug resistance
en-keyword=P-glycoprotein
kn-keyword=P-glycoprotein
en-keyword=Liposome
kn-keyword=Liposome
en-keyword=Tumor vascular endothelial cells
kn-keyword=Tumor vascular endothelial cells
en-keyword=Melanoma
kn-keyword=Melanoma
END

start-ver=1.4
cd-journal=joma
no-vol=209
cd-vols=
no-issue=
article-no=
start-page=114663
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Repeated sequential administration of pegylated emulsion of SU5416 and liposomal paclitaxel enhances anti-tumor effect in 4T1 breast cancer-bearing mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To improve vascular normalization strategy for intractable triple-negative breast cancer 4T1, we examined the anti-tumor effects of repeated sequential administration of polyethylene glycol (PEG)-modified emulsion of SU5416 (PE-SU5416), a vascular endothelial growth factor (VEGF) receptor-2 kinase inhibitor, and PEG-modified liposomal paclitaxel (PL-PTX) in mice bearing 4T1 cells. Three sequential administrations (Seq×3) of PE-SU5416 and PL-PTX exhibited significantly higher anti-tumor activity than a single sequential administration (Seq×1). The tumor vasculatures were structurally normalized until after two PE-SU5416 (PE-SU5416×2) or sequential (Seq×2) administrations, while the improvement in vascular function, such as oxygen supply, blood flow, and PEG-liposomal distribution, was evident until after three administrations of PE-SU5416 (PE-SU5416×3) and Seq×3. Although some discrepancies between the structural and functional improvement in tumor vasculatures were observed after PE-SU5416×3 and Seq×3, cancer-associated fibroblasts (CAFs) and collagen levels were significantly reduced after PE-SU5416×2, PE-SU5416×3, Seq×2, and Seq×3, suggesting that a possible decrease in interstitial fluid pressure due to the reduction in CAFs and collagen would have compensated for vascular function. Furthermore, PE-SU5416×2, PE-SU5416×3, Seq×2, and Seq×3 significantly decreased tumor growth factor-β (TGF-β), an activator of CAFs, in tumor tissues, suggesting that the reduction in TGF-β levels by PE-SU5416 suppresses CAF activation.
en-copyright=
kn-copyright=

en-aut-name=MaruyamaMasato
en-aut-sei=Maruyama
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ToriiReiya
en-aut-sei=Torii
en-aut-mei=Reiya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MatsuiHazuki
en-aut-sei=Matsui
en-aut-mei=Hazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HayashiHiroki
en-aut-sei=Hayashi
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OgawaraKen-ichi
en-aut-sei=Ogawara
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HigakiKazutaka
en-aut-sei=Higaki
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 Pharmaceutics, Faculty of Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Laboratory of Pharmaceutics, Kobe Pharmaceutical University
kn-affil=

affil-num=6
en-affil=Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Drug delivery
kn-keyword=Drug delivery
en-keyword=Vascular normalization
kn-keyword=Vascular normalization
en-keyword=Breast cancer
kn-keyword=Breast cancer
en-keyword=Liposome
kn-keyword=Liposome
en-keyword=Cancer-associated fibroblast
kn-keyword=Cancer-associated fibroblast
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=13
cd-vols=
no-issue=2
article-no=
start-page=61
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250129
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Study of Podoplanin-Deficient Mouse Bone with Mechanical Stress
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective: We investigated morphological differences in osteocyte processes between aged mice and our original podoplanin-conditional knockout (cKO) mice in which the floxed exon 3 of podoplanin was deleted by Dmp-1-driven Cre (Dmp1-Cre;PdpnΔ/Δ). Methods: SEM observation on osteocyte cell process, histochemistry for bone remodeling with mechanostress, and RT-PCR for RANKL and M-CSF in podoplanin cKO mouse bone with mechanostress was investigated. Results: SEM observations showed fewer and thinner osteocyte processes in femurs from 23-week-old Dmp1-Cre;PdpnΔ/Δ mice than from 23-week-old wild-type mice, while the numbers of osteocyte processes in femurs and calvarias were similar in 23-week-old Dmp1-Cre;PdpnΔ/Δ mice and 48-week-old wild-type mice. Furthermore, cell process numbers in femurs and calvarias were significantly smaller in 23-week-old Dmp1-Cre;PdpnΔ/Δ mice than in 48-week-old wild-type mice. In the test for differences in alveolar bone resorption under mechanical stress between Dmp1-Cre;PdpnΔ/Δ and wild-type mice, the area of TRAP-positive resorption pits was larger in wild-type mice than in Dmp1-Cre;PdpnΔ/Δ mice. In a quantitative tissue PCR analysis, the mRNA expression levels of RANKL and M-CSF in alveolar bone under mechanical stress were significantly lower in Dmp1-Cre;PdpnΔ/Δ mice than in wild-type mice. These results suggest that a reduction in cell process formation in osteocytes with podoplanin cKO affected the absorption of alveolar bone under mechanical stress in Dmp1-Cre;PdpnΔ/Δ mice. Conclusions: In podoplanin-deficient bone, the deformation of osteocyte processes by mechanical stimuli is not recognized as a stress due to the lower number of cell processes with podoplanin deficiency; therefore, the production of osteoclast migration/differentiation factors by activated osteocytes is not fully induced and macrophage migration to alveolar bone with mechanical stress appeared to be suppressed. These results indicate that podoplanin-dependent osteocyte process formation indirectly plays a key role in sensing mechanical stress in bone.
en-copyright=
kn-copyright=

en-aut-name=KanaiTakenori
en-aut-sei=Kanai
en-aut-mei=Takenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OsawaKyoko
en-aut-sei=Osawa
en-aut-mei=Kyoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KajiwaraKoichiro
en-aut-sei=Kajiwara
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SatoYoshiaki
en-aut-sei=Sato
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SawaYoshihiko
en-aut-sei=Sawa
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Orthodontics, Faculty of Dental Medicine and Graduate School of Dental Medicine, Hokkaido University
kn-affil=

affil-num=2
en-affil=Department of Orthodontics, Faculty of Dental Medicine and Graduate School of Dental Medicine, Hokkaido University
kn-affil=

affil-num=3
en-affil=Department of Oral Growth & Development, Hokkaido University
kn-affil=

affil-num=4
en-affil=Department of Orthodontics, Faculty of Dental Medicine and Graduate School of Dental Medicine, Hokkaido University
kn-affil=

affil-num=5
en-affil=Department of Oral Function & Anatomy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=podoplanin
kn-keyword=podoplanin
en-keyword=cKO
kn-keyword=cKO
en-keyword=osteocyte
kn-keyword=osteocyte
en-keyword=bone
kn-keyword=bone
en-keyword=remodeling
kn-keyword=remodeling
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=2
article-no=
start-page=267
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250122
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Abnormal Expression of Tubular SGLT2 and GULT2 in Diabetes Model Mice with Malocclusion-Induced Hyperglycemia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: A relationship between malocclusion and the promotion of diabetes has been suggested. In hyperglycemia, the expression of sodium-glucose cotransporter 2 (SGLT2) and the facilitative glucose transporter 2 (GLUT2) is upregulated in proximal tubular cells, leading to an increase in renal glucose reabsorption. The present study aimed to investigate whether malocclusion contributes to diabetic exacerbation. Methods: Streptozotocin (STZ)-induced diabetic mice with malocclusion due to cutting molars were investigated based on increased blood glucose levels. PCR and immunohistochemical analyses were performed on diabetic mice kidneys to investigate the expression of SGLT2 and GLUT2. Results: Animal experiments were performed using 32 mice for 21 days. The time to reach a diabetic condition in STZ-administered mice was shorter with malocclusion than without malocclusion. The increase and mean blood glucose levels in STZ-administered mice were steeper and higher with malocclusion than without malocclusion. Urea albumin, BUN, and CRE levels were higher in diabetic mice with malocclusion than in diabetic mice without. Immunoreaction with anti-SGLT2 and anti-GLUT2 in the renal tissue of STZ-administered mice was stronger with malocclusion than without malocclusion. The amounts of SGLT2 and GLUT2 mRNA in the renal tissue in STZ-administered mice were higher with malocclusion than without malocclusion. The amounts of TNF-a and IL-6 mRNA in the large intestinal tissue in STZ-administered mice were higher with malocclusion than without malocclusion. Conclusions: Our results indicate that malocclusion accelerates the tubular expression of SGLT2 and GLUT2 under hyperglycemia. Malocclusion may be a diabetes-exacerbating factor with increased poor glycemic control due to shortened occlusion time resulting from swallowing food without chewing.
en-copyright=
kn-copyright=

en-aut-name=KajiwaraKoichiro
en-aut-sei=Kajiwara
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TamaokiSachio
en-aut-sei=Tamaoki
en-aut-mei=Sachio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SawaYoshihiko
en-aut-sei=Sawa
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Oral Growth & Development, Fukuoka Dental College
kn-affil=

affil-num=2
en-affil=Department of Oral Growth & Development, Fukuoka Dental College
kn-affil=

affil-num=3
en-affil=Department of Oral Function & Anatomy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=malocclusion
kn-keyword=malocclusion
en-keyword= hyperglycemia
kn-keyword= hyperglycemia
en-keyword= SGLT2
kn-keyword= SGLT2
en-keyword= GLUT2
kn-keyword= GLUT2
END

start-ver=1.4
cd-journal=joma
no-vol=197
cd-vols=
no-issue=
article-no=
start-page=115301
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202503
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Fraglide-1 from traditional Chinese aromatic vinegar: A natural AhR antagonist for atopic dermatitis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Traditional Chinese Zhenjiang aromatic vinegar (Kozu) contains Fraglide-1 (FG1), a bioactive lactone with demonstrated peroxisome proliferator-activated receptor gamma (PPARγ) agonist and antioxidant activities. This study explored FG1's novel ability to antagonize the aryl hydrocarbon receptor (AhR) signaling pathway, which regulates artemin expression and contributes to itching and inflammation in atopic dermatitis. Through molecular docking simulations and cell-based assays in human keratinocytes, we demonstrated FG1's potent antagonistic activity against AhR signaling. FG1 effectively suppressed FICZ-induced inflammatory responses, including artemin expression, with potency (half maximal inhibitory concentration, IC50 = 5.1 μM) comparable to the synthetic antagonist StemRegenin 1 (SR1) while demonstrating a superior safety profile (median lethal concentration, LC50 > 100 μM vs. 27.5 μM for SR1). These findings expand our understanding of bioactive compounds from traditional fermented foods and their regulatory effects on AhR signaling, providing a foundation for future studies on FG1's role in modulating skin inflammation.
en-copyright=
kn-copyright=

en-aut-name=KatoKosuke
en-aut-sei=Kato
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AkamatsuMiki
en-aut-sei=Akamatsu
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KakimaruSaya
en-aut-sei=Kakimaru
en-aut-mei=Saya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakagiMasahiro
en-aut-sei=Takagi
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyashitaMasahiro
en-aut-sei=Miyashita
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MurataYoshiyuki
en-aut-sei=Murata
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
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=10
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 Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
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=School of Materials Science, Japan Advanced Institute of Science and Technology
kn-affil=

affil-num=6
en-affil=Graduate School of Agriculture, Kyoto University
kn-affil=

affil-num=7
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=9
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=10
en-affil=Graduate School of Science, Technology and Innovation, Kobe University
kn-affil=
en-keyword=AhR
kn-keyword=AhR
en-keyword=Xenobiotic responsive element
kn-keyword=Xenobiotic responsive element
en-keyword=StemRegenin 1
kn-keyword=StemRegenin 1
en-keyword=ARNT
kn-keyword=ARNT
en-keyword=Atopic dermatitis
kn-keyword=Atopic dermatitis
en-keyword=Artemin
kn-keyword=Artemin
END

start-ver=1.4
cd-journal=joma
no-vol=64
cd-vols=
no-issue=2
article-no=
start-page=97
end-page=106
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=2024
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Atypical lymphoplasmacytic and immunoblastic proliferation: A Systematic Review
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Atypical lymphoplasmacytic and immunoblastic proliferation (ALPIBP) was first reported in 1984 as characteristic histological findings in lymph nodes associated with autoimmune diseases, but it has not been clearly defined to date. To summarize the histological characteristics and clinical diagnoses associated with ALPIBP, we searched MEDLINE and EMBASE for all peer-reviewed articles using keywords including “atypical lymphoplasmacytic and immunoblastic lymphadenopathy” from their inception to December 27, 2023. We also summarized the courses of three cases with a pathological diagnosis of ALPIBP. Nine articles with 52 cases were included. Among the total of 55 cases, including the three from our institution, the median age of the cases was 63.5 years with a female predominance (69.5%). Lymphadenopathy was generalized in 65.6% and regional in 34.4% of cases. RA (24.4%), SLE (24.4%), and autoimmune hemolytic anemia (20.0%), were common clinical diagnoses. A combination of cytotoxic chemotherapy was used in 15.6% of cases due to the suspicion of malignancy. Nodal T-follicular helper cell lymphoma, angioimmunoblastic type, methotrexate-associated lymphoproliferative disorders, and IgG4-related diseases were listed as important diseases that need to be pathologically differentiated from ALPIBP. This review summarizes the current understanding of the characteristics of ALPIBP. Given that underrecognition of ALPIBP could lead to overdiagnosis of hematological malignancy and unnecessary treatment, increased awareness of the condition in pathologists and clinicians is crucial.
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=TakahashiToshiaki
en-aut-sei=Takahashi
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakaokaKensuke
en-aut-sei=Takaoka
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MacapagalSharina
en-aut-sei=Macapagal
en-aut-mei=Sharina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WannaphutChalothorn
en-aut-sei=Wannaphut
en-aut-mei=Chalothorn
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

en-aut-name=TodaHiroko
en-aut-sei=Toda
en-aut-mei=Hiroko
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=SatoYasuharu
en-aut-sei=Sato
en-aut-mei=Yasuharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

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

affil-num=2
en-affil=Department of Medicine, John A. Burns School of Medicine, University of Hawai’i
kn-affil=

affil-num=3
en-affil=Department of Medicine, John A. Burns School of Medicine, University of Hawai’i
kn-affil=

affil-num=4
en-affil=Department of Medicine, John A. Burns School of Medicine, University of Hawai’i
kn-affil=

affil-num=5
en-affil=Department of Medicine, John A. Burns School of Medicine, University of Hawai’i
kn-affil=

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

affil-num=7
en-affil=Department of Pathology, Chugoku Central Hospital
kn-affil=

affil-num=8
en-affil=Department of Medicine, John A. Burns School of Medicine, University of Hawai’i
kn-affil=

affil-num=9
en-affil=Department of Molecular Hematopathology, Okayama University Graduate School of Health Sciences
kn-affil=
en-keyword=systematic review
kn-keyword=systematic review
en-keyword=atypical lymphoplasmacytic and immunoblastic proliferation
kn-keyword=atypical lymphoplasmacytic and immunoblastic proliferation
en-keyword=IgG4-related disease
kn-keyword=IgG4-related disease
en-keyword=angioimmunoblastic T-cell lymphoma
kn-keyword=angioimmunoblastic T-cell lymphoma
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=20250212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Spatiotemporal expression pattern of dyslexia susceptibility 1 candidate 1 (DYX1C1) during rat cerebral cortex development
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Developmental dyslexia (DD) is a common learning disorder with significant consequences for affected individuals. Although several candidate genes, including dyslexia susceptibility 1 candidate 1 (DYX1C1), have been implicated in dyslexia, their role in brain development remains unclear. We aimed to elucidate the spatiotemporal expression patterns of DYX1C1 during cerebral cortex development in rats.<br>
Methods We investigated DYX1C1 expression during cerebral cortex development using rat embryos at various gestational stages (E13.5, 15.5, 17.5 and 20.5) by immunohistochemistry (n?=?7 embryos/stage), quantitative real-time PCR (n?=?6), and in situ hybridization (n?=?11?15).<br>
Results The DYX1C1-positive cells were predominantly located in the outermost layers of the cortical plate, particularly at E15.5. DYX1C1 mRNA expression peaked at E15.5 and subsequently declined. DYX1C1-positive cells did not co-localize with reelin-positive Cajal-Retzius cells, but co-localized with neuronal markers expressed during development, and had shorter primary cilia than DYX1C1-negative cells.<br>
Conclusions Our findings highlight the dynamic expression of DYX1C1 in the developing cerebral cortex of rats, implicating its involvement in neurodevelopmental processes. Further investigation of the functional interactions of DYX1C1, particularly its relationship with reelin and its role in cerebrocortical and hippocampal development, may provide insights into the pathophysiology of dyslexia and neurodevelopmental disorders.
en-copyright=
kn-copyright=

en-aut-name=ZenshoKazumasa
en-aut-sei=Zensho
en-aut-mei=Kazumasa
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=IsseAika
en-aut-sei=Isse
en-aut-mei=Aika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MisawaIchika
en-aut-sei=Misawa
en-aut-mei=Ichika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MasaiKaori
en-aut-sei=Masai
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OkaMakio
en-aut-sei=Oka
en-aut-mei=Makio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
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=8
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=

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

affil-num=6
en-affil=Department of Psychosocial Medicine, National Center for Child Health and Development
kn-affil=

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

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

start-ver=1.4
cd-journal=joma
no-vol=236
cd-vols=
no-issue=
article-no=
start-page=74
end-page=81
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Characteristics of porcine oocyte-cumulus complexes derived from various sizes of antral follicles and classified by brilliant cresyl blue staining, and developmental competence of the oocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The present study sought to determine the characteristics of porcine oocyte-cumulus complexes (OCCs) derived from very small and small antral follicles (with less than 1 mm and 1?3 mm in diameter, respectively; VSF and SF) in comparison with controls from medium ones (with 3?6 mm in diameter; MF). Additionally, the present study examined the utility of brilliant cresyl blue (BCB) staining for assessing these OCCs. The incidence of BCB- oocytes in VSF- and SF-derived OCCs was higher than that in MF-derived OCCs. Although the meiotic and developmental competences of BCB+ oocytes from MF were superior to those from VSF and SF, blastocysts were successfully obtained from BCB+ oocytes even derived from VSF. The mean numbers of both total and viable cumulus cells surrounding an oocyte were significantly affected not only by the origin of the OCCs, but also by the BCB status of the oocytes (largest in MF-derived OCCs containing BCB+ oocytes). Although the outer and inner diameters of zona pellucida were affected by the origin of OCCs and the BCB status of oocytes (largest in MF-derived oocytes), the ooplasmic diameter of BCB+ oocytes did not differ among those derived from VSF, SF, and MF. Regardless of the BCB status, the transcriptional levels of G6PD and TKT in cumulus cells decreased during follicular development from VSF to MF, whereas the RPIA mRNA level in cumulus cells of MF-derived BCB+ OCCs was lower than in the others. These results underscore the utility of BCB staining for selecting MF-, SF-, and even VSF-derived OCCs containing oocytes with relatively higher meiotic and developmental competences, as well as the importance of having a sufficient number of healthy cumulus cells expressing genes related to the pentose phosphate pathway at lower levels.
en-copyright=
kn-copyright=

en-aut-name=VanPhong Ngoc
en-aut-sei=Van
en-aut-mei=Phong Ngoc
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=DoSon Quang
en-aut-sei=Do
en-aut-mei=Son Quang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FonsekaWanniarachchige Tharindu Lakshitha
en-aut-sei=Fonseka
en-aut-mei=Wanniarachchige Tharindu Lakshitha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WakaiTakuya
en-aut-sei=Wakai
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FunahashiHiroaki
en-aut-sei=Funahashi
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Animal Science, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Animal Science, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Animal Science, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Animal Science, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Animal Science, Graduate School of Environmental and Life Science, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=2
article-no=
start-page=376
end-page=382
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250205
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A case of pancreatic ductal adenocarcinoma growing within the pancreatic duct mimicking an intraductal tubulopapillary neoplasm
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We herein report a case of pancreatic ductal adenocarcinoma (PDAC) that developed within the pancreatic duct and was initially diagnosed as an intraductal tubulopapillary neoplasm (ITPN). A 76-year-old man presented with weight loss and main pancreatic duct dilation. The imaging studies revealed a 30-mm hypovascular tumor within the main duct of the pancreatic head. An endoscopic examination with a biopsy revealed high-grade atypical epithelial cells with immunostaining patterns suggestive of ITPN. Following robot-assisted pancreaticoduodenectomy, postoperative pathology revealed conflicting features: nodular/cribriform infiltrations typical of ITPN and non-lobular replacement with scattered infiltrations characteristic of PDAC. A comprehensive genomic profiling test detected KRAS and TP53 mutations, leading to the final diagnosis of PDAC (fT3N1aM0, stage IIB). The patient received adjuvant S-1 chemotherapy and remained recurrence-free for 15 months post-surgery. This case highlights the diagnostic challenges of differentiating intraductal pancreatic tumors and demonstrates the utility of integrating genetic testing with conventional diagnostic modalities for an accurate diagnosis and appropriate treatment selection.
en-copyright=
kn-copyright=

en-aut-name=SatoRyosuke
en-aut-sei=Sato
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsumotoKazuyuki
en-aut-sei=Matsumoto
en-aut-mei=Kazuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UkaMayu
en-aut-sei=Uka
en-aut-mei=Mayu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=NishidaKenji
en-aut-sei=Nishida
en-aut-mei=Kenji
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=FujiiYuki
en-aut-sei=Fujii
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TsutsumiKoichiro
en-aut-sei=Tsutsumi
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HoriguchiShigeru
en-aut-sei=Horiguchi
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
ORCID=

affil-num=1
en-affil=Department of Gastroenterology and Hepatology, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Gastroenterology and Hepatology, Okayama University Hospital
kn-affil=

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

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

affil-num=7
en-affil=Department of Gastroenterology and Hepatology, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Gastroenterology and Hepatology, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Department of Gastroenterology and Hepatology, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of Gastroenterology and Hepatology, Okayama University Hospital
kn-affil=
en-keyword=Pancreatic intraductal neoplasms
kn-keyword=Pancreatic intraductal neoplasms
en-keyword=Pancreatic carcinoma
kn-keyword=Pancreatic carcinoma
en-keyword=Intraductal tubulopapillary neoplasm
kn-keyword=Intraductal tubulopapillary neoplasm
en-keyword=Genetic testing
kn-keyword=Genetic testing
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=74
cd-vols=
no-issue=3
article-no=
start-page=96
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250204
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cancer-associated fibroblasts promote pro-tumor functions of neutrophils in pancreatic cancer via IL-8: potential suppression by pirfenidone
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background The mechanisms by which neutrophils acquire pro-tumor properties remain poorly understood. In pancreatic cancer, cancer-associated fibroblasts (CAFs) may interact with neutrophils, directing them to promote tumor progression.<br>
Methods To validate the association between CAFs and neutrophils, the localization of neutrophils was examined in clinically resected pancreatic cancer specimens. CAFs were produced by culturing in cancer-conditioned media, and the effects of these CAFs on neutrophils were examined. In vitro migration and invasion assays assess the effect of CAF-activated neutrophils on cancer cells. The factors secreted by the activated neutrophils were also explored. Finally, pirfenidone (PFD) was tested to determine whether it could suppress the pro-tumor functions of activated neutrophils.<br>
Results In pancreatic cancer specimens, neutrophils tended to co-localize with IL-6-positive CAFs. Neutrophils co-cultured with CAFs increased migratory capacity and prolonged life span. CAF-affected neutrophils enhance the migratory and invasive activities of pancreatic cancer cells. IL-8 is the most upregulated cytokine secreted by the neutrophils. PFD suppresses IL-8 secretion from CAF-stimulated neutrophils and mitigates the malignant traits of pancreatic cancer cells.<br>
Conclusion CAFs activate neutrophils and enhance the malignant phenotype of pancreatic cancer. The interactions between cancer cells, CAFs, and neutrophils can be disrupted by PFD, highlighting a potential therapeutic approach.
en-copyright=
kn-copyright=

en-aut-name=YagiTomohiko
en-aut-sei=Yagi
en-aut-mei=Tomohiko
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=NogiShohei
en-aut-sei=Nogi
en-aut-mei=Shohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=YoshimotoMasashi
en-aut-sei=Yoshimoto
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=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=FujitaShuto
en-aut-sei=Fujita
en-aut-mei=Shuto
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=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=KakiuchiYoshihiko
en-aut-sei=Kakiuchi
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
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=12
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=13
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=14
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=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=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Departments of Pathology and Experimental Medicine, 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=

affil-num=16
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Cancer-associated fibroblasts
kn-keyword=Cancer-associated fibroblasts
en-keyword=Neutrophil
kn-keyword=Neutrophil
en-keyword=Anti-fibrotic agent
kn-keyword=Anti-fibrotic agent
en-keyword=Pirfenidone
kn-keyword=Pirfenidone
END

start-ver=1.4
cd-journal=joma
no-vol=79
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=7
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=Endothelial Cell Polarity in Health and Disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Endothelial cell polarity is fundamental to the organization and function of blood vessels, influencing processes such as angiogenesis, vascular stability, and response to shear stress. This review elaborates on the molecular mechanisms that regulate endothelial cell polarity, focusing on key players like the PAR polarity complex and Rho family GTPases. These pathways coordinate the front?rear, apical?basal and planar polarity of endothelial cells, which are essential for the proper formation and maintenance of vascular structures. In health, endothelial polarity ensures not only the orderly development of blood vessels, with tip cells adopting distinct polarities during angiogenesis, but also ensures proper vascular integrity and function. In disease states, however, disruptions in polarity contribute to pathologies such as coronary artery disease, where altered planar polarity exacerbates atherosclerosis, and cancer, where disrupted polarity in tumor vasculature leads to abnormal vessel growth and function. Understanding cell polarity and its disruption is fundamental not only to comprehending how cells interact with their microenvironment and organize themselves into complex, organ-specific tissues but also to developing novel, targeted, and therapeutic strategies for a range of diseases, from cardiovascular disorders to malignancies, ultimately improving patient outcomes.
en-copyright=
kn-copyright=

en-aut-name=ThihaMoe
en-aut-sei=Thiha
en-aut-mei=Moe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HikitaTakao
en-aut-sei=Hikita
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
ORCID=

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

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

affil-num=3
en-affil=Department of Pathophysiology and Drug Discovery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=blood vessel
kn-keyword=blood vessel
en-keyword=endothelial cell
kn-keyword=endothelial cell
en-keyword=cell polarity
kn-keyword=cell polarity
en-keyword=atherosclerosis
kn-keyword=atherosclerosis
en-keyword=cancer
kn-keyword=cancer
END

start-ver=1.4
cd-journal=joma
no-vol=121
cd-vols=
no-issue=35
article-no=
start-page=e2320189121
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240821
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Somatic mutations in tumor-infiltrating lymphocytes impact on antitumor immunity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Immune checkpoint inhibitors (ICIs) exert clinical efficacy against various types of cancers by reinvigorating exhausted CD8+ T cells that can expand and directly attack cancer cells (cancer-specific T cells) among tumor-infiltrating lymphocytes (TILs). Although some reports have identified somatic mutations in TILs, their effect on antitumor immunity remains unclear. In this study, we successfully established 18 cancer-specific T cell clones, which have an exhaustion phenotype, from the TILs of four patients with melanoma. We conducted whole-genome sequencing for these T cell clones and identified various somatic mutations in them with high clonality. Among the somatic mutations, an SH2D2A loss-of-function frameshift mutation and TNFAIP3 deletion could activate T cell effector functions in vitro. Furthermore, we generated CD8+ T cell?specific Tnfaip3 knockout mice and showed that Tnfaip3 function loss in CD8+ T cell increased antitumor immunity, leading to remarkable response to PD-1 blockade in vivo. In addition, we analyzed bulk CD3+ T cells from TILs in additional 12 patients and identified an SH2D2A mutation in one patient through amplicon sequencing. These findings suggest that somatic mutations in TILs can affect antitumor immunity and suggest unique biomarkers and therapeutic targets.
en-copyright=
kn-copyright=

en-aut-name=MukoharaFumiaki
en-aut-sei=Mukohara
en-aut-mei=Fumiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IwataKazuma
en-aut-sei=Iwata
en-aut-mei=Kazuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IshinoTakamasa
en-aut-sei=Ishino
en-aut-mei=Takamasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=InozumeTakashi
en-aut-sei=Inozume
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NagasakiJoji
en-aut-sei=Nagasaki
en-aut-mei=Joji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UedaYouki
en-aut-sei=Ueda
en-aut-mei=Youki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SuzawaKen
en-aut-sei=Suzawa
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UenoToshihide
en-aut-sei=Ueno
en-aut-mei=Toshihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IkedaHideki
en-aut-sei=Ikeda
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KawaseKatsushige
en-aut-sei=Kawase
en-aut-mei=Katsushige
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SaekiYuka
en-aut-sei=Saeki
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KawashimaShusuke
en-aut-sei=Kawashima
en-aut-mei=Shusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=YamashitaKazuo
en-aut-sei=Yamashita
en-aut-mei=Kazuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KawaharaYu
en-aut-sei=Kawahara
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NakamuraYasuhiro
en-aut-sei=Nakamura
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=Honobe-TabuchiAkiko
en-aut-sei=Honobe-Tabuchi
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=WatanabeHiroko
en-aut-sei=Watanabe
en-aut-mei=Hiroko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=DansakoHiromichi
en-aut-sei=Dansako
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=KawamuraTatsuyoshi
en-aut-sei=Kawamura
en-aut-mei=Tatsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=SuzukiYutaka
en-aut-sei=Suzuki
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=HondaHiroaki
en-aut-sei=Honda
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=ManoHiroyuki
en-aut-sei=Mano
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
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=23
ORCID=

en-aut-name=KawazuMasahito
en-aut-sei=Kawazu
en-aut-mei=Masahito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=TogashiYosuke
en-aut-sei=Togashi
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

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

affil-num=2
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Dermatology, Chiba University Graduate School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

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

affil-num=8
en-affil=Division of Cellular Signaling, National Cancer Center Research Institute
kn-affil=

affil-num=9
en-affil=Division of Cell Therapy, Chiba Cancer Research Institute
kn-affil=

affil-num=10
en-affil=Division of Cell Therapy, Chiba Cancer Research Institute
kn-affil=

affil-num=11
en-affil=Department of Dermatology, Chiba University Graduate School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Dermatology, Chiba University Graduate School of Medicine
kn-affil=

affil-num=13
en-affil=KOTAI Biotechnologies, Inc.
kn-affil=

affil-num=14
en-affil=Department of Dermatology, Chiba University Graduate School of Medicine
kn-affil=

affil-num=15
en-affil=Department of Skin Oncology/Dermatology, Saitama Medical University International Medical Center
kn-affil=

affil-num=16
en-affil=Department of Dermatology, University of Yamanashi
kn-affil=

affil-num=17
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=18
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=19
en-affil=Department of Dermatology, University of Yamanashi
kn-affil=

affil-num=20
en-affil=Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa
kn-affil=

affil-num=21
en-affil=Department of Pathology, Tokyo Women's Medical University
kn-affil=

affil-num=22
en-affil=Division of Cellular Signaling, National Cancer Center Research Institute
kn-affil=

affil-num=23
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine, Okayama University
kn-affil=

affil-num=24
en-affil=Division of Cell Therapy, Chiba Cancer Research Institute
kn-affil=

affil-num=25
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=cancer immunology
kn-keyword=cancer immunology
en-keyword=somatic mutation
kn-keyword=somatic mutation
en-keyword=T cell
kn-keyword=T cell
en-keyword=tumor-infiltrating lymphocytes
kn-keyword=tumor-infiltrating lymphocytes
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=1
article-no=
start-page=38
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250124
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Exacerbation of diabetes due to F. Nucleatum LPS-induced SGLT2 overexpression in the renal proximal tubular epithelial cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Diabetes treatments by the control of sodium-glucose cotransporter 2 (SGLT2) is commonly conducted while there are still uncertainties about the mechanisms for the SGLT2 overexpression in kidneys with diabetes. Previously, we have reported that glomeruli and proximal tubules with diabetic nephropathy express toll-like receptor TLR2/4, and that the TLR ligand lipopolysaccharide (LPS) of periodontal pathogens have caused nephropathy in diabetic model mice. Recently, many researchers suggested that the periodontal pathogenic bacteria Fusobacterium (F.) nucleatum has the TLR4-associated strong activator of the colorectal inflammation and cancer. The present study aimed to investigate the possibility of F. nucleatum as an exacerbation factor of diabetes through the renal SGLT2 induction.<br>
Methods The induction of the SGLT2 by F. nucleatum LPS (Fn-LPS) were investigated in the streptozotocin-induced diabetic mouse renal tissue and cultured renal proximal epithelial cells. The changes of blood glucose levels and survival curves in diabetic mice with Fn-LPS were analyzed. The Fn-LPS-induced SGLT2 production in the diabetic mouse renal tissue and in the cultured proximal epithelial cells was examined by ELISA, quantitative RT-PCR, and immunohistochemical analysis.<br>
Results The SGLT2 expression in the cultured mouse tubular epithelial cells was significantly increased by TNF- or co-culture with Fn-LPS-supplemented J774.1 cells. The period to reach diabetic condition was significantly shorter in Fn-LPS-administered diabetic mice than in diabetic mice. All Fn-LPS-administered-diabetic mice reached humane endpoints during the healthy period of all of the mice administered Fn-LPS only. The promotion of the SGLT2 expression at the inner lumen of proximal tubules were stronger in the Fn-LPS-administered-diabetic mice than in diabetic mice. The renal tissue SGLT2 mRNA amounts and the number of renal proximal tubules with overexpressed SGLT2 in the lumen were more in the Fn-LPS-administered-diabetic mice than in diabetic mice.<br>
Conclusions This study suggests that F. nucleatum causes the promotion of diabetes through the overexpression of SGLT2 in proximal tubules under the diabetic condition. Periodontitis with F. nucleatum may be a diabetic exacerbating factor.
en-copyright=
kn-copyright=

en-aut-name=SekiAiko
en-aut-sei=Seki
en-aut-mei=Aiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KajiwaraKoichiro
en-aut-sei=Kajiwara
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TeramachiJumpei
en-aut-sei=Teramachi
en-aut-mei=Jumpei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=EgusaMasahiko
en-aut-sei=Egusa
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyawakiTakuya
en-aut-sei=Miyawaki
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SawaYoshihiko
en-aut-sei=Sawa
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

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

affil-num=2
en-affil=Department of Oral Growth & Development, Fukuoka Dental College
kn-affil=

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

affil-num=4
en-affil=Department of Dental Anesthesiology & Special Care Dentistry, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Dental Anesthesiology & Special Care Dentistry, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Oral Function & Anatomy, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=
en-keyword=F. Nucleatum
kn-keyword=F. Nucleatum
en-keyword=Diabetic exacerbation
kn-keyword=Diabetic exacerbation
en-keyword=Diabetic nephropathy
kn-keyword=Diabetic nephropathy
en-keyword=SGLT2
kn-keyword=SGLT2
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=
cd-vols=
no-issue=
article-no=
start-page=4055-24
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=2025
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dyspnea with Hemidiaphragm Elevation in a Patient with Giant Cell Arteritis: A Case Report
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We herein report the first case of dyspnea with hemidiaphragm elevation in a 68-year-old woman with active giant cell arteritis (GCA), including successful treatment. Contrast-enhanced computed tomography showed a reduced density of the left ophthalmic artery and the left superficial temporal artery with increased soft tissue compared to the other side, indicating that the GCA had flared up and suggesting that the hemidiaphragm elevation might be caused by vasculitis-associated ischemia of the right phrenic nerve. Hemidiaphragm paralysis due to vasculitis-associated ischemia in patients with GCA needs to be distinguished from local infection, tumors, and hepatomegaly, which are the major causes of hemidiaphragm elevation.
en-copyright=
kn-copyright=

en-aut-name=AsanoYosuke
en-aut-sei=Asano
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=KubotaNatsuki
en-aut-sei=Kubota
en-aut-mei=Natsuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TerajimaYuya
en-aut-sei=Terajima
en-aut-mei=Yuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MatsumotoKazuya
en-aut-sei=Matsumoto
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShidaharaKenta
en-aut-sei=Shidahara
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HiroseKei
en-aut-sei=Hirose
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakadoiTakato
en-aut-sei=Nakadoi
en-aut-mei=Takato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NawachiShoichi
en-aut-sei=Nawachi
en-aut-mei=Shoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KatayamaYu
en-aut-sei=Katayama
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
ORCID=

en-aut-name=KatsuyamaEri
en-aut-sei=Katsuyama
en-aut-mei=Eri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KatsuyamaTakayuki
en-aut-sei=Katsuyama
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=Takano-NarazakiMariko
en-aut-sei=Takano-Narazaki
en-aut-mei=Mariko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=SadaKen-Ei
en-aut-sei=Sada
en-aut-mei=Ken-Ei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
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=16
ORCID=

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

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

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

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

affil-num=5
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

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

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

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

affil-num=10
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=giant cell arteritis
kn-keyword=giant cell arteritis
en-keyword=dyspnea
kn-keyword=dyspnea
en-keyword=hemidiaphragm elevation
kn-keyword=hemidiaphragm elevation
en-keyword=phrenic nerve paralysis
kn-keyword=phrenic nerve paralysis
en-keyword=FDG-PET
kn-keyword=FDG-PET
en-keyword=case report
kn-keyword=case report
END

start-ver=1.4
cd-journal=joma
no-vol=361
cd-vols=
no-issue=
article-no=
start-page=114657
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=Crosstalk between prolactin, insulin-like growth factors, and thyroid hormones in feather growth regulation in neonatal chick wings
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The elongation of primary feathers in neonatal chicks is delayed by the late-feathering K gene located on the Z chromosome. We recently found that the K gene slows feather growth by reducing the number of functional prolactin (PRL) receptor (PRLR) dimers. In this study, we investigated the molecular mechanisms by which PRL promotes feather elongation. RT-qPCR and immunohistochemistry analyses revealed that PRLRs are predominantly localized in the pulp rather than in the epidermal layer of the feather follicle. Treatment of primary cultured feather pulp cells with PRL increased the expression of mRNAs for insulin-like growth factors (IGFs; IGF-1 and IGF-2) and type 2 deiodinase (DIO2). Furthermore, treatments with IGF-1 and triiodothyronine (T3) reciprocally enhanced the expression of mRNAs for DIO2 and IGFs. Additionally, BrdU staining in neonatal chicks showed that T3 promoted cell proliferation in both the epidermal layer and pulp cells, while this effect was suppressed by an IGF-1 receptor (IGF1R) inhibitor. These findings suggest a novel model in which PRL upregulates IGFs and DIO2 in feather pulp cells, creating a positive feedback loop between IGFs and T3, ultimately leading to the promotion of cell proliferation in both the epidermal layer and the pulp cells by IGFs. This is the first report proposing crosstalk between PRL, thyroid hormone (TH), and IGFs in feather follicles.
en-copyright=
kn-copyright=

en-aut-name=NozawaYuri
en-aut-sei=Nozawa
en-aut-mei=Yuri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OkamuraAyako
en-aut-sei=Okamura
en-aut-mei=Ayako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FukuchiHibiki
en-aut-sei=Fukuchi
en-aut-mei=Hibiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShinoharaMasamichi
en-aut-sei=Shinohara
en-aut-mei=Masamichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AizawaSayaka
en-aut-sei=Aizawa
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

affil-num=1
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Prolactin
kn-keyword=Prolactin
en-keyword=Thyroid hormone
kn-keyword=Thyroid hormone
en-keyword=IGF
kn-keyword=IGF
en-keyword=Iodothyronine deiodinase
kn-keyword=Iodothyronine deiodinase
en-keyword=Feather growth
kn-keyword=Feather growth
END

start-ver=1.4
cd-journal=joma
no-vol=941
cd-vols=
no-issue=
article-no=
start-page=149244
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250315
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Identification of pennaceous barbule cell factor (PBCF), a novel gene with spatiotemporal expression in barbule cells during feather development
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Bird contour feathers exhibit a complex hierarchical structure composed of a rachis, barbs, and barbules, with barbules playing a crucial role in maintaining feather structure and function. Understanding the molecular mechanisms underlying barbule formation is essential for advancing our knowledge of avian biology and evolution. In this study, we identified a novel gene, pennaceous barbule cell factor (PBCF), using microarray analysis, RT-PCR, and in situ hybridization. PBCF is expressed in barbule cells adjacent to the ramus during pennaceous barbule formation, where these cells fuse with the ramus to establish the feather’s branching structure. PBCF expression occurs transiently after melanin pigmentation of the barbule plates but before the expression of barbule-specific keratin 1 (BlSK1). Orthologues of PBCF, predicted to be secreted proteins, are conserved across avian species, with potential homologues detected in reptiles, suggesting an evolutionary lineage-specific adaptation. Additionally, PBCF is expressed in non-vacuolated notochord cells and the extra-embryonic ectoderm of the yolk sac, hinting at its broader developmental significance. The PBCF gene produces two mRNA isoforms via alternative splicing, encoding a secreted protein and a glycophosphatidylinositol (GPI)-anchored membrane-bound protein, indicating functional versatility. These findings suggest that PBCF may be involved as an avian-specific extracellular matrix component in cell adhesion and/or communication, potentially contributing to both feather development and embryogenesis. Further investigation of PBCF’s role in feather evolution and its potential functions in other vertebrates could provide new insights into the interplay between development and evolution.
en-copyright=
kn-copyright=

en-aut-name=NakaokaMinori
en-aut-sei=Nakaoka
en-aut-mei=Minori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FukuchiHibiki
en-aut-sei=Fukuchi
en-aut-mei=Hibiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OgoshiMaho
en-aut-sei=Ogoshi
en-aut-mei=Maho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AizawaSayaka
en-aut-sei=Aizawa
en-aut-mei=Sayaka
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=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Feather
kn-keyword=Feather
en-keyword=Barbule
kn-keyword=Barbule
en-keyword=Branching
kn-keyword=Branching
en-keyword=Chicken
kn-keyword=Chicken
en-keyword=Yolk sac membrane
kn-keyword=Yolk sac membrane
en-keyword=Notochord
kn-keyword=Notochord
END

start-ver=1.4
cd-journal=joma
no-vol=145
cd-vols=
no-issue=1
article-no=
start-page=7
end-page=14
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250101
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Precision Medicine for Patients with Renal Cell Carcinoma Based on Drug-metabolizing Enzyme Expression Levels
kn-title=薬物代謝酵素の発現情報を活用した腎がん治療の個別適正化
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Notable advances have recently been achieved in drug therapies for renal cell carcinoma (RCC). Several tyrosine kinase inhibitors (TKIs) and immune checkpoint inhibitors (ICIs) have been approved for metastatic RCC (mRCC). The current first-line treatment for mRCC involves combination therapies using TKIs and ICIs. However, there is no consensus on which TKI+ICI therapy is best or how to select the appropriate therapy for individual patients with RCC. The kidney expresses various metabolic enzymes, including CYP and uridine diphosphate glucose (UDP)-glucuronosyltransferase (UGT). Although information on CYP and UGT expression in the kidney is limited compared to our understanding of liver expression, the main CYP and UGT subtypes expressed at high levels in the kidney are estimated to be CYP2B6, CYP3A5, CYP4A11, CYP4F2, UGT1A6, UGT1A9, and UGT2B7. In RCC, the expression profiles and levels of these enzymes are somewhat altered compared with normal kidney. The main known subtypes of CYP and UGT in RCC are CYP1B1, CYP3A5, CYP4A11, UGT1A6, UGT1A9, UGT1A10, and UGT2B7. High CYP expression has been reported in several cancers, possibly conferring resistance to anti-cancer drugs including TKIs, due to extensive drug metabolism. Additionally, CYP and UGT expression levels may possibly affect cancer prognosis by metabolizing endogenous substrates, regardless of their role in anti-cancer drug metabolism. In this review, I discuss CYP and UGT expression level profiles in RCC based on previously published papers, including ours, and examine possible relationships between these enzyme expression profiles and treatment outcomes for patients with RCC.
en-copyright=
kn-copyright=

en-aut-name=MatsumotoJun
en-aut-sei=Matsumoto
en-aut-mei=Jun
kn-aut-name=松本准
kn-aut-sei=松本
kn-aut-mei=准
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Personalized Medicine and Preventive Healthcare Sciences, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学学術研究院医歯薬学域（薬学系）疾患薬理制御科学分野
en-keyword=renal cell carcinoma (RCC)
kn-keyword=renal cell carcinoma (RCC)
en-keyword=kidney
kn-keyword=kidney
en-keyword=CYP
kn-keyword=CYP
en-keyword=uridine diphosphate glucose (UDP)-glucuronosyltransferase
kn-keyword=uridine diphosphate glucose (UDP)-glucuronosyltransferase
en-keyword=metabolism
kn-keyword=metabolism
END

start-ver=1.4
cd-journal=joma
no-vol=43
cd-vols=
no-issue=1
article-no=
start-page=4
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250114
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Differentially Expressed Nedd4-binding Protein Ndfip1 Protects Neurons Against Methamphetamine-induced Neurotoxicity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To identify factors involved in methamphetamine (METH) neurotoxicity, we comprehensively searched for genes which were differentially expressed in mouse striatum after METH administration using differential display (DD) reverse transcription-PCR method and sequent single-strand conformation polymorphism analysis, and found two DD cDNA fragments later identified as mRNA of Nedd4 (neural precursor cell expressed developmentally downregulated 4) WW domain-binding protein 5 (N4WBP5), later named Nedd4 family-interacting protein 1 (Ndfip1). It is an adaptor protein for the binding between Nedd4 of ubiquitin ligase (E3) and target substrate protein for ubiquitination. Northern blot analysis confirmed drastic increases in Ndfip1 mRNA in the striatum after METH injections, and in situ hybridization histochemistry showed that the mRNA expression was increased in the hippocampus and cerebellum at 2 h-2 days, in the cerebral cortex and striatum at 18 h-2 days after single METH administration. The knockdown of Ndfip1 expression with Ndfip1 siRNA significantly aggravated METH-induced neurotoxicity in the cultured monoaminergic neuronal cells. These results suggest that drastic increases in Ndfip1 mRNA is compensatory reaction to protect neurons against METH-induced neurotoxicity.
en-copyright=
kn-copyright=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
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=CadetJean Lud
en-aut-sei=Cadet
en-aut-mei=Jean Lud
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=Molecular Neuropsychiatry Section, Intramural Research Program, NIH/ NIDA
kn-affil=
en-keyword=Methamphetamine
kn-keyword=Methamphetamine
en-keyword=Neurotoxicity
kn-keyword=Neurotoxicity
en-keyword=Nedd4
kn-keyword=Nedd4
en-keyword=Ndfip1
kn-keyword=Ndfip1
en-keyword=Differential display
kn-keyword=Differential display
END

start-ver=1.4
cd-journal=joma
no-vol=741
cd-vols=
no-issue=
article-no=
start-page=151006
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241231
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=S-adenosylmethionine and S-adenosyl-L-homocysteine metabolism is involved in the sperm motility and in vitro fertility rate in mouse
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Increased fragmentation of sperm DNA has been implicated in male infertility. Folate deficiency results in impaired methionine synthesis, depletion of S-adenosylmethionine (SAM) levels, an increase in S-adenosyl-l-homocysteine (SAH) levels, and increased DNA fragmentation. Disruption of the dynamic balance between SAM and SAH may also contribute, although the details of this process are not yet fully understood. We investigated the localization of SAM, SAH, and S-adenosylhomocysteine hydrolase (SAHH), and whether SAM/SAH metabolism contributes to sperm motility and fertilization rate. SAM, SAH, and SAHH levels were assessed in the acrosome, midpiece, and tail of spermatozoa. Chemical inhibition of SAM/SAH metabolism and extracellular SAH significantly decreased the straight-line velocity (VSL), curvilinear velocity (VCL), and amplitude lateral head displacement (ALH) of sperm cells, which were thus unable to swim forward and perform oscillatory movements in place. This significantly reduced the fertilization rate. Therefore, the disruption of the SAM/SAH balance may contribute to male infertility.
en-copyright=
kn-copyright=

en-aut-name=KawaiTomoko
en-aut-sei=Kawai
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujimuraAtsushi
en-aut-sei=Fujimura
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

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

affil-num=2
en-affil=Department of Cellular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=SAM/SAH metabolism
kn-keyword=SAM/SAH metabolism
en-keyword=Sperm motility
kn-keyword=Sperm motility
en-keyword=Fertilization rate
kn-keyword=Fertilization rate
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=2577
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250120
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Plasma S100A8/A9 level predicts response to immune checkpoint inhibitors in patients with advanced non-small cell lung cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Blood-based predictive markers for the efficacy of immune checkpoint inhibitors (ICIs) have not yet been established. We investigated the association of the plasma level of S100A8/A9 with the efficacy of immunotherapy. We evaluated patients with unresectable stage III/IV or recurrent non-small cell lung cancer (NSCLC) who were treated with ICIs at Okayama University Hospital. The pre-treatment plasma levels of S100A8/A9 were analyzed. Eighty-one eligible patients were included (median age, 69 years). Sixty-two patients were men, 54 had adenocarcinoma, 74 had performance status (PS) 0?1, and 47 received ICIs as first-line treatment. The median time to treatment failure (TTF) for ICIs was 5.7 months, and the median overall survival (OS) was 19.6 months. The TTF and OS were worse in patients with high plasma S100A8/A9 levels (??2.475 ?g/mL) (median TTF: 4.3 vs. 8.5 months, p?=?0.009; median OS: 15.4 vs. 38.0 months, p?=?0.001). Multivariate analysis revealed that PS???2, liver metastasis, and high plasma S100A8/A9 levels were significantly associated with short TTF and OS. In conclusion, plasma S100A8/A9 level may have a limited effect on ICI therapy for NSCLC.
en-copyright=
kn-copyright=

en-aut-name=KuribayashiTadahiro
en-aut-sei=Kuribayashi
en-aut-mei=Tadahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
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=3
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=4
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=5
ORCID=

en-aut-name=RaiKammei
en-aut-sei=Rai
en-aut-mei=Kammei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
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=8
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=9
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=10
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=11
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=12
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=13
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=14
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 Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Center for Clinical Oncology, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
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=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=12
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=13
en-affil=Department of Cell Biology, 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=
en-keyword=S100A8/A9
kn-keyword=S100A8/A9
en-keyword=Lung cancer
kn-keyword=Lung cancer
en-keyword=Immune checkpoint inhibitors
kn-keyword=Immune checkpoint inhibitors
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=60
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250106
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Novel Drug Delivery Particles Can Provide Dual Effects on Cancer "Theranostics" in Boron Neutron Capture Therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Boron (B) neutron capture therapy (BNCT) is a novel non-invasive targeted cancer therapy based on the nuclear capture reaction 10B (n, alpha) 7Li that enables the death of cancer cells without damaging neighboring normal cells. However, the development of clinically approved boron drugs remains challenging. We have previously reported on self-forming nanoparticles for drug delivery consisting of a biodegradable polymer, namely, “AB-type” Lactosome? nanoparticles (AB-Lac particles)- highly loaded with hydrophobic B compounds, namely o-Carborane (Carb) or 1,2-dihexyl-o-Carborane (diC6-Carb), and the latter (diC6-Carb) especially showed the “molecular glue” effect. Here we present in vivo and ex vivo studies with human pancreatic cancer (AsPC-1) cells to find therapeutically optimal formulas and the appropriate treatment conditions for these particles. The biodistribution of the particles was assessed by the tumor/normal tissue ratio (T/N) in terms of tumor/muscle (T/M) and tumor/blood (T/B) ratios using near-infrared fluorescence (NIRF) imaging with indocyanine green (ICG). The in vivo and ex vivo accumulation of B delivered by the injected AB-Lac particles in tumor lesions reached a maximum by 12 h post-injection. Irradiation studies conducted both in vitro and in vivo showed that AB-Lac particles-loaded with either 10B-Carb or 10B-diC6-Carb significantly inhibited the growth of AsPC-1 cancer cells or strongly inhibited their growth, with the latter method being significantly more effective. Surprisingly, a similar in vitro and in vivo irradiation study showed that ICG-labeled AB-Lac particles alone, i.e., without any 10B compounds, also revealed a significant inhibition. Therefore, we expect that our ICG-labeled AB-Lac particles-loaded with 10B compound(s) may be a novel and promising candidate for providing not only NIRF imaging for a practical diagnosis but also the dual therapeutic effects of induced cancer cell death, i.e., “theranostics”.
en-copyright=
kn-copyright=

en-aut-name=FithroniAbdul Basith
en-aut-sei=Fithroni
en-aut-mei=Abdul Basith
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=InoueHaruki
en-aut-sei=Inoue
en-aut-mei=Haruki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ZhouShengli
en-aut-sei=Zhou
en-aut-mei=Shengli
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HakimTaufik Fatwa Nur
en-aut-sei=Hakim
en-aut-mei=Taufik Fatwa Nur
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TadaTakashi
en-aut-sei=Tada
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SuzukiMinoru
en-aut-sei=Suzuki
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakuraiYoshinori
en-aut-sei=Sakurai
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IshimotoManabu
en-aut-sei=Ishimoto
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YamadaNaoyuki
en-aut-sei=Yamada
en-aut-mei=Naoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SauriasariRani
en-aut-sei=Sauriasari
en-aut-mei=Rani
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SauerweinWolfgang A. G.
en-aut-sei=Sauerwein
en-aut-mei=Wolfgang A. G.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=WatanabeKazunori
en-aut-sei=Watanabe
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
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=14
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 Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
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=

affil-num=6
en-affil=Institute for Integrated Radiation and Nuclear Science, Kyoto University
kn-affil=

affil-num=7
en-affil=Institute for Integrated Radiation and Nuclear Science, Kyoto University
kn-affil=

affil-num=8
en-affil=J-BEAM, Inc.
kn-affil=

affil-num=9
en-affil=Nihon Fukushi Fuiin Holding, Co., Ltd.
kn-affil=

affil-num=10
en-affil=Faculty of Pharmacy, Universitas Indonesia
kn-affil=

affil-num=11
en-affil=Deutsche Gesellschaft f?r Bor-Neutroneneinfangtherapie DGBNCT e.V., University Hospital Essen, Klinik f?r Strahlentherapie
kn-affil=

affil-num=12
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=13
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=14
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=boron neutron capture therapy (BNCT)
kn-keyword=boron neutron capture therapy (BNCT)
en-keyword=dual therapeutic effects
kn-keyword=dual therapeutic effects
en-keyword=Lactosome ?
kn-keyword=Lactosome ?
en-keyword=hydrophobic boron compound
kn-keyword=hydrophobic boron compound
en-keyword=neutron irradiation
kn-keyword=neutron irradiation
en-keyword=theranostics
kn-keyword=theranostics
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=52
article-no=
start-page=35202
end-page=35213
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241216
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Bright Quantum-Grade Fluorescent Nanodiamonds
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Optically accessible spin-active nanomaterials are promising as quantum nanosensors for probing biological samples. However, achieving bioimaging-level brightness and high-quality spin properties for these materials is challenging and hinders their application in quantum biosensing. Here, we demonstrate bright fluorescent nanodiamonds (NDs) containing 0.6?1.3-ppm negatively charged nitrogen-vacancy (NV) centers by spin-environment engineering via enriching spin-less 12C-carbon isotopes and reducing substitutional nitrogen spin impurities. The NDs, readily introduced into cultured cells, exhibited improved optically detected magnetic resonance (ODMR) spectra; peak splitting (E) was reduced by 2?3 MHz, and microwave excitation power required was 20 times lower to achieve a 3% ODMR contrast, comparable to that of conventional type-Ib NDs. They show average spin-relaxation times of T1 = 0.68 ms and T2 = 3.2 μs (1.6 ms and 5.4 μs maximum) that were 5- and 11-fold longer than those of type-Ib, respectively. Additionally, the extended T2 relaxation times of these NDs enable shot-noise-limited temperature measurements with a sensitivity of approximately 0.28K/√Hz. The combination of bulk-like NV spin properties and enhanced fluorescence significantly improves the sensitivity of ND-based quantum sensors for biological applications.
en-copyright=
kn-copyright=

en-aut-name=OshimiKeisuke
en-aut-sei=Oshimi
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IshiwataHitoshi
en-aut-sei=Ishiwata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakashimaHiromu
en-aut-sei=Nakashima
en-aut-mei=Hiromu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=Mandi?Sara
en-aut-sei=Mandi?
en-aut-mei=Sara
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KobayashiHina
en-aut-sei=Kobayashi
en-aut-mei=Hina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TeramotoMinori
en-aut-sei=Teramoto
en-aut-mei=Minori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TsujiHirokazu
en-aut-sei=Tsuji
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NishibayashiYoshiki
en-aut-sei=Nishibayashi
en-aut-mei=Yoshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShikanoYutaka
en-aut-sei=Shikano
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AnToshu
en-aut-sei=An
en-aut-mei=Toshu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=FujiwaraMasazumi
en-aut-sei=Fujiwara
en-aut-mei=Masazumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Chemistry, Graduate School of Life, Environmental, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=The National Institutes for Quantum Science and Technology (QST), Institute for Quantum Life Science (iQLS)
kn-affil=

affil-num=3
en-affil=Department of Chemistry, Graduate School of Life, Environmental, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Chemistry, Graduate School of Life, Environmental, Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Chemistry, Graduate School of Life, Environmental, Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Advanced Materials Laboratory, Sumitomo Electric Industries, Ltd.
kn-affil=

affil-num=7
en-affil=Advanced Materials Laboratory, Sumitomo Electric Industries, Ltd.
kn-affil=

affil-num=8
en-affil=Advanced Materials Laboratory, Sumitomo Electric Industries, Ltd.
kn-affil=

affil-num=9
en-affil=Institute of Systems and Information Engineering, University of Tsukuba
kn-affil=

affil-num=10
en-affil=School of Materials Science, Japan Advanced Institute of Science and Technology
kn-affil=

affil-num=11
en-affil=Department of Chemistry, Graduate School of Life, Environmental, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=nanodiamonds
kn-keyword=nanodiamonds
en-keyword=nitrogen-vacancy centers
kn-keyword=nitrogen-vacancy centers
en-keyword=spins
kn-keyword=spins
en-keyword=spin-relaxation times
kn-keyword=spin-relaxation times
en-keyword=quantum biosensor
kn-keyword=quantum biosensor
en-keyword=cellular probes
kn-keyword=cellular probes
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=
article-no=
start-page=1439705
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241211
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=HOMA-beta independently predicts survival in patients with advanced cancer on treatment with immune checkpoint inhibitors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Although immune checkpoint inhibitors (ICIs) are effective cancer drugs, ICI-induced diabetes is a rare but a life-threatening adverse event for patients. The deleterious action of ICI on pancreatic beta-cell function is a concern. However, the influence of ICI on insulin synthesis and secretion in patients with cancer without diabetes remains unknown. <br>
Methods: This study included 87 patients diagnosed with advanced cancer. Glucose metabolism markers (HbA1c, HOMA-IR) and indicators of insulin secretory capacity (HOMA-beta, C-peptide) were prospectively evaluated in patients with ICI-treated cancers to determine their association with cancer prognosis. <br>
Results: Patients with overall survival (OS) >= 7 months had substantially higher HOMA-beta levels at baseline (p=0.008) and 1 month after ICI administration (p=0.006) compared to those with OS <7 months. The median OS was significantly longer in patients with HOMA-beta >= 64.24 (13 months, 95%CI: 5.849-20.151, 37 events) than in those with HOMA-beta < 64.24 (5 months, 95%CI: 3.280-6.720, 50 events) (p=0.013). Further, the median progression-free survival (PFS) was significantly longer in patients with HOMA-beta >= 66.43 (4 months, 95%CI: 3.073-4.927, 33 events) than in those with HOMA-beta < 66.43 (2 months, 95%CI: 1.410-2.590, 54 events) (p=0.025). Additionally, multivariable logistic regression analysis revealed that a HOMA-beta value >= 64.24 independently predicted longer OS in ICI-treated patients. <br>
Conclusions: Pre-ICI HOMA-beta level is linked to longer OS in ICI-treated patients. This connection is significant and shows that insulin secretory capacity may predict ICI efficacy.
en-copyright=
kn-copyright=

en-aut-name=WatanabeMayu
en-aut-sei=Watanabe
en-aut-mei=Mayu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakamotoAtsushi
en-aut-sei=Takamoto
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KanzakiHiromitsu
en-aut-sei=Kanzaki
en-aut-mei=Hiromitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NodaYohei
en-aut-sei=Noda
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KagawaSyunsuke
en-aut-sei=Kagawa
en-aut-mei=Syunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=

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

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

affil-num=3
en-affil=Department of Urology, Fukuyama City Hospital
kn-affil=

affil-num=4
en-affil=Department of Internal Medicine, Tsuyama Chuo Hospital
kn-affil=

affil-num=5
en-affil=Department of Urology, Fukuyama City Hospital
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 Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=anti-PD1 immune checkpoint inhibitors
kn-keyword=anti-PD1 immune checkpoint inhibitors
en-keyword= insulin secretory capacity
kn-keyword= insulin secretory capacity
en-keyword= cancer prognosis
kn-keyword= cancer prognosis
en-keyword= insulin secretion
kn-keyword= insulin secretion
en-keyword= glucose metabolism markers
kn-keyword= glucose metabolism markers
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=24
article-no=
start-page=2045
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241211
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=iPSC-Derived Biological Pacemaker-From Bench to Bedside
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Induced pluripotent stem cell (iPSC)-derived biological pacemakers have emerged as an alternative to traditional electronic pacemakers for managing cardiac arrhythmias. While effective, electronic pacemakers face challenges such as device failure, lead complications, and surgical risks, particularly in children. iPSC-derived pacemakers offer a promising solution by mimicking the sinoatrial node's natural pacemaking function, providing a more physiological approach to rhythm control. These cells can differentiate into cardiomyocytes capable of autonomous electrical activity, integrating into heart tissue. However, challenges such as achieving cellular maturity, long-term functionality, and immune response remain significant barriers to clinical translation. Future research should focus on refining gene-editing techniques, optimizing differentiation, and developing scalable production processes to enhance the safety and effectiveness of these biological pacemakers. With further advancements, iPSC-derived pacemakers could offer a patient-specific, durable alternative for cardiac rhythm management. This review discusses key advancements in differentiation protocols and preclinical studies, demonstrating their potential in treating dysrhythmias.
en-copyright=
kn-copyright=

en-aut-name=VoQuan Duy
en-aut-sei=Vo
en-aut-mei=Quan Duy
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
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=3
ORCID=

en-aut-name=IidaToshihiro
en-aut-sei=Iida
en-aut-mei=Toshihiro
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=AmiokaNaofumi
en-aut-sei=Amioka
en-aut-mei=Naofumi
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=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YuasaShinsuke
en-aut-sei=Yuasa
en-aut-mei=Shinsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

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

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

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

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

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

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

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

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

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=sinoatrial node
kn-keyword=sinoatrial node
en-keyword=HCN channels
kn-keyword=HCN channels
en-keyword=induced pluripotent stem cell
kn-keyword=induced pluripotent stem cell
END

start-ver=1.4
cd-journal=joma
no-vol=169
cd-vols=
no-issue=1
article-no=
start-page=e16291
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241222
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Exploring the Role of Ccn3 in Type III Cell of Mice Taste Buds
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Different taste cells express unique cell-type markers, enabling researchers to distinguish them and study their functional differentiation. Using single-cell RNA-Seq of taste cells in mouse fungiform papillae, we found that Cellular Communication Network Factor 3 (Ccn3) was highly expressed in Type III taste cells but not in Type II taste cells. Ccn3 is a protein-coding gene involved in various biological processes, such as cell proliferation, angiogenesis, tumorigenesis, and wound healing. Therefore, in this study, we aimed to explore the expression and function of Ccn3 in mouse taste bud cells. Using reverse transcription polymerase chain reaction (RT-PCR), in situ hybridization, and immunohistochemistry (IHC), we confirmed that Ccn3 was predominantly expressed in Type III taste cells. Through IHC, quantitative real-time RT-PCR, gustatory nerve recordings, and short-term lick tests, we observed that Ccn3 knockout (Ccn3-KO) mice did not exhibit any significant differences in the expression of taste cell markers and taste responses compared to wild-type controls. To explore the function of Ccn3 in taste cells, bioinformatics analyses were conducted and predicted possible roles of Ccn3 in tissue regeneration, perception of pain, protein secretion, and immune response. Among them, an immune function is the most plausible based on our experimental results. In summary, our study indicates that although Ccn3 is strongly expressed in Type III taste cells, its knockout did not influence the basic taste response, but bioinformatics provided valuable insights into the possible role of Ccn3 in taste buds and shed light on future research directions.
en-copyright=
kn-copyright=

en-aut-name=WangKuanyu
en-aut-sei=Wang
en-aut-mei=Kuanyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MitohYoshihiro
en-aut-sei=Mitoh
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HorieKengo
en-aut-sei=Horie
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

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

affil-num=2
en-affil=Department of Oral Physiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral Physiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Oral Physiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=bioinformatics
kn-keyword=bioinformatics
en-keyword=Ccn3
kn-keyword=Ccn3
en-keyword=Type III taste cell
kn-keyword=Type III taste cell
END

start-ver=1.4
cd-journal=joma
no-vol=145
cd-vols=
no-issue=8
article-no=
start-page=881
end-page=896
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250220
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Oral Inflammation and Microbiome Dysbiosis Exacerbate Chronic Graft-versus-host Disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The oral microbiota, second in abundance to the gut, is implicated in chronic systemic diseases, but its specific role in graft-versus-host disease (GVHD) pathogenesis has been unclear. Our study finds that mucositis-induced oral dysbiosis in patients after hematopoietic cell transplantation (HCT) associated with increased chronic GVHD (cGVHD), even in patients receiving posttransplant cyclophosphamide. In murine HCT models, oral dysbiosis caused by bilateral molar ligatures exacerbated cGVHD and increased bacterial load in the oral cavity and gut, with Enterococcaceae significantly increasing in both organs. In this model, the migration of Enterococcaceae to cervical lymph nodes both before and after transplantation activated antigen-presenting cells, thereby promoting the expansion of donor-derived inflammatory T cells. Based on these results, we hypothesize that pathogenic bacteria increase in the oral cavity might not only exacerbate local inflammation but also enhance systemic inflammation throughout the HCT course. Additionally, these bacteria translocated to the gut and formed ectopic colonies, further amplifying systemic inflammation. Furthermore, interventions targeting the oral microbiome mitigated murine cGVHD. Collectively, our findings highlight the importance of oral dysbiosis in cGVHD and suggest that modulation of the oral microbiome during transplantation may be an effective approach for preventing or treating cGVHD.
en-copyright=
kn-copyright=

en-aut-name=KambaraYui
en-aut-sei=Kambara
en-aut-mei=Yui
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=YamamotoAkira
en-aut-sei=Yamamoto
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=GotohKazuyoshi
en-aut-sei=Gotoh
en-aut-mei=Kazuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TsujiShuma
en-aut-sei=Tsuji
en-aut-mei=Shuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KunihiroMari
en-aut-sei=Kunihiro
en-aut-mei=Mari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OyamaTadashi
en-aut-sei=Oyama
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TeraoToshiki
en-aut-sei=Terao
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SatoAyame
en-aut-sei=Sato
en-aut-mei=Ayame
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
ORCID=

en-aut-name=PeltierDaniel
en-aut-sei=Peltier
en-aut-mei=Daniel
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
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=12
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=13
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=14
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=15
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=16
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=17
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=18
ORCID=

en-aut-name=SogaYoshihiko
en-aut-sei=Soga
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=ReddyPavan
en-aut-sei=Reddy
en-aut-mei=Pavan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=YoshinobuMaeda
en-aut-sei=Yoshinobu
en-aut-mei=Maeda
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 Medical School
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 Medical Laboratory Science, Okayama University Graduate School of Health Sciences
kn-affil=

affil-num=5
en-affil=Department of Microbiology and Genetics, Okayama University Graduate School of Health 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=Division of Hospital Dentistry, Okayama University Hospital
kn-affil=

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

affil-num=11
en-affil=Division of Pediatric Hematology, Oncology, and Stem Cell Transplantation, Department of Pediatrics, Herman B Wells Center for Pediatric Research, Simon Cancer Center, Indiana University School of Medicine
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=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=16
en-affil=Department of Clinical Laboratory, Okayama University Hospital
kn-affil=

affil-num=17
en-affil=Division of Blood Transfusion, Okayama University Hospital
kn-affil=

affil-num=18
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=19
en-affil=Division of Hospital Dentistry, Okayama University Hospital
kn-affil=

affil-num=20
en-affil=Dan L Duncan Comprehensive Cancer Center, Baylor College of Medicine
kn-affil=

affil-num=21
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=44
cd-vols=
no-issue=2
article-no=
start-page=249
end-page=260
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241005
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Loss of Nr4a1 ameliorates endothelial cell injury and vascular leakage in lung transplantation from circulatory-death donor
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Ischemia-reperfusion injury (IRI) stands as a major trigger for primary graft dysfunction (PGD) in lung transplantation (LTx). Especially in LTx from donation after cardiac death (DCD), effective control of IRI following warm ischemia (WIRI) is crucial to prevent PGD. This study aimed to identify the key factors affecting WIRI in LTx from DCD.<br>
Methods: Previously reported RNA-sequencing dataset of lung WIRI was reanalyzed to identify nuclear receptor subfamily 4 group A member 1 (NR4A1) as the immediate early gene for WIRI. Dynamics of NR4A1 expression were verified using a mouse hilar clamp model. To investigate the role of NR4A1 in WIRI, a mouse model of LTx from DCD was established using Nr4a1 knockout (Nr4a1?/?) mice.<br>
Results: NR4A1 was located around vascular cells, and its protein levels in the lungs increased rapidly and transiently during WIRI. LTｘ from Nr4a1?/? donors significantly improved pulmonary graft function compared to wild-type donors. Histological analysis showed decreased microvascular endothelial cell death, neutrophil infiltration, and albumin leakage. Evans blue permeability assay demonstrated maintained pulmonary microvascular barrier integrity in grafts from Nr4a1?/? donors, correlating with diminished pulmonary edema. However, NR4A1 did not significantly affect the inflammatory response during WIRI, and IRI was not suppressed when a wild-type donor lung was transplanted into the Nr4a1?/? recipient.<br>
Conclusions: Donor NR4A1 plays a specialized role in the positive regulation of endothelial cell injury and microvascular hyperpermeability. These findings demonstrate the potential of targeting NR4A1 interventions to alleviate PGD and improve outcomes in LTx from DCD.
en-copyright=
kn-copyright=

en-aut-name=KawanaShinichi
en-aut-sei=Kawana
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=SakaueTomohisa
en-aut-sei=Sakaue
en-aut-mei=Tomohisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HashimotoKohei
en-aut-sei=Hashimoto
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakataKentaro
en-aut-sei=Nakata
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ChoshiHaruki
en-aut-sei=Choshi
en-aut-mei=Haruki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TanakaShin
en-aut-sei=Tanaka
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

en-aut-name=OhtaniShinji
en-aut-sei=Ohtani
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=SugimotoSeiichiro
en-aut-sei=Sugimoto
en-aut-mei=Seiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MatsukawaAkihiro
en-aut-sei=Matsukawa
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=13
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 Cardiovascular and Thoracic Surgery, Ehime University Graduate School of Medicine
kn-affil=

affil-num=4
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=5
en-affil=Department of Surgery, Division of Cardiovascular and Thoracic Surgery, Duke University School of Medicine
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 Cell Growth and Tumor Regulation, Proteo-Science Center (PROS), Ehime University
kn-affil=

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

affil-num=11
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=12
en-affil=Department of Pathology and Experimental Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
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
kn-keyword=lung transplantation
en-keyword=ischemia-reperfusion injury
kn-keyword=ischemia-reperfusion injury
en-keyword=donation after circulatory death
kn-keyword=donation after circulatory death
en-keyword=nuclear receptor subfamily 4 group A member 1
kn-keyword=nuclear receptor subfamily 4 group A member 1
en-keyword=endothelial cell
kn-keyword=endothelial cell
END

start-ver=1.4
cd-journal=joma
no-vol=226
cd-vols=
no-issue=
article-no=
start-page=158
end-page=166
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240915
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The impact of cumulus cell viability and pre-culture with the healthy cell mass on brilliant cresyl blue (BCB) staining assessment and meiotic competence of suboptimal porcine oocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objectives of the present study were to investigate the characteristics including glucose-6-phosphate dehydrogenase activity, as determined by Brilliant Cresyl Blue (BCB) staining, of suboptimal porcine oocytes and to enhance the meiotic competence of those through pre-culture with cumulus cell masses (CCMs). Percentage of oocyte-cumulus complexes (OCCs) derived from small follicles (SF; <3 mm in diameter) containing the oocytes that were assessed as BCB-negative (BCB-) was significantly higher than those derived from medium follicles (MF; 3?6 mm in diameter). Degrees of dead cumulus cells were significantly higher in OCCs containing BCB- oocytes, regardless of the origin of OCCs (MF vs. SF), than those containing BCB-positive (BCB+) ones. Exposing OCCs containing BCB+ oocytes to the apoptosis inducer, carbonyl cyanide m-chlorophenylhydrazone, for 20 h significantly induced the transition to BCB- and meiotic progression of exposed OCCs were significantly reduced in both SF and MF derived ones. Transit of BCB- oocytes to BCB+ was induced when OCCs were pre-cultured with CCMs of MF derived OCCs containing BCB+ oocytes for 20 h before IVM. This pre-culture also significantly increased the meiotic competence of BCB- oocytes, particularly in SF derived ones. However, reactive oxygen species levels were significantly higher in BCB+ oocytes as compared with BCB- ones, regardless of pre-culture with CCMs, whereas no significant differences were found in the ATP contents among the treatment groups. In conclusion, the BCB result of oocytes could be regulated by the healthy status and content of surrounding cumulus cells and the meiotic competence of suboptimal BCB- porcine oocytes is improved by pre-culture with healthy CCMs.
en-copyright=
kn-copyright=

en-aut-name=FonsekaWanniarachchige Tharindu Lakshitha
en-aut-sei=Fonseka
en-aut-mei=Wanniarachchige Tharindu Lakshitha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=DoSon Quang
en-aut-sei=Do
en-aut-mei=Son Quang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=VanPhong Ngoc
en-aut-sei=Van
en-aut-mei=Phong Ngoc
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NguyenHai Thanh
en-aut-sei=Nguyen
en-aut-mei=Hai Thanh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WakaiTakuya
en-aut-sei=Wakai
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FunahashiHiroaki
en-aut-sei=Funahashi
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Animal Science, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Animal Science, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Animal Science, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Animal Science, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Animal Science, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Animal Science, Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=Oocytes
kn-keyword=Oocytes
en-keyword=Meiotic competence
kn-keyword=Meiotic competence
en-keyword=Brilliant cresyl blue
kn-keyword=Brilliant cresyl blue
en-keyword=Cumulus cells
kn-keyword=Cumulus cells
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=13
cd-vols=
no-issue=1
article-no=
start-page=e70097
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250107
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Eyelid Spindle Cell Lipoma: Case Report and Review of Three Patients in Literature
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A 39-year-old woman presented a saucer-shaped mass in the left upper eyelid and underwent the extirpation at local anesthesia. Pathologically, collagen fibers, capillaries, small vessels, and CD34-positive spindle cells were dispersed among mature adipose tissues, indicative of spindle cell lipoma. Long-lasting cyst-like eyelid masses would be usually dermoid cysts, and spindle cell lipoma would be listed as a rare pathological diagnosis in differential diagnoses of cyst-like lesions in the upper and lower eyelid.
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=YamadaKiyoshi
en-aut-sei=Yamada
en-aut-mei=Kiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MonobeYasumasa
en-aut-sei=Monobe
en-aut-mei=Yasumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=Plastic and Reconstructive Surgery, Kousei Hospital
kn-affil=

affil-num=3
en-affil=Department of Pathology, General Medical Center, Kawasaki Medical School
kn-affil=

affil-num=4
en-affil=Department of Pathology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=CD34
kn-keyword=CD34
en-keyword=eyelid
kn-keyword=eyelid
en-keyword=orbital bony edge
kn-keyword=orbital bony edge
en-keyword=pathology
kn-keyword=pathology
en-keyword=spindle cell lipoma
kn-keyword=spindle cell lipoma
END

start-ver=1.4
cd-journal=joma
no-vol=45
cd-vols=
no-issue=1
article-no=
start-page=11
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230323
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mutation and apoptosis are well-coordinated for protecting against DNA damage-inducing toxicity in Drosophila
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Apoptotic cell death is an important survival system for multicellular organisms because it removes damaged cells. Mutation is also a survival method for dealing with damaged cells in multicellular and also unicellular organisms, when DNA lesions are not removed. However, to the best of our knowledge, no reports have comprehensively explored the direct relationship between apoptosis and somatic cell mutations induced by various mutagenic factors.<br>
Results Mutation was examined by the wing-spot test, which is used to detect somatic cell mutations, including chromosomal recombination. Apoptosis was observed in the wing discs by acridine orange staining in situ. After treatment with chemical mutagens, ultraviolet light (UV), and X-ray, both the apoptotic frequency and mutagenic activity increased in a dose-dependent manner at non-toxic doses. When we used DNA repair-deficient Drosophila strains, the correlation coefficient of the relationship between apoptosis and mutagenicity, differed from that of the wild-type. To explore how apoptosis affects the behavior of mutated cells, we determined the spot size, i.e., the number of mutated cells in a spot. In parallel with an increase in apoptosis, the spot size increased with MNU or X-ray treatment dose-dependently; however, this increase was not seen with UV irradiation. In addition, BrdU incorporation, an indicator of cell proliferation, in the wing discs was suppressed at 6 h, with peak at 12 h post-treatment with X-ray, and that it started to increase again at 24 h; however, this was not seen with UV irradiation.<br>
Conclusion Damage-induced apoptosis and mutation might be coordinated with each other, and the frequency of apoptosis and mutagenicity are balanced depending on the type of DNA damage. From the data of the spot size and BrdU incorporation, it is possible that mutated cells replace apoptotic cells due to their high frequency of cell division, resulting in enlargement of the spot size after MNU or X-ray treatment. We consider that the induction of mutation, apoptosis, and/or cell growth varies in multi-cellular organisms depending on the type of the mutagens, and that their balance and coordination have an important function to counter DNA damage for the survival of the organism.
en-copyright=
kn-copyright=

en-aut-name=Toyoshima-SasataniMegumi
en-aut-sei=Toyoshima-Sasatani
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ImuraFumika
en-aut-sei=Imura
en-aut-mei=Fumika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HamatakeYuko
en-aut-sei=Hamatake
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FukunagaAkihiro
en-aut-sei=Fukunaga
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NegishiTomoe
en-aut-sei=Negishi
en-aut-mei=Tomoe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

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

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

affil-num=4
en-affil=School of Nursing, Osaka City University
kn-affil=

affil-num=5
en-affil=Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Drosophila
kn-keyword=Drosophila
en-keyword=Apoptosis
kn-keyword=Apoptosis
en-keyword=Mutation
kn-keyword=Mutation
en-keyword=Larval wing disc
kn-keyword=Larval wing disc
en-keyword=X-ray
kn-keyword=X-ray
en-keyword=Ultraviolet
kn-keyword=Ultraviolet
en-keyword=Alkylating agents
kn-keyword=Alkylating agents
en-keyword=Tobacco smoke
kn-keyword=Tobacco smoke
en-keyword=Acridine orange
kn-keyword=Acridine orange
en-keyword=BrdU
kn-keyword=BrdU
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=04
article-no=
start-page=E351
end-page=E357
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230213
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Degree of pharyngeal deformation caused by pharyngeal endoscopic submucosal dissection is associated with the incidence of aspiration pneumonia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background and study aims?Endoscopic submucosal dissection (ESD) is one of the most minimally invasive treatments for superficial squamous cell cancer of the pharynx. However, aspiration pneumonia (AsP) associated with postoperative deformity of the pharynx may occur. The purpose of this study was to investigate the frequency of AsP and the degree of pharyngeal deformity after pharyngeal ESD.<br>
Patients and methods?This was a retrospective observational study of patients who underwent pharyngeal ESD at Okayama University Hospital between 2006 and 2017.?The degree of pharyngeal deformation was assessed using the pharyngeal deformation grade (PDG). The primary endpoint was the frequency of AsP as a long-term adverse event.<br>
Results?Among the 52 patients enrolled, nine developed aspiration pneumonia, with a 3-year cumulative incidence of 9.0?% (95?% confidence interval [CI], 3.3?%?22.0?%). There were 16, 18, 16, and two patients that had PDG 0, 1, 2, and 3, respectively. Patients with a history of radiotherapy, as a treatment of head and neck cancer (44.4?% vs. 11.6?%; P?=?0.02) and the high PDG group (PDG 2 and 3) (77.8?% vs. 25.6?%; P?=?0.005) had a significantly higher incidence of AsP. The 3-year cumulative incidence rate of AsP after ESD in the high PDG group was significantly higher than that in the low PDG group (PDG 0 and 1) (23.9?% [95?%CI, 9.2.?49.5%] vs. 0?%; P?=?0.03).<br>
Conclusions?The incidence of aspiration pneumonia in the long-term course after pharyngeal ESD was revealed. The incidence of aspiration pneumonia may be associated with pharyngeal deformity, but further studies are needed.
en-copyright=
kn-copyright=

en-aut-name=AbeMakoto
en-aut-sei=Abe
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawaharaYoshiro
en-aut-sei=Kawahara
en-aut-mei=Yoshiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ObayashiYuka
en-aut-sei=Obayashi
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=BabaYuki
en-aut-sei=Baba
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HamadaKenta
en-aut-sei=Hamada
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SakaeHiroyuki
en-aut-sei=Sakae
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=

en-aut-name=KanzakiHiromitu
en-aut-sei=Kanzaki
en-aut-mei=Hiromitu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
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=10
ORCID=

en-aut-name=MakinoTakuma
en-aut-sei=Makino
en-aut-mei=Takuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NodaYohei
en-aut-sei=Noda
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MarunakaHidenori
en-aut-sei=Marunaka
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
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=14
ORCID=

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

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

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

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

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

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

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

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

affil-num=9
en-affil=Department of Gastroenterology, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of Gastroenterology, Okayama University Hospital
kn-affil=

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

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

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

affil-num=14
en-affil=Department of Gastroenterology, Okayama University Hospital
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=33
cd-vols=
no-issue=4
article-no=
start-page=213
end-page=218
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=2024
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=β-catenin Binds to Gsk-3β in Liquid-Liquid Phase Separation Compartment in HEK293 Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Liquid-liquid phase separation (LLPS) has emerged as a significant mechanism for cellular organization, impacting various biological processes, including Wnt/β-catenin signaling. This study investigates the role of LLPS in the regulation of β-catenin in HEK293 cells, particularly in response to Wnt3a signaling. Our findings demonstrate that β-catenin is regulated by LLPS, forming spherical droplets indicative of this phenomenon. Fluorescence recovery after photobleaching (FRAP) assays revealed that these droplets exhibit reversible dynamics, further confirming their phase-separated nature. Importantly, treatment with Wnt3a led to an increase in β-catenin levels, while simultaneously reducing the recovery of fluorescence intensity in FRAP experiments, suggesting that enhanced Wnt signaling may stimulate the release of β-catenin from LLPS. Immunoprecipitation studies indicated that β-catenin binds to glycogen synthase kinase 3β (Gsk-3β) within the LLPS state, highlighting a potential regulatory mechanism whereby LLPS facilitates the phosphorylation and subsequent degradation of β-catenin. The addition of 1,6-hexanediol disrupted the β-catenin/Gsk-3β interaction, reinforcing the idea that LLPS plays a critical role in modulating these biochemical interactions. The findings presented in this study suggest that LLPS is not only crucial for the spatial organization of β-catenin but also serves as a regulatory mechanism for its signaling functions in the Wnt pathway. Given the association of aberrant Wnt signaling with various diseases, including cancer and neurodegenerative disorders, understanding the role of LLPS in this context may provide new insights into therapeutic strategies targeting these pathological conditions.
en-copyright=
kn-copyright=

en-aut-name=KatoMari
en-aut-sei=Kato
en-aut-mei=Mari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanaiAiri
en-aut-sei=Tanai
en-aut-mei=Airi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FukuharaYoko
en-aut-sei=Fukuhara
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ZhengXinyu
en-aut-sei=Zheng
en-aut-mei=Xinyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SitosariHeriati
en-aut-sei=Sitosari
en-aut-mei=Heriati
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

en-aut-name=IkegameMika
en-aut-sei=Ikegame
en-aut-mei=Mika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

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

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

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

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

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

affil-num=6
en-affil=The Center for Graduate Medical Education (Dental Division), Okayama University Hospital
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 Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=β-catenin
kn-keyword=β-catenin
en-keyword=Gsk-3β
kn-keyword=Gsk-3β
en-keyword=LLPS
kn-keyword=LLPS
en-keyword=Wnt
kn-keyword=Wnt
END

start-ver=1.4
cd-journal=joma
no-vol=136
cd-vols=
no-issue=3
article-no=
start-page=97
end-page=99
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241202
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The 2023 Incentive Award of the Okayama Medical Association in Cardiovascular and Pulmonary Research (2023 Sunada Prize)
kn-title=令和５年度岡山医学会賞　胸部・循環研究奨励賞（砂田賞）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TaniguchiAkihiko
en-aut-sei=Taniguchi
en-aut-mei=Akihiko
kn-aut-name=谷口暁彦
kn-aut-sei=谷口
kn-aut-mei=暁彦
aut-affil-num=1
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=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=126
cd-vols=
no-issue=
article-no=
start-page=110572
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=Laparoscopic resection for oesophageal duplication cyst: A case report
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction: Oesophageal duplication cyst is a congenital malformation and rare tumour, clinically manifesting as dysphagia, epigastric pain, or respiratory distress. Duplicate cysts associated with abscess formation or mediastinal penetration and malignancies have been reported, necessitating surgical resection. <br>
Presentation of case: A 55-year-old woman had chest discomfort for 1 year. Preoperative imaging, including computed tomography (CT), upper gastrointestinal endoscopy, and endoscopic ultrasound, revealed a tumour extending from the anterior wall to the lesser curvature of the near the oesophagogastric junction (OGJ) and a suspected mural nodule within the tumour. Contrast-enhanced CT revealed a cystic nodule on the wall of the lesser curvature of the OGJ, with an unclear boundary between the cystic nodule and the oesophageal wall. Magnetic resonance imaging showed an isointense signal on T1-weighted imaging and hyperintensity on T2weighted imaging. Laparoscopic lower oesophagectomy and proximal gastrectomy with lymph node dissection were performed to the confirm mucinous cyst. Pathological findings revealed a cystic lesion in the muscularis propria of the OGJ filled with mucinous components and lined with multilayered columnar epithelial cells. The cyst was diagnosed as a duplicate without malignancy. <br>
Discussion: Since the border between the cyst and the oesophageal walls was unclear, and the cyst potentially contained a malignant component, instead of cystectomy, lower oesophagectomy and proximal gastrectomy with lymph node dissection were performed with oesophagogastric anastomosis using the double-flap technique, tailored specifically for OGJ cancer. <br>
Conclusions: Oesophageal duplication cysts are rare. Lower oesophagectomy and proximal gastrectomy are selective surgical approaches for cyst duplication at the OGJ.
en-copyright=
kn-copyright=

en-aut-name=HamazakiTomohiro
en-aut-sei=Hamazaki
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=KawasakiKento
en-aut-sei=Kawasaki
en-aut-mei=Kento
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HashimotoMasashi
en-aut-sei=Hashimoto
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TanabeShunsuke
en-aut-sei=Tanabe
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
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=
en-keyword=Oesophageal duplication cyst
kn-keyword=Oesophageal duplication cyst
en-keyword=Laparoscopic surgery
kn-keyword=Laparoscopic surgery
en-keyword=Lower oesophagectomy
kn-keyword=Lower oesophagectomy
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=28
end-page=36
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=Local Control of Conjunctival Malignant Melanoma by Proton Beam Therapy in a Patient With No Metastasis in Six Years From in Situ to Nodular Lesions
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Conjunctival malignant melanoma is extremely rare, with no standard of care established at moment. Here we report a 65-year-old woman, as a hepatitis B virus (HBV) carrier, who presented concurrently a liver mass and lower bulbar conjunctival pigmented lesions in the right eye. Needle liver biopsy and excisional conjunctival biopsy showed hepatocellular carcinoma and conjunctival malignant melanoma in situ, respectively. The priority was given to segmental liver resection for hepatocellular carcinoma after transcatheter arterial chemoembolization. In 1 year, she underwent second and third resection of bulbar conjunctival pigmented lesions, and the pathological examinations constantly showed melanoma in situ. In the course, she showed gradual widening of pigmented lesions to upper bulbar conjunctiva and lower palpebral conjunctiva and lower eyelid. About 2.5 years from the initial visit, the lower eyelid lesion was resected for a genomic DNA-based test of BRAF mutations which turned out to be absent, and then, she began to have intravenous anti-programmed cell death-1 (PD-1), nivolumab every 3 or 4 weeks. She developed iritis in the right eye with conjunctival melanoma as an immune-related adverse event, 3 months after the beginning of nivolumab, and so she used daily topical 0.1% betamethasone eye drops to control the intraocular inflammation. She showed no metastasis in 6 years of follow-up, but later in the course, 5 years from the initial visit, she developed abruptly a non-pigmented nodular lesion on the temporal side of the bulbar conjunctiva along the corneal limbus, accompanied by two pigmented nodular lesions in the upper and lower eyelids in a few months. She thus, underwent proton beam therapy toward the conjunctival melanoma and achieved the successful local control. Proton beam therapy is a treatment option in place of orbital exenteration, and multidisciplinary team collaboration is desirable to achieve better cosmetic and functional outcomes in conjunctival malignant melanoma.
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=OgataTakeshi
en-aut-sei=Ogata
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WakiTakahiro
en-aut-sei=Waki
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=TachibanaKota
en-aut-sei=Tachibana
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
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=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=

affil-num=1
en-affil=Regenerative and Reconstructive Medicine (Ophthalmology), Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Radiology, Proton Beam Center, Tsuyama Chuo Hospital
kn-affil=

affil-num=3
en-affil=Department of Radiology, Proton Beam Center, Tsuyama Chuo Hospital
kn-affil=

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

affil-num=7
en-affil=Department of Gastroenterology and Hepatology, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Dermatology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Ocular surface
kn-keyword=Ocular surface
en-keyword=Conjunctiva
kn-keyword=Conjunctiva
en-keyword=Malignant melanoma
kn-keyword=Malignant melanoma
en-keyword=Proton beam therapy
kn-keyword=Proton beam therapy
en-keyword=Nivolumab
kn-keyword=Nivolumab
en-keyword=PD-1 inhibitor
kn-keyword=PD-1 inhibitor
en-keyword=Immune checkpoint inhibitor
kn-keyword=Immune checkpoint inhibitor
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=23
article-no=
start-page=4089
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241206
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Frequency and Significance of Body Weight Loss During Immunochemotherapy in Patients with Advanced Non-Small Cell Lung Cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Limited data are available on the frequency and significance of body weight loss during cancer therapy. This study investigated the frequency of patients who experienced body weight loss during immune checkpoint inhibitor (ICI) plus chemotherapy for advanced non-small cell lung cancer (NSCLC) and the impact of weight loss on treatment outcomes. Methods: Using the clinical data of 370 patients with NSCLC who received a combination of ICI and chemotherapy at 13 institutions, this study investigated the frequency of body weight loss > 5% during treatment and determined the impact of body weight loss on patient outcomes. Results: Of the 370 included patients, 141 (38.1%) lost more than 5% of their body weight during ICI plus chemotherapy (WL group). The 2-month landmark analysis showed that patients who experienced body weight loss of >5% during treatment had worse overall survival (OS) and progression-free survival (PFS) than those who did not (OS 14.0 and 31.1 months in the WL non-WL groups, respectively, p < 0.001; PFS 6.8 and 10.9 months in the WL non-WL groups, respectively, p = 0.002). Furthermore, a negative impact of body weight loss on survival was observed even in those who had obesity (body mass index [BMI] >= 25.0) at the start of therapy (OS 12.8 and 25.4 months in the WL non-WL groups, respectively, p < 0.001; PFS 5.7 and 10.7 months in the WL non-WL groups, respectively, p = 0.038). Conclusions: In conclusion, weight loss of >5% during ICI plus chemotherapy negatively influenced patient outcomes. Further and broader studies should investigate the role of nutritional status, specifically weight change and nutritional support, in responsiveness to ICI plus chemotherapy.
en-copyright=
kn-copyright=

en-aut-name=TaokaMasataka
en-aut-sei=Taoka
en-aut-mei=Masataka
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=YokoyamaToshihide
en-aut-sei=Yokoyama
en-aut-mei=Toshihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=InoueKoji
en-aut-sei=Inoue
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TamuraTomoki
en-aut-sei=Tamura
en-aut-mei=Tomoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SatoAkiko
en-aut-sei=Sato
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
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=8
ORCID=

en-aut-name=NakamuraKayo
en-aut-sei=Nakamura
en-aut-mei=Kayo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KawaiHaruyuki
en-aut-sei=Kawai
en-aut-mei=Haruyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=InoueMasaaki
en-aut-sei=Inoue
en-aut-mei=Masaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OchiNobuaki
en-aut-sei=Ochi
en-aut-mei=Nobuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=FujimotoNobukazu
en-aut-sei=Fujimoto
en-aut-mei=Nobukazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
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=14
ORCID=

en-aut-name=AndoChihiro
en-aut-sei=Ando
en-aut-mei=Chihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=OzeIsao
en-aut-sei=Oze
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
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=17
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=18
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=19
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=Center for Clinical Oncology, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Respiratory Medicine, Ohara Healthcare Foundation, Kurashiki Central Hospital
kn-affil=

affil-num=4
en-affil=Department of Respiratory Medicine, Ehime Prefectural Central Hospital
kn-affil=

affil-num=5
en-affil=Department of Respiratory Medicine, NHO Iwakuni Clinical Center
kn-affil=

affil-num=6
en-affil=Department of Internal Medicine, National Hospital Organization Okayama Medical Center
kn-affil=

affil-num=7
en-affil=Department of Respiratory Medicine, Fukuyama City Hospital
kn-affil=

affil-num=8
en-affil=Department of Respiratory Medicine, Japanese Red Cross Okayama Hospital
kn-affil=

affil-num=9
en-affil=Department of Respiratory Medicine, Japanese Red Cross Himeji Hospital
kn-affil=

affil-num=10
en-affil=Department of Internal Medicine, Okayama Saiseikai General Hospital
kn-affil=

affil-num=11
en-affil=Department of Chest Surgery, Shimonoseki City Hospital
kn-affil=

affil-num=12
en-affil=Department of General Internal Medicine 4 , Kawasaki Medical School
kn-affil=

affil-num=13
en-affil=Department of Respiratory Medicine, Okayama Rosai Hospital
kn-affil=

affil-num=14
en-affil=Department of Respiratory Medicine, KKR Takamatsu Hospital
kn-affil=

affil-num=15
en-affil=Department of Respiratory Medicine, Japanese Red Cross Okayama Hospital
kn-affil=

affil-num=16
en-affil=Division of Cancer Information and Control, Aichi Cancer Center Research Institute
kn-affil=

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

affil-num=18
en-affil=Department of Hematology and Oncology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=19
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=
en-keyword=non-small cell lung cancer
kn-keyword=non-small cell lung cancer
en-keyword=body weight loss
kn-keyword=body weight loss
en-keyword=immune checkpoint inhibitors
kn-keyword=immune checkpoint inhibitors
en-keyword=chemotherapy
kn-keyword=chemotherapy
END

start-ver=1.4
cd-journal=joma
no-vol=20
cd-vols=
no-issue=
article-no=
start-page=3215
end-page=3220
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241209
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Ceratinadin G, a new psammaplysin derivative possessing a cyano group from a sponge of the genus Pseudoceratina
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A new psammaplysin derivative, ceratinadin G (1), was obtained from the Okinawan marine sponge Pseudoceratina sp., and the gross structure was clarified through spectroscopic and spectrometric analyses. The absolute configuration of compound 1 was established by comparing its NMR and ECD data with those of the known psammaplysin derivative, psammaplysin F (2). Ceratinadin G (1) is a rare nitrile containing a cyano group as aminoacetonitrile, and is the first psammaplysin derivative possessing a cyano group. In vitro assays indicated that compound 1 displayed moderate cytotoxicity against L1210 murine leukemia cells and KB epidermoid carcinoma cells.
en-copyright=
kn-copyright=

en-aut-name=KurimotoShin-Ichiro
en-aut-sei=Kurimoto
en-aut-mei=Shin-Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=InoueKouta
en-aut-sei=Inoue
en-aut-mei=Kouta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OhnoTaito
en-aut-sei=Ohno
en-aut-mei=Taito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KubotaTakaaki
en-aut-sei=Kubota
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

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

affil-num=2
en-affil=Showa Pharmaceutical University
kn-affil=

affil-num=3
en-affil=Showa Pharmaceutical University
kn-affil=

affil-num=4
en-affil=Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=ceratinadin
kn-keyword=ceratinadin
en-keyword=cytotoxicity
kn-keyword=cytotoxicity
en-keyword=marine sponge
kn-keyword=marine sponge
en-keyword=psammaplysin
kn-keyword=psammaplysin
en-keyword=Pseudoceratina sp
kn-keyword=Pseudoceratina sp
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=6
article-no=
start-page=469
end-page=474
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202412
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Treatment of Tenosynovial Giant Cell Tumor of the Cervical Spine with Postoperative Anti-RANKL Antibody (Denosumab) Administration
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Tenosynovial giant cell tumor (TGCT) is a fibrous histiocytic tumor originating in the synovial membrane. While cervical TGCT may not be considered a common diagnosis preoperatively because it is relatively rare, it has a high recurrence rate and should be considered. Total resection is preferable, but it can be challenging due to the risk of damaging the vertebral artery. Denosumab has shown effectiveness as a postoperative treatment for osteolytic bone lesion. Denosumab administration coupled with close follow-up might offer an effective postoperative treatment option for unresectable TGCT with bone invasion.
en-copyright=
kn-copyright=

en-aut-name=HirataYuichi
en-aut-sei=Hirata
en-aut-mei=Yuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NagaseTakayuki
en-aut-sei=Nagase
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SasadaSusumu
en-aut-sei=Sasada
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AyadaYoshiyuki
en-aut-sei=Ayada
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyakeHayato
en-aut-sei=Miyake
en-aut-mei=Hayato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SugaharaChiaki
en-aut-sei=Sugahara
en-aut-mei=Chiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamamotoHidetaka
en-aut-sei=Yamamoto
en-aut-mei=Hidetaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OdaYoshinao
en-aut-sei=Oda
en-aut-mei=Yoshinao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YasuharaTakao
en-aut-sei=Yasuhara
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TanakaShota
en-aut-sei=Tanaka
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

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

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

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

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

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

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

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

affil-num=8
en-affil=Department of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University
kn-affil=

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

affil-num=10
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=tenosynovial giant cell tumor
kn-keyword=tenosynovial giant cell tumor
en-keyword=bone tumor
kn-keyword=bone tumor
en-keyword=spine
kn-keyword=spine
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=29419
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241127
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=ADAR1 could be a potential diagnostic target for intrauterine infection patients
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Intrauterine infection (IUI) is mainly an ascending infection in which vaginal and cervical pathogens ascend to the uterus and can affect the fetus. Until now, there is still no effective diagnostic biomarker for IUI, such as chorioamnionitis (CAM) and funisitis (FUN). Deoxyribonucleic acid (DNA)/Ribonucleic acid (RNA) editing molecules such as apolipoprotein-B mRNA-editing complex (APOBEC) 3 families and Adenosine deaminase family acting on RNA (ADAR)1 were examined in chorioamniotic membranes and umbilical cord of 83 patient samples. Furthermore, Ureaplasma parvum induced ADAR1 was investigated in human HTR-8/SVneo EVT cell line. ADAR1 had a significantly higher area under the curve (AUC) (0.721 and 0.745) than other APOBEC3s or cytokines in CAM and FUN patients. In vitro, ureaplasma parvum was demonstrated to activate ADAR1 (p?=?0.025) and reduce RIG-I, IRF3, IFN-α, and IFN-β expression in EVT cell line (p?=?0.005, p?=?0.010, p?<?0.001, and p?=?0.018, respectively). High expression of ADAR1 was strongly associated with CAM and FUN patients (multivariate analyses; p?=?0.035 and p?=?0.002). ADAR1 could be a potential diagnostic target for IUI, such as CAM and FUN patients.
en-copyright=
kn-copyright=

en-aut-name=NakamuraKeiichiro
en-aut-sei=Nakamura
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShigeyasuKunitoshi
en-aut-sei=Shigeyasu
en-aut-mei=Kunitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=VuThuy Ha
en-aut-sei=Vu
en-aut-mei=Thuy Ha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=5
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=6
ORCID=

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

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

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

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

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

affil-num=6
en-affil=Department of Obstetrics and Gynecology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=
en-keyword=ADAR1
kn-keyword=ADAR1
en-keyword=Chorioamnionitis
kn-keyword=Chorioamnionitis
en-keyword=Funisitis
kn-keyword=Funisitis
en-keyword=Intrauterine infection
kn-keyword=Intrauterine infection
en-keyword=Diagnostic biomarker
kn-keyword=Diagnostic biomarker
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=6
article-no=
start-page=465
end-page=468
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202412
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Secondary Polymyalgia Rheumatica Following SARS-CoV-2 Infection
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=An 81-year-old Japanese man with a medical history of diabetes mellitus and hypertension was diagnosed with the novel coronavirus disease 2019 (COVID-19). The patient developed pain in the bilateral shoulders and hips 3 days after the disease onset and presented to our outpatient clinic after 1 month. Referring to diagnostic criteria, we diagnosed him with polymyalgia rheumatica (PMR). We initiated prednisolone at 15 mg per day and his symptoms improved immediately. The clinical course of the patient indicated that the SARS-CoV-2 infection triggered the onset of autoimmune disease, PMR in this case.
en-copyright=
kn-copyright=

en-aut-name=OchoKazuki
en-aut-sei=Ocho
en-aut-mei=Kazuki
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=IshikawaHisashi
en-aut-sei=Ishikawa
en-aut-mei=Hisashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

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

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

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

affil-num=4
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=COVID-19
kn-keyword=COVID-19
en-keyword=SARS-CoV-2
kn-keyword=SARS-CoV-2
en-keyword=polymyalgia rheumatica
kn-keyword=polymyalgia rheumatica
en-keyword=autoimmune diseases
kn-keyword=autoimmune diseases
en-keyword=human leukocyte antigen
kn-keyword=human leukocyte antigen
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=6
article-no=
start-page=439
end-page=447
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202412
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Risk Factors for Gangrenous Cholecystitis and the Outcomes of Early Cholecystectomy: A Retrospective Study of a Single-Center City General Hospital
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Gangrenous cholecystitis (GC) is classified as moderate acute cholecystitis according to the Tokyo Guidelines from 2018 (TG18). We evaluated the risk factors for GC and the outcomes of early cholecystectomy. A total of 136 patients who underwent emergency cholecystectomy for acute cholecystitis were retrospectively analyzed; 58 of these patients (42.6%) were diagnosed with GC (GC group) based on our retrospective pathologic diagnosis. We comparatively evaluated the patient backgrounds and surgical outcomes between the GC group and non-GC group. The GC group was significantly older and included more hypertensive patients than the non-GC group. The GC group was prescribed more antibiotics as initial treatment than the non-GC group, and they had more days between onset and surgery. The preoperative white blood cell count and C-reactive protein values were significantly higher in the GC group than in the non-GC group, and these values were predictive factors for GC. Cholecystectomy required a longer operation time and caused greater blood loss in the GC group. The GC group also had longer hospitalization times than the non-GC group; however, no significant differences were observed in terms of postoperative complications. In conclusion, gangrenous changes should be assessed when diagnosing cholecystitis, and appropriate treatment, such as surgery or drainage, should be undertaken.
en-copyright=
kn-copyright=

en-aut-name=YamashitaMampei
en-aut-sei=Yamashita
en-aut-mei=Mampei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanakaTakayuki
en-aut-sei=Tanaka
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SumidaYorihisa
en-aut-sei=Sumida
en-aut-mei=Yorihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamazakiShoto
en-aut-sei=Yamazaki
en-aut-mei=Shoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HaraYuki
en-aut-sei=Hara
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FukudaAkiko
en-aut-sei=Fukuda
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HisanagaMakoto
en-aut-sei=Hisanaga
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WakataKoki
en-aut-sei=Wakata
en-aut-mei=Koki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ArakiMasato
en-aut-sei=Araki
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=EguchiSusumu
en-aut-sei=Eguchi
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Surgery, Sasebo City General Hospital
kn-affil=

affil-num=2
en-affil=Department of Surgery, Sasebo City General Hospital
kn-affil=

affil-num=3
en-affil=Department of Surgery, Sasebo City General Hospital
kn-affil=

affil-num=4
en-affil=Department of Surgery, Sasebo City General Hospital
kn-affil=

affil-num=5
en-affil=Department of Surgery, Sasebo City General Hospital
kn-affil=

affil-num=6
en-affil=Department of Surgery, Sasebo City General Hospital
kn-affil=

affil-num=7
en-affil=Department of Surgery, Sasebo City General Hospital
kn-affil=

affil-num=8
en-affil=Department of Surgery, Sasebo City General Hospital
kn-affil=

affil-num=9
en-affil=Department of Surgery, Sasebo City General Hospital
kn-affil=

affil-num=10
en-affil=Department of Surgery, Nagasaki University Graduate School of Biomedical Science
kn-affil=
en-keyword=gangrenous
kn-keyword=gangrenous
en-keyword=cholecystitis
kn-keyword=cholecystitis
en-keyword=acute cholecystitis
kn-keyword=acute cholecystitis
en-keyword=laparoscopic cholecystectomy
kn-keyword=laparoscopic cholecystectomy
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=6
article-no=
start-page=429
end-page=437
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202412
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Partial versus Radical Nephrectomy for Small Renal Cancer: Comparative Propensity Score-Matching Analysis of Cardiovascular Event Risk
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Although partial nephrectomy (PN) is preferred over radical nephrectomy (RN) for preserving renal function in patients with cT1 renal cancer, its impact on cardiovascular events (CVe) remains controversial. This study aimed to compare PN and RN in regard to the occurrence of CVe, including cerebrovascular events and exacerbation of hypertension (HT). We retrospectively analyzed 418 consecutive patients who underwent PN or RN for cT1 renal cancer. Propensity score-matching analysis was used to adjust for imbalances between patients who underwent PN and RN, leaving 102 patients in each group. The 5-year probability of cumulative CVe incidence was 6% in the PN group and 12% in the RN group (p=0.03), with a median follow-up of 73.5 months. The statistical significance was retained after propensity score matching for patients without preoperative proteinuria (p=0.03). For all CVe including cerebrovascular events and exacerbation of HT analyzed, PN provided a lower probability of occurrence than RN in patients with small renal cancers.
en-copyright=
kn-copyright=

en-aut-name=KubotaRisa
en-aut-sei=Kubota
en-aut-mei=Risa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=BekkuKensuke
en-aut-sei=Bekku
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KatayamaSatoshi
en-aut-sei=Katayama
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=NishimuraShingo
en-aut-sei=Nishimura
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=EdamuraKohei
en-aut-sei=Edamura
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KobayashiTomoko
en-aut-sei=Kobayashi
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KobayashiYasuyuki
en-aut-sei=Kobayashi
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ArakiMotoo
en-aut-sei=Araki
en-aut-mei=Motoo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

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

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

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

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

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

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

affil-num=9
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=chronic kidney disease
kn-keyword=chronic kidney disease
en-keyword=hypertension
kn-keyword=hypertension
en-keyword=nephrectomy
kn-keyword=nephrectomy
en-keyword=proteinuria
kn-keyword=proteinuria
END

start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=2
article-no=
start-page=292
end-page=305
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241128
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The role of C1orf50 in breast cancer progression and prognosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Although the prognosis of breast cancer has significantly improved compared to other types of cancer, there are still some patients who expire due to recurrence or metastasis. Therefore, it is necessary to develop a method to identify patients with poor prognosis at the early stages of cancer. In the process of discovering new prognostic markers from genes of unknown function, we found that the expression of C1orf50 determines the prognosis of breast cancer patients, especially for those with Luminal A breast cancer. This study aims to elucidate the molecular role of C1orf50 in breast cancer progression. Bioinformatic analyses of the breast cancer dataset of TCGA, and in vitro analyses, reveal the molecular pathways influenced by C1orf50 expression. C1orf50 knockdown suppressed the cell cycle of breast cancer cells and weakened their ability to maintain the undifferentiated state and self-renewal capacity. Interestingly, upregulation of C1orf50 increased sensitivity to CDK4/6 inhibition. In addition, C1orf50 was found to be more abundant in breast cancer cells than in normal breast epithelium, suggesting C1orf50’s involvement in breast cancer pathogenesis. Furthermore, the mRNA expression level of C1orf50 was positively correlated with the expression of PD-L1 and its related factors. These results suggest that C1orf50 promotes breast cancer progression through cell cycle upregulation, maintenance of cancer stemness, and immune evasion mechanisms. Our study uncovers the biological functions of C1orf50 in Luminal breast cancer progression, a finding not previously reported in any type of cancer.
en-copyright=
kn-copyright=

en-aut-name=OtaniYusuke
en-aut-sei=Otani
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanakaAtsushi
en-aut-sei=Tanaka
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MaekawaMasaki
en-aut-sei=Maekawa
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=Pe?aTirso
en-aut-sei=Pe?a
en-aut-mei=Tirso
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=RogachevskayaAnna
en-aut-sei=Rogachevskaya
en-aut-mei=Anna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AndoTeruhiko
en-aut-sei=Ando
en-aut-mei=Teruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ItanoTakuto
en-aut-sei=Itano
en-aut-mei=Takuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KatayamaHaruyoshi
en-aut-sei=Katayama
en-aut-mei=Haruyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakataEiji
en-aut-sei=Nakata
en-aut-mei=Eiji
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=

en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=DoiharaHiroyoshi
en-aut-sei=Doihara
en-aut-mei=Hiroyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=RoehrlMichael H.
en-aut-sei=Roehrl
en-aut-mei=Michael H.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=FujimuraAtsushi
en-aut-sei=Fujimura
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA Harvard Medical School
kn-affil=

affil-num=2
en-affil=Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA Harvard Medical School
kn-affil=

affil-num=3
en-affil=Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA Harvard Medical School
kn-affil=

affil-num=4
en-affil=Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA Harvard Medical School
kn-affil=

affil-num=5
en-affil=Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA Harvard Medical School
kn-affil=

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

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

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

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

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

affil-num=11
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=12
en-affil=Department of General Surgery, Kawasaki Medical School General Medical Center
kn-affil=

affil-num=13
en-affil=Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA Harvard Medical School
kn-affil=

affil-num=14
en-affil=Department of Cellular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=C1orf50
kn-keyword=C1orf50
en-keyword=Luminal A breast cancer
kn-keyword=Luminal A breast cancer
en-keyword=Cell cycle
kn-keyword=Cell cycle
en-keyword=Immune evasion
kn-keyword=Immune evasion
en-keyword=YAP/TAZ
kn-keyword=YAP/TAZ
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=60
end-page=63
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241129
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Successful immunotherapy with ipilimumab and nivolumab in a patient with pulmonary sclerosing pneumocytoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pulmonary sclerosing pneumocytoma (PSP) is a rare form of lung cancer that occasionally presents with lymph node and extrapulmonary metastases, and multiple lesions. The treatment of metastatic PSP remains undefined. This study reports the case of a 48-year-old female patient diagnosed with PSP following surgical intervention for a solitary nodule in the left lower lobe. Four years later, recurrence occurred in the left hilar and mediastinal lymph nodes, necessitating an additional resection. Concurrently, sacral metastases developed and required palliative radiotherapy. Genetic analysis identified an AKT1 E17K mutation, characteristic of PSP, and absence of programmed cell death ligand 1 (PD-L1) expression in the tumor. Two years post-recurrence, the tumor recurred in the left mammary gland and mediastinal lymph nodes. Combination immunotherapy with ipilimumab and nivolumab yielded a significantly positive response in this metastatic PSP case. This is the first reported case of successful treatment of multiple distant metastatic PSP with ipilimumab and nivolumab, following the failure of various local treatments. Further case series are warranted to validate the efficacy of immunotherapy in metastatic PSP.
en-copyright=
kn-copyright=

en-aut-name=Inukai-MotokuraYumi
en-aut-sei=Inukai-Motokura
en-aut-mei=Yumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=BabaTakahiro
en-aut-sei=Baba
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OmoriHiroki
en-aut-sei=Omori
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakeguchiTetsuya
en-aut-sei=Takeguchi
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UnoMari
en-aut-sei=Uno
en-aut-mei=Mari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AyadaYoshiyuki
en-aut-sei=Ayada
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=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=

en-aut-name=OhashiKadoaki
en-aut-sei=Ohashi
en-aut-mei=Kadoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

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

affil-num=4
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

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

affil-num=8
en-affil=Department of Pathology and Oncology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
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 Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=
en-keyword=Pulmonary sclerosing pneumocytoma
kn-keyword=Pulmonary sclerosing pneumocytoma
en-keyword=Ipilimumab
kn-keyword=Ipilimumab
en-keyword=Nivolumab
kn-keyword=Nivolumab
en-keyword=Programmed cell death ligand 1
kn-keyword=Programmed cell death ligand 1
en-keyword=Case report
kn-keyword=Case report
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=20
article-no=
start-page=e70288
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241023
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=New Anti-Angiogenic Therapy for Glioblastoma With the Anti-Depressant Sertraline
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background and Aims: Anti-angiogenic therapies prolong patient survival in some malignancies but not glioblastoma. We focused on the relationship between the differentiation of glioma stem like cells (GSCs) into tumor derived endothelial cells (TDECs) and, anti-angiogenic therapy resistance. Especially we aimed to elucidate the mechanisms of drug resistance of TDECs to anti-angiogenic inhibitors and identify novel anti-angiogenic drugs with clinical applications.<br>
Results: The mouse GSCs, 005, were differentiated into TDECs under hypoxic conditions, and TDECs had endothelial cell characteristics independent of the vascular endothelial growth factor (VEGF) pathway. In vivo, inhibition of the VEGF pathway had no anti-tumor effect and increased the percentage of TDECs in the 005 mouse model. Novel anti-angiogenic drugs for glioblastoma were evaluated using a tube formation assay and a drug repositioning strategy with existing blood-brain barrier permeable drugs. Drug screening revealed that the antidepressant sertraline inhibited tube formation of TDECs. Sertraline was administered to differentiated TDECs in vitro and 005 mouse models in vivo to evaluate genetic changes by RNA-Seq and tumor regression effects by immunohistochemistry and MRI. Sertraline reduced Lama4 and Ang2 expressions of TDEC, which play an important role in non-VEGF-mediated angiogenesis in tumors. The combination of a VEGF receptor inhibitor axitinib, and sertraline improved survival and reduced tumor growth in the 005 mouse model.<br>
Conclusion: Collectively, our findings showed the diversity of tumor vascular endothelial cells across VEGF and non-VEGF pathways led to anti-angiogenic resistance. The combination of axitinib and sertraline can represent an effective anti-angiogenic therapy for glioblastoma with safe, low cost, and fast availability.
en-copyright=
kn-copyright=

en-aut-name=TsuboiNobushige
en-aut-sei=Tsuboi
en-aut-mei=Nobushige
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OtaniYoshihiro
en-aut-sei=Otani
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UnedaAtsuhito
en-aut-sei=Uneda
en-aut-mei=Atsuhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=SurugaYasuki
en-aut-sei=Suruga
en-aut-mei=Yasuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsumotoYuji
en-aut-sei=Matsumoto
en-aut-mei=Yuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FujimuraAtsushi
en-aut-sei=Fujimura
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FujiiKentaro
en-aut-sei=Fujii
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MatsuiHideki
en-aut-sei=Matsui
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KurozumiKazuhiko
en-aut-sei=Kurozumi
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
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=12
ORCID=

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

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

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

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

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

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

affil-num=7
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

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

affil-num=9
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Neurosurgery, Hamamatsu University School of Medicine
kn-affil=

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

affil-num=12
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=
en-keyword=anti-angiogenic therapy
kn-keyword=anti-angiogenic therapy
en-keyword=antidepressant sertraline
kn-keyword=antidepressant sertraline
en-keyword=drug repositioning
kn-keyword=drug repositioning
en-keyword=glioblastoma
kn-keyword=glioblastoma
en-keyword=tumor derived endothelial cells
kn-keyword=tumor derived endothelial cells
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=線維化を伴う膵がん微小環境の立体培養法による新規in vitroモデルの構築と解析
kn-title=Establishment and Analysis of Novel In Vitro 3D Cell Culture Models of the Fibrotic Tumor Microenvironment in Pancreatic Cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TANAKAHiroyoshi
en-aut-sei=TANAKA
en-aut-mei=Hiroyoshi
kn-aut-name=田中啓祥
kn-aut-sei=田中
kn-aut-mei=啓祥
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Okayama University
kn-affil=岡山大学大学院
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=がん細胞へのsiRNA送達のためのペプチドナノミセルの開発
kn-title=Development of Peptide Nanomicelle for siRNA Delivery into Cancer Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TAUFIK FATWA NUR HAKIM
en-aut-sei=TAUFIK FATWA NUR HAKIM
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=岡山大学大学院ヘルスシステム統合科学研究科
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=腫瘍ホーミングペプチド修飾磁性ナノ粒子の磁気温熱療法および腫瘍検出への応用
kn-title=Application of novel tumor-homing peptide-modified magnetic nanoparticles for magnetic hyperthermia and tumor cell detection
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=ZHOUSHENGLI
en-aut-sei=ZHOU
en-aut-mei=SHENGLI
kn-aut-name=周聖力
kn-aut-sei=周
kn-aut-mei=聖力
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=岡山大学大学院ヘルスシステム統合科学研究科
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=卵丘細胞の生存率と前培養が低品質ブタ卵母細胞におけるグルコース-6-リン酸デヒドロゲナーゼ (G6PDH) 活性、減数分裂の進行および発生能力に及ぼす影響
kn-title=The impact of cumulus cell viability and pre-culture on glucose-6-phosphate dehydrogenase (G6PDH) activity, meiotic progression, and developmental competence in suboptimal porcine oocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=WANNIARACHCHIGE THARINDU LAKSHITHA FONSEKA
en-aut-sei=WANNIARACHCHIGE THARINDU LAKSHITHA FONSEKA
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=岡山大学大学院環境生命科学研究科
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=植物細胞における亜硫酸の毒性機構に関する研究−亜硫酸毒性への細胞質酸性化と細胞酸化の関与の評価
kn-title=A study on toxic mechanisms of SO2 in plant cells - Evaluation of the involvement of cytosolic acidification and cellular oxidation in SO2 toxicity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MAHDI MOZHGANI
en-aut-sei=MAHDI MOZHGANI
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=岡山大学大学院環境生命科学研究科
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=高悪性度口腔扁平上皮癌において、CX3CL1はリンパ管新生を増強しリンパ節転移に寄与する
kn-title=Double-faced CX3CL1 enhances lymphangiogenesis-dependent metastasis in an aggressive subclone of oral squamous cell carcinoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=Htoo Shwe Eain
en-aut-sei=Htoo Shwe Eain
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=一細胞解析を応用した軟骨細胞分化を制御する転写因子の遡及的な再発見法　
kn-title=Retrospective re-discovery of the transcription factor that controls chondrocyte differentiation by single cell RNA-sequencing
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=DO Thuy Hang
en-aut-sei=DO Thuy Hang
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=悪性末梢神経鞘腫瘍のがん幹細胞性維持に対するカテコラミン合成酵素の役割
kn-title=Role of catecholamine synthases in the maintenance of cancer stem-like cells in malignant peripheral nerve sheath tumors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KATAYAMAHaruyoshi
en-aut-sei=KATAYAMA
en-aut-mei=Haruyoshi
kn-aut-name=片山晴喜
kn-aut-sei=片山
kn-aut-mei=晴喜
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=PAI-1は非小細胞肺がんにおけるMET標的治療の獲得耐性に関与する
kn-title=PAI-1 mediates acquired resistance to MET-targeted therapy in non-small cell lung cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=YIN MIN THU
en-aut-sei=YIN MIN THU
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=角化の調節因子の探索： 口腔粘膜におけるBMP-2の役割
kn-title=Exploring the Regulators of Keratinization: Role of BMP-2 in Oral Mucosa
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MUXINDI
en-aut-sei=MU
en-aut-mei=XINDI
kn-aut-name=穆欣迪
kn-aut-sei=穆
kn-aut-mei=欣迪
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Lysyl oxidase-like 4は、細胞表面にAnnexin A2/S100A11複合体形成を促進することで、トリプルネガティブ乳がん細胞の浸潤能を促進する
kn-title=Lysyl oxidase-like 4 promotes the invasiveness of triple-negative breast cancer cells by orchestrating the invasive machinery formed by annexin A2 and S100A11 on the cell surface
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TAKAHASHITetta
en-aut-sei=TAKAHASHI
en-aut-mei=Tetta
kn-aut-name=��橋徹多
kn-aut-sei=��橋
kn-aut-mei=徹多
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=非小細胞肺癌における腫瘍免疫状態の指標としての好中球リンパ球比の有用性
kn-title=Utility of neutrophil-to-lymphocyte ratio as an indicator of tumor immune status in non-small cell lung cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=IWATAKazuma
en-aut-sei=IWATA
en-aut-mei=Kazuma
kn-aut-name=岩田一馬
kn-aut-sei=岩田
kn-aut-mei=一馬
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=SPRED2は、肝細胞癌細胞および正常肝細胞におけるオートファジーの新しい調節因子です
kn-title=SPRED2 Is a Novel Regulator of Autophagy in Hepatocellular Carcinoma Cells and Normal Hepatocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=WANGTIANYI
en-aut-sei=WANG
en-aut-mei=TIANYI
kn-aut-name=王天?
kn-aut-sei=王
kn-aut-mei=天?
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=LOXL4によるトリプルネガティブ乳がん細胞浸潤亢進のシグナル伝達機構の解明
kn-title=Dissection of the signal transduction machinery responsible for the lysyl oxidase-like 4-mediated increase in invasive motility in triple-negative breast cancer cells: mechanistic insight into the integrin-β1-NF-κB-MMP9 axis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=JIANGFAN
en-aut-sei=JIANG
en-aut-mei=FAN
kn-aut-name=江帆
kn-aut-sei=江
kn-aut-mei=帆
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=T細胞腫瘍におけるα-ピネンの抗腫瘍活性
kn-title=Antitumor activity of α-pinene in T-cell tumors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=ABEMasaya
en-aut-sei=ABE
en-aut-mei=Masaya
kn-aut-name=阿部将也
kn-aut-sei=阿部
kn-aut-mei=将也
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=老化線維芽細胞はIL-8のクロストークを介し、びまん性胃癌細胞の腹膜転移を促進する
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=
en-copyright=
kn-copyright=

en-aut-name=LIYUNCHENG
en-aut-sei=LI
en-aut-mei=YUNCHENG
kn-aut-name=李云成
kn-aut-sei=李
kn-aut-mei=云成
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=4D-CT Angiographyによる腎細胞癌の栄養動脈の描出率
kn-title=Depiction rate of feeding arteries of renal cell carcinoma on four?dimensional computed tomography angiography
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MUNETOMOKazuaki
en-aut-sei=MUNETOMO
en-aut-mei=Kazuaki
kn-aut-name=宗友一晃
kn-aut-sei=宗友
kn-aut-mei=一晃
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=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=血中循環遊離DNAのメチル化パターンは、原発巣遺伝子変異プロファイルによらず、大腸癌の治療効果モニタリングを可能とする非侵襲的なバイオマーカーである
kn-title=Circulating cell?free DNA methylation patterns as non?invasive biomarkers to monitor colorectal cancer treatment efficacy without referencing primary site mutation profiles
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=YASUIKazuya
en-aut-sei=YASUI
en-aut-mei=Kazuya
kn-aut-name=安井和也
kn-aut-sei=安井
kn-aut-mei=和也
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=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=25
cd-vols=
no-issue=22
article-no=
start-page=12063
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241110
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Efficient Production of Chondrocyte Particles from Human iPSC-Derived Chondroprogenitors Using a Plate-Based Cell Self-Aggregation Technique
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The limited capacity of articular cartilage for self-repair is a critical challenge in orthopedic medicine. Here, we aimed to develop a simplified method of generating chondrocyte particles from human-induced pluripotent stem cell-derived expandable limb-bud mesenchymal cells (ExpLBM) using a cell self-aggregation technique (CAT). ExpLBM cells were induced to form chondrocyte particles through a stepwise differentiation protocol performed on a CAT plate (prevelex-CAT (R)), which enables efficient and consistent production of an arbitrary number of uniformly sized particles. Histological and immunohistochemical analyses confirmed that the generated chondrocyte particles expressed key cartilage markers, such as type II collagen and aggrecan, but not hypertrophic markers, such as type X collagen. Additionally, when these particles were transplanted into osteochondral defects in rats with X-linked severe combined immunodeficiency, they demonstrated successful engraftment and extracellular matrix production, as evidenced by Safranin O and Toluidine Blue staining. These data suggest that the plate-based CAT system offers a robust and scalable approach to produce a large number of chondrocyte particles in a simplified and efficient manner, with potential application to cartilage regeneration. Future studies will focus on refining the system and exploring its clinical applications to the treatment of cartilage defects.
en-copyright=
kn-copyright=

en-aut-name=HanakiShojiro
en-aut-sei=Hanaki
en-aut-mei=Shojiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamadaDaisuke
en-aut-sei=Yamada
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakaoTomoka
en-aut-sei=Takao
en-aut-mei=Tomoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IwaiRyosuke
en-aut-sei=Iwai
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakaradaTakeshi
en-aut-sei=Takarada
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

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

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

affil-num=4
en-affil=Institute of Frontier Science and Technology, Okayama University of Science
kn-affil=

affil-num=5
en-affil=Department of Regenerative Science, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=
en-keyword=tissue engineering
kn-keyword=tissue engineering
en-keyword=chondrocyte particles
kn-keyword=chondrocyte particles
en-keyword=cartilaginous particles
kn-keyword=cartilaginous particles
en-keyword=ExpLBM
kn-keyword=ExpLBM
en-keyword=hiPSC
kn-keyword=hiPSC
en-keyword=chondrocyte
kn-keyword=chondrocyte
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=2
article-no=
start-page=35
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230511
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Development of the Follow-Up Human 3D Oral Cancer Model in Cancer Treatment
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=As function preservation cancer therapy, targeted radiation therapies have been developed for the quality of life of cancer patients. However, preclinical animal studies evaluating the safety and efficacy of targeted radiation therapy is challenging from the viewpoints of animal welfare and animal protection, as well as the management of animal in radiation-controlled areas under the regulations. We fabricated the human 3D oral cancer model that considers the time axis of the follow up in cancer treatment. Therefore, in this study, the 3D model with human oral cancer cells and normal oral fibroblasts was treated based on clinical protocol. After cancer treatment, the histological findings of the 3D oral cancer model indicated the clinical correlation between tumor response and surrounding normal tissue. This 3D model has potential as a tool for preclinical studies alternative to animal studies.
en-copyright=
kn-copyright=

en-aut-name=IgawaKazuyo
en-aut-sei=Igawa
en-aut-mei=Kazuyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IzumiKenji
en-aut-sei=Izumi
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SakuraiYoshinori
en-aut-sei=Sakurai
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=2
en-affil=Division of Biomimetics, Faculty of Dentistry & Graduate School of Medical and Dental Sciences, Niigata University
kn-affil=

affil-num=3
en-affil=Institute for Integrated Radiation and Nuclear Science, Kyoto University
kn-affil=
en-keyword=3D cancer model
kn-keyword=3D cancer model
en-keyword=preclinical study
kn-keyword=preclinical study
en-keyword=cancer treatment
kn-keyword=cancer treatment
en-keyword=quality of life
kn-keyword=quality of life
en-keyword=multidisciplinary treatment
kn-keyword=multidisciplinary treatment
END

start-ver=1.4
cd-journal=joma
no-vol=193
cd-vols=
no-issue=3
article-no=
start-page=2122
end-page=2140
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230720
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Calredoxin regulates the chloroplast NADPH-dependent thioredoxin reductase in Chlamydomonas reinhardtii
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Calredoxin (CRX) is a calcium (Ca2+)-dependent thioredoxin (TRX) in the chloroplast of Chlamydomonas (Chlamydomonas reinhardtii) with a largely unclear physiological role. We elucidated the CRX functionality by performing in-depth quantitative proteomics of wild-type cells compared with a crx insertional mutant (IMcrx), two CRISPR/Cas9 KO mutants, and CRX rescues. These analyses revealed that the chloroplast NADPH-dependent TRX reductase (NTRC) is co-regulated with CRX. Electron transfer measurements revealed that CRX inhibits NADPH-dependent reduction of oxidized chloroplast 2-Cys peroxiredoxin (PRX1) via NTRC and that the function of the NADPH-NTRC complex is under strict control of CRX. Via non-reducing SDS-PAGE assays and mass spectrometry, our data also demonstrated that PRX1 is more oxidized under high light (HL) conditions in the absence of CRX. The redox tuning of PRX1 and control of the NADPH-NTRC complex via CRX interconnect redox control with active photosynthetic electron transport and metabolism, as well as Ca2+ signaling. In this way, an economic use of NADPH for PRX1 reduction is ensured. The finding that the absence of CRX under HL conditions severely inhibited light-driven CO2 fixation underpins the importance of CRX for redox tuning, as well as for efficient photosynthesis.
en-copyright=
kn-copyright=

en-aut-name=ZinziusKaren
en-aut-sei=Zinzius
en-aut-mei=Karen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MarchettiGiulia Maria
en-aut-sei=Marchetti
en-aut-mei=Giulia Maria
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FischerRonja
en-aut-sei=Fischer
en-aut-mei=Ronja
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MilradYuval
en-aut-sei=Milrad
en-aut-mei=Yuval
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OltmannsAnne
en-aut-sei=Oltmanns
en-aut-mei=Anne
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KelterbornSimon
en-aut-sei=Kelterborn
en-aut-mei=Simon
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YacobyIftach
en-aut-sei=Yacoby
en-aut-mei=Iftach
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HegemannPeter
en-aut-sei=Hegemann
en-aut-mei=Peter
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ScholzMartin
en-aut-sei=Scholz
en-aut-mei=Martin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HipplerMichael
en-aut-sei=Hippler
en-aut-mei=Michael
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Institute of Plant Biology and Biotechnology, University of M?nster
kn-affil=

affil-num=2
en-affil=Institute of Plant Biology and Biotechnology, University of M?nster
kn-affil=

affil-num=3
en-affil=Institute of Plant Biology and Biotechnology, University of M?nster
kn-affil=

affil-num=4
en-affil=School of Plant Sciences and Food Security, The George S. Wise Faculty of Life Sciences, Tel Aviv University
kn-affil=

affil-num=5
en-affil=Institute of Plant Biology and Biotechnology, University of M?nster
kn-affil=

affil-num=6
en-affil=Institute of Biology, Experimental Biophysics, Humboldt University of Berlin
kn-affil=

affil-num=7
en-affil=School of Plant Sciences and Food Security, The George S. Wise Faculty of Life Sciences, Tel Aviv University
kn-affil=

affil-num=8
en-affil=Institute of Biology, Experimental Biophysics, Humboldt University of Berlin
kn-affil=

affil-num=9
en-affil=Institute of Plant Biology and Biotechnology, University of M?nster
kn-affil=

affil-num=10
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=22
article-no=
start-page=e038137
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241119
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Eight-Year Outcomes of Cardiosphere-Derived Cells in Single Ventricle Congenital Heart Disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Cardiosphere‐derived cell (CDC) infusion was associated with better clinical outcomes at 2?years in patients with single ventricle heart disease. The current study investigates time‐to‐event outcomes at 8?years.<br>
Methods and Results: This cohort enrolled patients with single ventricles who underwent stage 2 or stage 3 palliation from January 2011 to January 2015 at 8 centers in Japan. The primary outcomes were time‐dependent CDC treatment effects on death and late complications during 8?years of follow‐up, assessed by restricted mean survival time. Among 93 patients enrolled (mean age, 2.3±1.3?years; 56% men), 40 received CDC infusion. Overall survival for CDC‐treated versus control patients did not differ at 8?years (hazard ratio [HR], 0.60 [95% CI, 0.21?1.77]; P=0.35). Treatment effect had nonproportional hazards for death favoring CDCs at 4?years (restricted mean survival time difference +0.33?years [95% CI, 0.01?0.66]; P=0.043). In patients with heart failure with reduced ejection fraction, CDC treatment effect on survival was greater over 8?years (restricted mean survival time difference +1.58?years [95% CI, 0.05?3.12]; P=0.043). Compared with control participants, CDC‐treated patients showed lower incidences of late failure (HR, 0.45 [95% CI, 0.21?0.93]; P=0.027) and adverse events (subdistribution HR, 0.50 [95% CI, 0.27?0.94]; P=0.036) at 8?years.<br>
Conclusions: By 8?years, CDC infusion was associated with lower hazards of late failure and adverse events in single ventricle heart disease. CDC treatment effect on survival was notable by 4?years and showed a durable clinical benefit in patients with heart failure with reduced ejection fraction over 8?years.<br>
Registration: URL: https://www.clinicaltrials.gov; Unique identifiers: NCT01273857 and NCT01829750.
en-copyright=
kn-copyright=

en-aut-name=HiraiKenta
en-aut-sei=Hirai
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SawadaRyusuke
en-aut-sei=Sawada
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HayashiTomohiro
en-aut-sei=Hayashi
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ArakiToru
en-aut-sei=Araki
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakagawaNaomi
en-aut-sei=Nakagawa
en-aut-mei=Naomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KondoMaiko
en-aut-sei=Kondo
en-aut-mei=Maiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YasudaKenji
en-aut-sei=Yasuda
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HirataTakuya
en-aut-sei=Hirata
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SatoTomoyuki
en-aut-sei=Sato
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakatsukaYuki
en-aut-sei=Nakatsuka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YoshidaMichihiro
en-aut-sei=Yoshida
en-aut-mei=Michihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KasaharaShingo
en-aut-sei=Kasahara
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=BabaKenji
en-aut-sei=Baba
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=OhHidemasa
en-aut-sei=Oh
en-aut-mei=Hidemasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=the TICAP/PERSEUS Study Group
en-aut-sei=the TICAP/PERSEUS Study Group
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
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 Pharmacology Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Pediatrics Kurashiki Central Hospital
kn-affil=

affil-num=4
en-affil=Department of Pediatrics National Hospital Organization Fukuyama Medical Center
kn-affil=

affil-num=5
en-affil=Department of Pediatric Cardiology Hiroshima City Hiroshima Citizens Hospital
kn-affil=

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

affil-num=7
en-affil=Department of Pediatrics Shimane University Faculty of Medicine
kn-affil=

affil-num=8
en-affil=Department of Pediatrics Kyoto University Graduate School of Medicine
kn-affil=

affil-num=9
en-affil=Department of Pediatrics Jichi Medical University
kn-affil=

affil-num=10
en-affil=Department of Data Science, Center for Innovative Clinical Medicine Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of Data Science, Center for Innovative Clinical Medicine Okayama University Hospital
kn-affil=

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

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

affil-num=14
en-affil=Department of Regenerative Medicine, Center for Innovative Clinical Medicine Okayama University Hospital
kn-affil=

affil-num=15
en-affil=
kn-affil=
en-keyword=cardiosphere
kn-keyword=cardiosphere
en-keyword=heart failure
kn-keyword=heart failure
en-keyword=restricted mean survival time
kn-keyword=restricted mean survival time
en-keyword=single ventricle
kn-keyword=single ventricle
en-keyword=survival
kn-keyword=survival
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=1
article-no=
start-page=198
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241112
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical practice pattern of Pneumocystis pneumonia prophylaxis in systemic lupus erythematosus: a cross-sectional study from lupus registry of nationwide institutions (LUNA)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Pneumocystis jirovecii pneumonia (PCP) is an opportunistic infection in patients undergoing immunosuppressive therapy, such as glucocorticoid (GC) medication, for systemic autoimmune diseases like systemic lupus erythematosus (SLE). Despite the confirmed effectiveness of PCP prophylaxis, its clinical administration, especially in conjunction with GC dosage, remains unclear. We aimed to describe the clinical practice of PCP prophylaxis in association with SLE in Japan, evaluate the relationship between GC dosage and PCP prophylaxis, and explore the practice patterns associated with PCP prophylaxis. <br>
Methods This cross-sectional study used data from the Lupus Registry of Nationwide Institutions in Japan from 2016 to 2021 and included patients diagnosed with SLE. Using descriptive statistics, multivariate analysis, and decision tree analysis, we examined the prevalence of PCP prophylaxis and its association with the GC dosage. <br>
Results Out of 1,460 patients, 21% underwent PCP prophylaxis. The frequency of prophylaxis decreased with a decrease in GC dosage. After adjusting for confounders, logistic regression revealed the odds ratio of PCP prophylaxis increased with higher prednisolone (PSL) doses: 3.7 for 5 <= PSL < 7.5 mg, 5.2 for 7.5 <= PSL < 10 mg, 9.0 for 10 <= PSL < 20 mg, and 43.1 for PSL >= 20 mg, using PSL < 5 mg as the reference. Decision tree analysis indicated that a PSL dosage of < 11 mg/day and immunosuppressant use were key determinants of PCP prophylaxis. <br>
Conclusion This study provides valuable insights into PCP prophylaxis practices in patients with SLE in Japan, underscoring the importance of GC dosage and concomitant immunosuppressant use.
en-copyright=
kn-copyright=

en-aut-name=OnishiTakahisa
en-aut-sei=Onishi
en-aut-mei=Takahisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SadaKen-Ei
en-aut-sei=Sada
en-aut-mei=Ken-Ei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HayashiKeigo
en-aut-sei=Hayashi
en-aut-mei=Keigo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=YoshimiRyusuke
en-aut-sei=Yoshimi
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShimojimaYasuhiro
en-aut-sei=Shimojima
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OhnoShigeru
en-aut-sei=Ohno
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KajiyamaHiroshi
en-aut-sei=Kajiyama
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IchinoseKunihiro
en-aut-sei=Ichinose
en-aut-mei=Kunihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SatoShuzo
en-aut-sei=Sato
en-aut-mei=Shuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=FujiwaraMichio
en-aut-sei=Fujiwara
en-aut-mei=Michio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
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=12
ORCID=

en-aut-name=KidaTakashi
en-aut-sei=Kida
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MatsuoYusuke
en-aut-sei=Matsuo
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NishimuraKeisuke
en-aut-sei=Nishimura
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=YamaneTakashi
en-aut-sei=Yamane
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

affil-num=1
en-affil=Department of Rheumatology, Kakogawa Central City Hospital
kn-affil=

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

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

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

affil-num=5
en-affil=Department of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine
kn-affil=

affil-num=7
en-affil=Center for Rheumatic Diseases, Yokohama City University Medical Center
kn-affil=

affil-num=8
en-affil=Department of Rheumatology and Applied Immunology, Faculty of Medicine, Saitama Medical University
kn-affil=

affil-num=9
en-affil=Department of Immunology and Rheumatology, Division of Advanced Preventive Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences
kn-affil=

affil-num=10
en-affil=Department of Rheumatology, Fukushima Medical University School of Medicine
kn-affil=

affil-num=11
en-affil=Department of Rheumatology, Yokohama Rosai Hospital
kn-affil=

affil-num=12
en-affil=Division of Rheumatology, Department of Medicine, Showa University School of Medicine
kn-affil=

affil-num=13
en-affil=Infammation and Immunology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=14
en-affil=Department of Rheumatology, Tokyo Kyosai Hospital
kn-affil=

affil-num=15
en-affil=Department of Rheumatology and Clinical Immunology, Kobe University Graduate School of Medicine
kn-affil=

affil-num=16
en-affil=Department of Rheumatology, Kakogawa Central City Hospital
kn-affil=
en-keyword=Systemic lupus erythematosus
kn-keyword=Systemic lupus erythematosus
en-keyword=Pneumocystis jirovecii pneumonia
kn-keyword=Pneumocystis jirovecii pneumonia
en-keyword=Glucocorticoid
kn-keyword=Glucocorticoid
en-keyword=Immunosuppressant
kn-keyword=Immunosuppressant
en-keyword=Practice pattern
kn-keyword=Practice pattern
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=21
article-no=
start-page=11592
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241029
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Epigenetic Regulation of CXC Chemokine Expression by Environmental Electrophiles Through DNA Methyltransferase Inhibition
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ubiquitously distributed environmental electrophiles covalently modify DNA and proteins, potentially leading to adverse health effects. However, the impacts of specific electrophiles on target proteins and their physiological roles remain largely unknown. In the present study, we focused on DNA methylation, which regulates gene expression and physiological responses. A total of 45 environmental electrophiles were screened for inhibitory effects on the activity of DNA methyltransferase 3B (DNMT3B), a key enzyme in DNA methylation, and four compounds were identified. We focused on 1,2-naphthoquinone (1,2-NQ), an air pollutant whose toxicity has been reported previously. Interestingly, we found that 1,2-NQ modified multiple lysine and histidine residues in DNMT3B, one of which was near the active site in DNMT3B. It was found that 1,2-NQ altered gene expression and evoked inflammatory responses in lung adenocarcinoma cell lines. Furthermore, we found that 1,2-NQ upregulated CXCL8 expression through DNA demethylation of the distal enhancer and promoted cancer cell growth. Our study reveals novel mechanisms of epigenetic regulation by environmental electrophiles through the inhibition of DNMT3B activity and suggests their physiological impact.
en-copyright=
kn-copyright=

en-aut-name=TsuchidaTomoki
en-aut-sei=Tsuchida
en-aut-mei=Tomoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KubotaSho
en-aut-sei=Kubota
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KamiuezonoShizuki
en-aut-sei=Kamiuezono
en-aut-mei=Shizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ItoAkihiro
en-aut-sei=Ito
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KumagaiYoshito
en-aut-sei=Kumagai
en-aut-mei=Yoshito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

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

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

affil-num=3
en-affil=Department of Medicinal Pharmacology, Faculty of Pharmaceutical Sciences, Okayama University
kn-affil=

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

affil-num=5
en-affil=School of Life Sciences, Tokyo University of Pharmacy and Life Sciences
kn-affil=

affil-num=6
en-affil=Graduate School of Pharmaceutical Sciences, Kyushu University
kn-affil=

affil-num=7
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=DNA methylation
kn-keyword=DNA methylation
en-keyword=DNA methyltransferase
kn-keyword=DNA methyltransferase
en-keyword=chemical modification
kn-keyword=chemical modification
en-keyword=chemokine
kn-keyword=chemokine
en-keyword=cell proliferation
kn-keyword=cell proliferation
en-keyword=toxicology
kn-keyword=toxicology
en-keyword=exposome
kn-keyword=exposome
en-keyword=environmental electrophiles
kn-keyword=environmental electrophiles
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=1
article-no=
start-page=195
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241111
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Association between discontinuity of care and patient trust in the usual rheumatologist among patients with systemic lupus erythematosus: a cross-sectional study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Patient trust plays a central role in the patient-physician relationship. This study aimed to determine whether the number of outpatient visits with a covering rheumatologist is associated with patient trust in their usual rheumatologist.<br>
Methods Japanese adults with systemic lupus erythematosus (SLE) who met the 1997 revised classification criteria of the American College of Rheumatology and had outpatient visits with a covering rheumatologist in the past year were included.<br>
We used the 11-item Japanese version of the modified Trust in Physician Scale (range 0?100) to assess patient trust. A general linear model with cluster-robust variance estimation was used to evaluate the association between the number of outpatient visits with covering rheumatologists and the patient’s trust in their usual rheumatologist.<br>
Results Of the 515 enrolled participants, 421 patients with SLE were included in our analyses. Patients were divided into groups according to the number of outpatient visits with a covering rheumatologist in the past year as follows: no visits (59.9%; reference group), one to three visits (24.2%; low-frequency group), and four or more visits (15.9%; high-frequency group). The median Trust in Physician Scale score was 81.8 (interquartile range: 72.7?93.2). Both the low-frequency group (mean difference: -3.03; 95% confidence interval [CI] -5.93 to -0.80) and high-frequency group (mean difference: -4.17; 95% CI -7.77 to -0.58) exhibited lower trust in their usual rheumatologist.<br>
Conclusion This study revealed that the number of outpatient visits with a covering rheumatologist was associated with lower trust in a patient’s usual rheumatologist.
en-copyright=
kn-copyright=

en-aut-name=KatayamaYu
en-aut-sei=Katayama
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=ShidaharaKenta
en-aut-sei=Shidahara
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NawachiShoichi
en-aut-sei=Nawachi
en-aut-mei=Shoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AsanoYosuke
en-aut-sei=Asano
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KatsuyamaEri
en-aut-sei=Katsuyama
en-aut-mei=Eri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KatsuyamaTakayuki
en-aut-sei=Katsuyama
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=Takano-NarazakiMariko
en-aut-sei=Takano-Narazaki
en-aut-mei=Mariko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
ORCID=

en-aut-name=OguroNao
en-aut-sei=Oguro
en-aut-mei=Nao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
ORCID=

en-aut-name=IshikawaYuichi
en-aut-sei=Ishikawa
en-aut-mei=Yuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=SakuraiNatsuki
en-aut-sei=Sakurai
en-aut-mei=Natsuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=HidekawaChiharu
en-aut-sei=Hidekawa
en-aut-mei=Chiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=YoshimiRyusuke
en-aut-sei=Yoshimi
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=OhnoShigeru
en-aut-sei=Ohno
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=IchikawaTakanori
en-aut-sei=Ichikawa
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=KishidaDai
en-aut-sei=Kishida
en-aut-mei=Dai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=ShimojimaYasuhiro
en-aut-sei=Shimojima
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=SadaKen-Ei
en-aut-sei=Sada
en-aut-mei=Ken-Ei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
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=21
ORCID=

en-aut-name=ThomDavid H.
en-aut-sei=Thom
en-aut-mei=David H.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=KuritaNoriaki
en-aut-sei=Kurita
en-aut-mei=Noriaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

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

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

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

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

affil-num=5
en-affil=Department of Nephrology, Rheumatology, Endocrinology, and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
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 Nephrology, Rheumatology, Endocrinology, and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

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

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

affil-num=10
en-affil=Division of Rheumatology, Department of Medicine, Showa University School of Medicine
kn-affil=

affil-num=11
en-affil=Division of Rheumatology, Department of Medicine, Showa University School of Medicine
kn-affil=

affil-num=12
en-affil=The First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health
kn-affil=

affil-num=13
en-affil=Department of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine
kn-affil=

affil-num=14
en-affil=Department of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine
kn-affil=

affil-num=15
en-affil=Department of Stem Cell and Immune Regulation, Yokohama City University Graduate School of Medicine
kn-affil=

affil-num=16
en-affil=Centre for Rheumatic Disease, Yokohama City University Medical Centre
kn-affil=

affil-num=17
en-affil=Department of Clinical Epidemiology, Graduate School of Medicine, Fukushima Medical University
kn-affil=

affil-num=18
en-affil=Department of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine
kn-affil=

affil-num=19
en-affil=Department of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine
kn-affil=

affil-num=20
en-affil=Department of Nephrology, Rheumatology, Endocrinology, and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=21
en-affil=Department of Nephrology, Rheumatology, Endocrinology, and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=22
en-affil=Department of Medicine, Stanford University School of Medicine
kn-affil=

affil-num=23
en-affil=Division of Rheumatology, Department of Medicine, Showa University School of Medicine
kn-affil=
en-keyword=Systemic lupus erythematosus
kn-keyword=Systemic lupus erythematosus
en-keyword=Patient-physician relationship
kn-keyword=Patient-physician relationship
en-keyword=Outpatient visits
kn-keyword=Outpatient visits
en-keyword=Patient trust
kn-keyword=Patient trust
en-keyword=Discontinuity of care
kn-keyword=Discontinuity of care
END

start-ver=1.4
cd-journal=joma
no-vol=74
cd-vols=
no-issue=1
article-no=
start-page=12
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241105
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dendritic cell maturation is induced by p53-armed oncolytic adenovirus via tumor-derived exosomes enhancing systemic antitumor immunity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Dendritic cells (DCs) are crucial in cancer immunity, because they activate cytotoxic T cells by presenting tumor antigens. Recently, oncolytic virus therapy has been recognized as a systemic immune stimulator. We previously developed a telomerase-specific oncolytic adenovirus (OBP-301) and a p53-armed OBP-301 (OBP-702), demonstrating that these viruses strongly activate systemic antitumor immunity. However, their effects on DCs remained unclear. In the present study, the aim was to elucidate the mechanisms of DC activation by OBP-702, focusing particularly on tumor-derived exosomes. Exosomes (Exo53, Exo301, or Exo702) were isolated from conditioned media of human or murine pancreatic cancer cell lines (Panc-1, MiaPaCa-2, and PAN02) after treatment with Ad-p53, OBP-301, or OBP-702. Exo702 derived from Panc-1 and MiaPaCa-2 cells significantly upregulated CD86, CD80, CD83 (markers of DC maturation), and IFN-γ in DCs in vitro. Similarly, Exo702 derived from PAN02 cells upregulated CD86 and IFN-γ in bone marrow-derived DCs in a bilateral PAN02 subcutaneous tumor model. This DC maturation was inhibited by GW4869, an inhibitor of exosome release, and anti-CD63, an antibody targeting the exosome marker. Intratumoral injection of OBP-702 into PAN02 subcutaneous tumors significantly increased the presence of mature DCs and CD8-positive T cells in draining lymph nodes, leading to long-lasting antitumor effects through the durable activation of systemic antitumor immunity. In conclusion, tumor-derived exosomes play a significant role in DC maturation following OBP-702 treatment and are critical for the systemic activation of antitumor immunity, leading to the abscopal effect.
en-copyright=
kn-copyright=

en-aut-name=OhtaniTomoko
en-aut-sei=Ohtani
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
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=3
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=4
ORCID=

en-aut-name=KumonKento
en-aut-sei=Kumon
en-aut-mei=Kento
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HashimotoMasashi
en-aut-sei=Hashimoto
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YagiChiaki
en-aut-sei=Yagi
en-aut-mei=Chiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SugimotoRyoma
en-aut-sei=Sugimoto
en-aut-mei=Ryoma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=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=TazawaHiroshi
en-aut-sei=Tazawa
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
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=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=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Oncolys BioPharma, Inc
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=Oncolytic adenovirus
kn-keyword=Oncolytic adenovirus
en-keyword=p53
kn-keyword=p53
en-keyword=Dendritic cells
kn-keyword=Dendritic cells
en-keyword=Anti-tumor immunity
kn-keyword=Anti-tumor immunity
en-keyword=Exosome
kn-keyword=Exosome
END

start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=
article-no=
start-page=foae032
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241018
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Improving the Z3EV promoter system to create the strongest yeast promoter
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Promoters for artificial control of gene expression are central tools in genetic engineering. In the budding yeast Saccharomyces cerevisiae, a variety of constitutive and controllable promoters with different strengths have been constructed using endogenous gene promoters, synthetic transcription factors and their binding sequences, and artificial sequences. However, there have been no attempts to construct the highest strength promoter in yeast cells. In this study, by incrementally increasing the binding sequences of the synthetic transcription factor Z3EV, we were able to construct a promoter (P36) with ~1.4 times the strength of the TDH3 promoter. This is stronger than any previously reported promoter. Although the P36 promoter exhibits some leakage in the absence of induction, the expression induction by estradiol is maintained. When combined with a multicopy plasmid, it can express up to ~50% of total protein as a heterologous protein. This promoter system can be used to gain knowledge about the cell physiology resulting from the ultimate overexpression of excess proteins and is expected to be a useful tool for heterologous protein expression in yeast.
en-copyright=
kn-copyright=

en-aut-name=HiguchiRina
en-aut-sei=Higuchi
en-aut-mei=Rina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujitaYuri
en-aut-sei=Fujita
en-aut-mei=Yuri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NambaShotaro
en-aut-sei=Namba
en-aut-mei=Shotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MoriyaHisao
en-aut-sei=Moriya
en-aut-mei=Hisao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=yeast
kn-keyword=yeast
en-keyword=overexpression
kn-keyword=overexpression
en-keyword=promoter
kn-keyword=promoter
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=11
article-no=
start-page=e73775
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241115
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Axillary Reactive Lymphoid Hyperplasia, Likely Due to Unicentric Castleman Disease, and the Concurrent Presence of Orbital Mucosa-Associated Lymphoid Tissue (MALT) Lymphoma: A Six-Year Follow-Up Study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Castleman disease is a lymphadenopathy of unknown cause at a single site, which is designated as unicentric Castleman disease, or at multiple sites designated as multicentric Castleman disease. We present a patient who showed axillary reactive lymphoid hyperplasia, likely due to unicentric Castleman disease, and orbital extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) lymphoma in a six-year follow-up. A 76-year-old man had a painless left axillary mass for an unknown period and also left complete blepharoptosis with no other systemic symptoms. Suspected of lymphoma, iliac bone marrow biopsy showed no anomalous cells, and positron emission tomography demonstrated abnormal uptake at the left axilla and in the left superior anterior orbit. Incisional biopsy of the left axillary mass demonstrated hyperplastic lymphoid follicles with an atrophic germinal center and prominent small vessels in the follicular center, indicative of unicentric Castleman disease. One year later, annual follow-up positron emission tomography disclosed a high uptake site, next to the previously-identified cyst, in the pancreatic body. Trans-gastric fine needle pancreatic biopsy proved adenocarcinoma and he underwent subtotal stomach-preserving pancreaticoduodenectomy with jejunal anastomosis. He was well for six months after the surgery and thus, underwent resection of the left orbital lesion at 78 years old. The pathology of the orbital lesion showed ambiguous nodular structure with massive infiltration with CD20-positive medium-sized lymphoid cells which were κ monotype in immunoglobulin light chain restriction, indicative of MALT lymphoma. In the four-year period of the COVID-19 pandemic, he was healthy and followed with no treatment until the age of 82 years when he underwent radiation (46 Gy) to the left axillary lesion which did not regress. He then underwent eyelid levator muscle plication for left blepharoptosis since the left orbital lesion remained unpalpable. The six-year follow-up showed that concurrent and independent orbital MALT lymphoma and axillary reactive lymphoid hyperplasia, likely due to unicentric Castleman disease, were both stable. The present case illustrates how important it is to make pathological diagnoses in different anatomical lesions after the initial diagnosis of Castleman disease.
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=FujiTomokazu
en-aut-sei=Fuji
en-aut-mei=Tomokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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 Gastroenterological Surgery, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Hematology and Oncology, Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=
en-keyword=blepharoptosis
kn-keyword=blepharoptosis
en-keyword=castleman disease
kn-keyword=castleman disease
en-keyword=extranodal marginal zone b-cell lymphoma of mucosa-associated lymphoid tissue (malt) lymphoma
kn-keyword=extranodal marginal zone b-cell lymphoma of mucosa-associated lymphoid tissue (malt) lymphoma
en-keyword=pancreatic cancer
kn-keyword=pancreatic cancer
en-keyword=radiation
kn-keyword=radiation
en-keyword=reactive lymphoid hyperplasia
kn-keyword=reactive lymphoid hyperplasia
END

start-ver=1.4
cd-journal=joma
no-vol=300
cd-vols=
no-issue=3
article-no=
start-page=105679
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202403
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Methyl vinyl ketone and its analogs covalently modify PI3K and alter physiological functions by inhibiting PI3K signaling
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Reactive carbonyl species (RCS), which are abundant in the environment and are produced in vivo under stress, covalently bind to nucleophilic residues such as Cys in proteins. Disruption of protein function by RCS exposure is predicted to play a role in the development of various diseases such as cancer and metabolic disorders, but most studies on RCS have been limited to simple cytotoxicity validation, leaving their target proteins and resulting physiological changes unknown. In this study, we focused on methyl vinyl ketone (MVK), which is one of the main RCS found in cigarette smoke and exhaust gas. We found that MVK suppressed PI3K-Akt signaling, which regulates processes involved in cellular homeostasis, including cell proliferation, autophagy, and glucose metabolism. Interestingly, MVK inhibits the interaction between the epidermal growth factor receptor and PI3K. Cys656 in the SH2 domain of the PI3K p85 subunit, which is the covalently binding site of MVK, is important for this interaction. Suppression of PI3K- Akt signaling by MVK reversed epidermal growth factor- induced negative regulation of autophagy and attenuated glucose uptake. Furthermore, we analyzed the effects of the 23 RCS compounds with structures similar to MVK and showed that their analogs also suppressed PI3K-Akt signaling in a manner that correlated with their similarities to MVK. Our study demonstrates the mechanism of MVK and its analogs in suppressing PI3K-Akt signaling and modulating physiological functions, providing a model for future studies analyzing environmental reactive species.
en-copyright=
kn-copyright=

en-aut-name=MorimotoAtsushi
en-aut-sei=Morimoto
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=PanYuexuan
en-aut-sei=Pan
en-aut-mei=Yuexuan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KubotaSho
en-aut-sei=Kubota
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=DohmaeNaoshi
en-aut-sei=Dohmae
en-aut-mei=Naoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AbikoYumi
en-aut-sei=Abiko
en-aut-mei=Yumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=UchidaKoji
en-aut-sei=Uchida
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KumagaiYoshito
en-aut-sei=Kumagai
en-aut-mei=Yoshito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
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 Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

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

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

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

affil-num=5
en-affil=Biomolecular Characterization Unit, Technology Platform Division, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=6
en-affil=Graduate School of Biomedical Science, Nagasaki University
kn-affil=

affil-num=7
en-affil=Laboratory of Food Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo
kn-affil=

affil-num=8
en-affil=Graduate School of Pharmaceutical Sciences, Kyushu University
kn-affil=

affil-num=9
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=phosphatidylinositol 3-kinase (PI 3-kinase)
kn-keyword=phosphatidylinositol 3-kinase (PI 3-kinase)
en-keyword=cell signaling
kn-keyword=cell signaling
en-keyword=chemical modification
kn-keyword=chemical modification
en-keyword=autophagy
kn-keyword=autophagy
en-keyword=glucose uptake
kn-keyword=glucose uptake
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=24968
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241023
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Apolipoprotein-B mRNA-editing complex 3B could be a new potential therapeutic target in endometriosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This study investigated the correlation of Apolipoprotein-B mRNA-editing complex 3B (APOBEC3B) expression with hypoxia inducible factor 1α (HIF-1α), Kirsten rat sarcoma virus (KRAS) and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) in endometriosis patients, and the inhibitory effects of APOBEC3B knockdown in a human endometriotic cell line. Here, APOBEC3B, HIF-1α, KRAS, and PIK3CA were examined in patients with and without endometriosis using reverse transcription polymerase chain reaction (RT-PCR). The apoptosis, cell proliferation, invasion, migration, and biological function of APOBEC3B knockdown were explored in 12Z immortalized human endometriotic cell line. We observed APOBEC3B, HIF-1α, KRAS and PIK3CA expressions were significantly higher in endometriosis patients (p?<?0.001, p?<?0.001, p?=?0.029, p?=?0.001). Knockdown of APOBEC3B increased apoptosis, which was 28.03% and 22.27% higher than in mock and control siRNA samples, respectively. APOBEC3B knockdown also decreased PIK3CA expression and increased Caspase 8 expression, suggesting a potential role in the regulation of apoptosis. Furthermore, knockdown of APOBEC3B significantly inhibited cell proliferation, invasion, and migration compared to mock and control siRNA. (Cell proliferation: mock: p?<?0.001 and control siRNA: p?=?0.049. Cell invasion: mock: p?<?0.001 and control siRNA: p?=?0.029. Cell migration: mock: p?=?0.004, and control siRNA: p?=?0.014). In conclusion, this study suggests that APOBEC3B may be a new potential therapeutic target for endometriosis.
en-copyright=
kn-copyright=

en-aut-name=VuThuy Ha
en-aut-sei=Vu
en-aut-mei=Thuy Ha
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=ShigeyasuKunitoshi
en-aut-sei=Shigeyasu
en-aut-mei=Kunitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KashinoChiaki
en-aut-sei=Kashino
en-aut-mei=Chiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=

en-aut-name=KuboKotaro
en-aut-sei=Kubo
en-aut-mei=Kotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KamadaYasuhiko
en-aut-sei=Kamada
en-aut-mei=Yasuhiko
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, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

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

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

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

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

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

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

affil-num=8
en-affil=Department of Obstetrics and Gynecology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=
en-keyword=Apolipoprotein-B mRNA-editing complex 3B
kn-keyword=Apolipoprotein-B mRNA-editing complex 3B
en-keyword=Endometriosis
kn-keyword=Endometriosis
en-keyword=Apoptosis
kn-keyword=Apoptosis
en-keyword=Potential therapeutic target
kn-keyword=Potential therapeutic target
END

start-ver=1.4
cd-journal=joma
no-vol=99
cd-vols=
no-issue=2
article-no=
start-page=563
end-page=574
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241027
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Therapeutic potential of 4-phenylbutyric acid against methylmercury-induced neuronal cell death in mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Methylmercury (MeHg) is an environmental neurotoxin that induces damage to the central nervous system and is the causative agent in Minamata disease. The mechanisms underlying MeHg neurotoxicity remain largely unknown, and there is a need for effective therapeutic agents, such as those that target MeHg-induced endoplasmic reticulum (ER) stress and the unfolded protein response (UPR), which is activated as a defense mechanism. We investigated whether intraperitoneal administration of the chemical chaperone, 4-phenylbutyric acid (4-PBA), at 120 mg/kg/day can alleviate neurotoxicity in the brains of mice administered 50 ppm MeHg in drinking water for 5 weeks. 4-PBA significantly reduced MeHg-induced ER stress, neuronal apoptosis, and neurological symptoms. Furthermore, 4-PBA was effective even when administered 2 weeks after the initiation of exposure to 30 ppm MeHg in drinking water. Our results strongly indicate that ER stress and the UPR are key processes involved in MeHg toxicity, and that 4-PBA is a novel therapeutic candidate for MeHg-induced neurotoxicity.
en-copyright=
kn-copyright=

en-aut-name=MikiRyohei
en-aut-sei=Miki
en-aut-mei=Ryohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NomuraRyosuke
en-aut-sei=Nomura
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IijimaYuta
en-aut-sei=Iijima
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KubotaSho
en-aut-sei=Kubota
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IwawakiTakao
en-aut-sei=Iwawaki
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FujimuraMasatake
en-aut-sei=Fujimura
en-aut-mei=Masatake
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

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

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

affil-num=6
en-affil=Division of Cell Medicine, Department of Life Science, Medical Research Institute, Kanazawa Medical University
kn-affil=

affil-num=7
en-affil=Department of International Affairs and Research, National Institute for Minamata Disease
kn-affil=

affil-num=8
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Methylmercury
kn-keyword=Methylmercury
en-keyword=Neuronal cell death
kn-keyword=Neuronal cell death
en-keyword=Endoplasmic reticulum stress
kn-keyword=Endoplasmic reticulum stress
en-keyword=Unfolded protein response
kn-keyword=Unfolded protein response
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=4
article-no=
start-page=557
end-page=564
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241019
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical Significance of Prior Ramucirumab Use on the Effectiveness of Nivolumab as the Third-Line Regimen in Gastric Cancer: A Multicenter Retrospective Study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background and Objective Because vascular endothelial growth factor inhibition has been suggested to improve immune cell function in the cancer microenvironment, we examined whether using ramucirumab (RAM) before nivolumab usage is more effective in advanced gastric cancer. <br>
Methods This was a multicenter retrospective observational study. We analyzed patients who received nivolumab monotherapy as the third-line regimen for unresectable advanced or recurrent gastric cancer between October 2017 and December 2022. They were divided into the RAM (RAM-treated) group and the non-RAM (non-treated) group according to the RAM usage in the second-line regimen. The primary outcome was to compare the overall survival after nivolumab administration in the third-line regimen between the RAM and non-RAM groups. <br>
Results Fifty-two patients were included in the present study: 42 patients in the RAM group and ten patients in the non-RAM group. The median overall survival was significantly longer in the RAM group than in the non-RAM group (8.5 months vs 6.9 months, p < 0.05). In the RAM group, patients without peritoneal metastasis had significantly better median overall survival than those with peritoneal metastasis (23.8 months vs 7.7 months, p = 0.0033). Multivariate Cox-proportional hazards analyses showed that the presence of peritoneal metastasis (hazard ratio, 2.4; 95% confidence interval 1.0-5.7) alone was significantly associated with overall survival in the RAM group. <br>
Conclusions The use of RAM prior to nivolumab monotherapy may contribute to prolonged survival in patients with gastric cancer, especially those without peritoneal metastasis.
en-copyright=
kn-copyright=

en-aut-name=ObayashiYuka
en-aut-sei=Obayashi
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HirataShoichiro
en-aut-sei=Hirata
en-aut-mei=Shoichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
ORCID=

en-aut-name=AbeMakoto
en-aut-sei=Abe
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyaharaKoji
en-aut-sei=Miyahara
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakagawaMasahiro
en-aut-sei=Nakagawa
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IshidaMichihiro
en-aut-sei=Ishida
en-aut-mei=Michihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ChodaYasuhiro
en-aut-sei=Choda
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HamadaKenta
en-aut-sei=Hamada
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
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=11
ORCID=

en-aut-name=KawaharaYoshiro
en-aut-sei=Kawahara
en-aut-mei=Yoshiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=13
ORCID=

affil-num=1
en-affil=Department of Internal Medicine, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

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

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

affil-num=4
en-affil=Department of Internal Medicine, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=5
en-affil=Department of Internal Medicine, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=6
en-affil=Department of Endoscopy, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=7
en-affil=Department of Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=8
en-affil=Department of Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=9
en-affil=Department of Practical Gastrointestinal Endoscopy, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Gastroenterology, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of Gastroenterology, Okayama University Hospital
kn-affil=

affil-num=12
en-affil=Department of Practical Gastrointestinal Endoscopy, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=13
en-affil=Department of Gastroenterology and Hepatology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=5
article-no=
start-page=423
end-page=428
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Occult Nesidioblastosis Detected by 111In-Pentetreotide Single-Photon Emission Computed Tomography
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Nesidioblastosis, also known as persistent hyperinsulinemic hypoglycemia, is usually observed in children and infants, although more recently adult-onset nesidioblastosis has also been described. We present a case of nesidioblastosis in a 78-year-old man that was detected by 111In-pentetreotide single photon emission computed tomography (SPECT/CT). The patient was transferred to our hospital’s emergency department in a hypoglycemic coma. Dynamic enhanced CT could detect no lesion in the pancreas, but an 111In-pentetreotide SPECT/CT scan performed after a similar episode four weeks later showed increased focal uptake at the head of the pancreas. The results of a selective arterial calcium injection test were negative. After careful consideration and discussion among colleagues, surgical intervention was selected, and a pancreaticoduodenectomy was performed. On histology, there were elevated numbers of Langerhans islets in the pancreatic head, and the islets themselves appeared enlarged. Hypertrophic β-cells comprised the majority, but α-cells, δ-cells and pancreatic polypeptide were also detected in the islets. Based on the histopathological results and repeated hyperinsulinemic hypoglycemic crises, the patient was finally diagnosed with adult-onset nesidioblastosis. He had no hypoglycemic symptoms during outpatient follow-up examination. Since 111In-pentetreotide SPECT/CT may be able to detect nesidioblastosis, clinicians should consider this relatively new-modality examination when encountering such cases.
en-copyright=
kn-copyright=

en-aut-name=SakamotoShinya
en-aut-sei=Sakamoto
en-aut-mei=Shinya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=YoshimatsuRika
en-aut-sei=Yoshimatsu
en-aut-mei=Rika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HishidaAi
en-aut-sei=Hishida
en-aut-mei=Ai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MatsumotoManabu
en-aut-sei=Matsumoto
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IwataJun
en-aut-sei=Iwata
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OkabayashiTakehiro
en-aut-sei=Okabayashi
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Gastroenteorlogical Surgery, Kochi Health Sciences Center
kn-affil=

affil-num=2
en-affil=Department of Gastroenteorlogical Surgery, Kochi Health Sciences Center
kn-affil=

affil-num=3
en-affil=Department of Radiology, Kochi Health Sciences Center
kn-affil=

affil-num=4
en-affil=Department of Endocrinology and Metabolism, Kochi Health Sciences Center
kn-affil=

affil-num=5
en-affil=Department of Diagnostic Pathology, Kochi Health Sciences Center
kn-affil=

affil-num=6
en-affil=Department of Diagnostic Pathology, Kochi Health Sciences Center
kn-affil=

affil-num=7
en-affil=Department of Gastroenteorlogical Surgery, Kochi Health Sciences Center
kn-affil=
en-keyword=111In-pentetreotide
kn-keyword=111In-pentetreotide
en-keyword=nesidioblastosis
kn-keyword=nesidioblastosis
en-keyword=single-photon emission computed tomography
kn-keyword=single-photon emission computed tomography
en-keyword=hyperinsulinemic hypoglycemia
kn-keyword=hyperinsulinemic hypoglycemia
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=5
article-no=
start-page=407
end-page=412
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The First Report of Bickerstaff Brainstem Encephalitis Induced by Atezolizumab for Metastatic Breast Cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Immune checkpoint inhibitors (ICIs) have revolutionized cancer treatment, but they have been known to cause immune-related adverse events (irAEs) by promoting T-cell activation. Neurological irAEs are rare (1%) but have a high fatality rate (11.5%). Here we report the first case of Bickerstaff brainstem encephalitis (BBE) induced by an ICI. A woman in her 60s with metastatic breast cancer was treated with atezolizumab plus nab-paclitaxel once intravenously. Eighteen days later, she lost consciousness with ophthalmoplegia and was diagnosed with a neurological irAE. She recovered consciousness immediately with the administration of intravenous immunoglobulin (IVIG) but suffered severe permanent peripheral neuropathy. Although it is just one case, this experience shows that BBE occurring as a neurological irAE of ICI cancer treatment may be associated with more severe outcomes than conventional BBE in metastatic cancer. Creating a system for multidisciplinary treatment is essential for ICI therapy.
en-copyright=
kn-copyright=

en-aut-name=ShimoyamaKyoko
en-aut-sei=Shimoyama
en-aut-mei=Kyoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakajimaAtsushi
en-aut-sei=Nakajima
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MinariYoshimitsu
en-aut-sei=Minari
en-aut-mei=Yoshimitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Breast Surgery, Takatsuki General Hospital
kn-affil=

affil-num=2
en-affil=Department of Rehabilitation, Aijinkai Rehabilitation Hospital
kn-affil=

affil-num=3
en-affil=Department of Breast Surgery, Takatsuki General Hospital
kn-affil=
en-keyword=Bickerstaff brainstem encephalitis
kn-keyword=Bickerstaff brainstem encephalitis
en-keyword=immune checkpoint inhibitor
kn-keyword=immune checkpoint inhibitor
en-keyword=atezolizumab
kn-keyword=atezolizumab
en-keyword=neurological immune-related adverse event
kn-keyword=neurological immune-related adverse event
en-keyword=breast cancer
kn-keyword=breast cancer
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=5
article-no=
start-page=387
end-page=399
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of Radon Inhalation on Murine Brain Proteins: Investigation Using Proteomic and Multivariate Analyses
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Radon is a known risk factor for lung cancer; however, it can be used beneficially, such as in radon therapy. We have previously reported the enhancement of antioxidant effects associated with trace amounts of oxidative stress as one of the positive biological effects of radon inhalation. However, the biological effects of radon inhalation are incompletely understood, and more detailed and comprehensive studies are required. Although several studies have used proteomics to investigate the effects of radon inhalation on body proteins, none has focused on brain proteins. In this study, we evaluated the expression status of proteins in murine brains using proteomic and multivariate analyses to identify those whose expressions changed following two days of radon inhalation at a concentration of 1,500 Bq/m3. We found associations of radon inhalation with the expressions of seven proteins related to neurotransmission and heat shock. These proteins may be proposed as biomarkers indicative of radon inhalation. Although further studies are required to obtain the detailed biological significance of these protein alterations, this study contributes to the elucidation of the biological effects of radon
inhalation as a low-dose radiation.
en-copyright=
kn-copyright=

en-aut-name=NaoeShota
en-aut-sei=Naoe
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=KanzakiNorie
en-aut-sei=Kanzaki
en-aut-mei=Norie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakenakaReiju
en-aut-sei=Takenaka
en-aut-mei=Reiju
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakodaAkihiro
en-aut-sei=Sakoda
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyajiTakaaki
en-aut-sei=Miyaji
en-aut-mei=Takaaki
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=

en-aut-name=KataokaTakahiro
en-aut-sei=Kataoka
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Graduate School 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=Ningyo-toge Environmental Engineering Center, Japan Atomic Energy Agency
kn-affil=

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

affil-num=5
en-affil=Ningyo-toge Environmental Engineering Center, Japan Atomic Energy Agency
kn-affil=

affil-num=6
en-affil=Advanced Science Research Center, Okayama University
kn-affil=

affil-num=7
en-affil=Faculty of Health Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Faculty of Health Sciences, Okayama University
kn-affil=
en-keyword=radon inhalation
kn-keyword=radon inhalation
en-keyword=proteomics
kn-keyword=proteomics
en-keyword=multivariate analysis
kn-keyword=multivariate analysis
en-keyword=brain
kn-keyword=brain
en-keyword=oxidative stress
kn-keyword=oxidative stress
END

start-ver=1.4
cd-journal=joma
no-vol=33
cd-vols=
no-issue=4
article-no=
start-page=294
end-page=301
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202307
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Role of lymphadenectomy during primary surgery for kidney cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose of review <br>
Lymph node dissection (LND) during radical nephrectomy (RN) for renal cell carcinoma (RCC) is not considered as a standard. The emergence of robot-assisted surgery and effective immune checkpoint inhibitors (ICI) in recent years may change this and lymph node (LN) staging has become easier and has a clinical impact. In this review, we aimed to reconsider the role of LND today.<br>
<br>
Recent findings <br>
Although the extent of LND has still not been well established, removal of more LN seems to provide better oncologic outcomes for a select group of patients with high-risk factors such as clinical T3-4. Adjuvant therapy using pembrolizumab has been shown to improve disease free survival if complete resection of metastatic lesions as well as the primary site is obtained in combination. Robot assisted RN for localized RCC has been widespread and the studies regarding LND for RCC has been recently appeared.<br>
<br>
Summary <br>
The staging and surgical benefits and its extent of LND during RN for RCC remains unclear, but it is becoming increasingly important. Technologies that allow an easier LND and adjuvant ICI that improve survival in LN-positive patients are engaging the role of LND, a procedure that was needed, but almost never done, is now indicated sometimes. Now, the goal is to identify the clinical and molecular imaging tools that can help identify with sufficient accuracy who needs a LND and which LNs to remove in a targeted personalized approach.
en-copyright=
kn-copyright=

en-aut-name=BekkuKensuke
en-aut-sei=Bekku
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawadaTatsushi
en-aut-sei=Kawada
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YanagisawaTakafumi
en-aut-sei=Yanagisawa
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KarakiewiczPierre I.
en-aut-sei=Karakiewicz
en-aut-mei=Pierre I.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShariatShahrokh F.
en-aut-sei=Shariat
en-aut-mei=Shahrokh F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

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

affil-num=3
en-affil=Department of Urology, Comprehensive Cancer Center, Medical University of Vienna
kn-affil=

affil-num=4
en-affil=Cancer Prognostic and Health Outcomes Unit, Division of Urology, University of Montreal Health Center
kn-affil=

affil-num=5
en-affil=Department of Urology, Comprehensive Cancer Center, Medical University of Vienna
kn-affil=
en-keyword=lymph node dissection
kn-keyword=lymph node dissection
en-keyword=lymph node metastasis
kn-keyword=lymph node metastasis
en-keyword=lymphadenectomy
kn-keyword=lymphadenectomy
en-keyword=lymphadenopathy
kn-keyword=lymphadenopathy
en-keyword=Renal cell carcinoma
kn-keyword=Renal cell carcinoma
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=1
article-no=
start-page=229
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241004
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Primary ileal myeloid sarcoma presenting with bowel obstruction: a case report
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Myeloid sarcoma (MS) is an extramedullary tumor constituted by myeloid blasts or immature myeloid cells. It frequently occurs in conjunction with acute myeloid leukemia (AML); however, it can exceptionally manifest in patients without leukemia. Here, we present a rare case of primary MS originating in the small bowel without evidence of bone marrow involvement.<br>
Case representation A 33 year-old female with no relevant medical history was admitted to our hospital with recurrent abdominal pain. Computed tomography (CT) revealed bowel obstruction due to thickening of the ileum wall, which was suspected to be an ileal tumor. Initially, ectopic endometriosis was suspected because of abdominal pain associated with the menstrual cycle and changes observed on a follow-up CT scan. The lesion could not be detected by double-balloon endoscopy. Despite conservative treatment, the obstruction persisted, and laparoscopic partial ileal resection was performed, which revealed extensive involvement of the ileum and mesentery. Additionally, the mesentery of the resected ileum was extremely thickened. Histopathological and immunohistochemical examinations of the surgical specimen indicated ileal MS. Bone marrow aspiration after discharge was negative for cytological findings of leukemia, leading to a final diagnosis of primary ileal MS. Her postoperative course was uneventful, and she is currently undergoing systemic chemotherapy tailored to AML at another hospital.<br>
Conclusions Even though MS of the small bowel is rare and may not be considered preoperatively, similar surgical treatment to that of other small bowel malignancies can ensure proper postoperative diagnosis and appropriate chemotherapy. Given the potential need for chemotherapy, ensuring surgical safety that allows for its rapid initiation is critical.
en-copyright=
kn-copyright=

en-aut-name=MinagiHitoshi
en-aut-sei=Minagi
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=KondoYoshitaka
en-aut-sei=Kondo
en-aut-mei=Yoshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=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=KashimaHajime
en-aut-sei=Kashima
en-aut-mei=Hajime
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MatsumiYuki
en-aut-sei=Matsumi
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
ORCID=

en-aut-name=ShigeyasuKunitoshi
en-aut-sei=Shigeyasu
en-aut-mei=Kunitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
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=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, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

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

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

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

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

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

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

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

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

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

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

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

affil-num=13
en-affil=Department of Gastroenterological Surgery, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=
en-keyword=Myeloid sarcoma
kn-keyword=Myeloid sarcoma
en-keyword=Chloroma
kn-keyword=Chloroma
en-keyword=Granulocytic sarcoma
kn-keyword=Granulocytic sarcoma
en-keyword=Bowel obstruction
kn-keyword=Bowel obstruction
en-keyword=Abdominal pain
kn-keyword=Abdominal pain
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=9
article-no=
start-page=1781
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240828
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Novel C-Terminal Truncated Bacteriocin Found by Comparison between Leuconostoc mesenteroides 406 and 213M0 Isolated from Mongolian Traditional Fermented Milk, Airag
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Bacteriocins produced by lactic acid bacteria are known to be useful tools for food biopreservation and fermentation control. Leuconostoc mesenteroides subsp. mesenteroides 406 and 213M0 isolated from different samples of Mongolian traditional fermented milk, airag, had been reported to produce listericidal bacteriocin-like inhibitory substances with similar but slightly different properties. In this study, the antibacterial properties and the related gene sequences of both strains were compared, and then their bacteriocins were purified and identified. Strain 406 was superior to strain 213M0 in cell growth and antibacterial activity against many strains. However, the activity of 213M0 was stronger than that of 406 against a few strains. DNA sequencing revealed two and three plasmids in 406 and 213M0, respectively, and each one of them harbored an almost identical mesentericin Y105-B105 gene cluster. Removal of these plasmids resulted in a complete loss of activity, indicating that the antibacterial activity of both strains was generated by bacteriocins encoded on the plasmids. Mesentericins Y105 and B105 were purified from both cultures, and another novel bacteriocin, named mesentericin M, was identified from the 213M0 culture only. Its structural gene was coded on a 213M0 plasmid and, surprisingly, its C-terminal three amino acid residues were post-translationally cleaved. To our knowledge, this is the first report of a C-terminal truncated bacteriocin. In conclusion, the novel bacteriocin should be mainly responsible for the difference in antibacterial properties between the two strains.
en-copyright=
kn-copyright=

en-aut-name=HasiqimugeChihiro
en-aut-sei=Hasiqimuge
en-aut-mei=Chihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HanoChihiro
en-aut-sei=Hano
en-aut-mei=Chihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ArakawaKensuke
en-aut-sei=Arakawa
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YoshidaSaki
en-aut-sei=Yoshida
en-aut-mei=Saki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ZhaoJunliang
en-aut-sei=Zhao
en-aut-mei=Junliang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TohHidehiro
en-aut-sei=Toh
en-aut-mei=Hidehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MoritaHidetoshi
en-aut-sei=Morita
en-aut-mei=Hidetoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MiyamotoTaku
en-aut-sei=Miyamoto
en-aut-mei=Taku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=6
en-affil=Advanced Genomics Center, National Institute of Genetics
kn-affil=

affil-num=7
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=Leuconostoc mesenteroides
kn-keyword=Leuconostoc mesenteroides
en-keyword=antimicrobial peptide
kn-keyword=antimicrobial peptide
en-keyword=bacteriocin
kn-keyword=bacteriocin
en-keyword=Listeria monocytogenes
kn-keyword=Listeria monocytogenes
en-keyword=fermented milk
kn-keyword=fermented milk
en-keyword=biopreservation
kn-keyword=biopreservation
en-keyword=fermentation control
kn-keyword=fermentation control
en-keyword=post-translational modification
kn-keyword=post-translational modification
en-keyword=C-terminal cleavage
kn-keyword=C-terminal cleavage
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=10
article-no=
start-page=e70865
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241004
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Presumed Choroidopathy of IgG4-Related Disease Discovered During 16-Year Follow-Up of a Patient With Polycystic Kidney Disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Immunoglobulin G4 (IgG4)-related disease is characterized by infiltration with IgG4-producing plasma cells in different organs and the elevation of serum IgG4. We present a patient with polycystic kidney disease in long-term follow-up who developed bilateral lacrimal gland enlargement and presumed IgG4-related choroidopathy at different time points. A 45-year-old woman developed bilateral upper eyelid swelling. Head MRI showed bilateral lacrimal gland enlargement, and the resection on both sides revealed foci of infiltration with lymphocytes and plasma cells in bilateral lacrimal glands. The IgG4-immunostaining did not satisfy the diagnostic criteria. She had been taking oral valsartan 40 mg daily for hypertension with polycystic kidney disease.<br>
<br>
The patient was well until the age of 49 years, when she noticed yellowish vision in the right eye compared to the left eye. The right eye showed multiple yellowish spotty lesions in the deep retina to choroid with a mildly hyperemic optic disc, while the left eye showed the normal fundus. No inflammation was noted in the anterior segments of both eyes. Fundus angiography demonstrated early-phase no-filling with late-phase leakage by fluorescein dye and both early-phase and late-phase no-filling by indocyanine green dye, leading to the diagnosis of acute posterior multifocal placoid pigment epitheliopathy (APMPPE). She began to have oral prednisolone tapered from 30 mg daily and discontinued in a year. At the age of 52 years, she switched to candesartan 8 mg daily and began to have tolvaptan (a selective competitive vasopressin receptor 2 (V2) antagonist) 90 mg daily for polycystic kidney disease with liver cysts. At that time, the lesions in the right eye had mild degeneration.<br>
<br>
The patient was followed once a year ophthalmologically to maintain good vision. At 57 years, serum IgG4, which was measured for the first time on suspicion of IgG4-related disease, was elevated to 269.6 mg/dL. In the following four years to the latest visit at 61 years, she kept stable but high levels of serum IgG4 around 300 mg/dL. Serum IgG4 measurement is helpful to make a clinical diagnosis and, hence, a clinical decision since the spectrum of IgG4-related disease remains obscure.
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=TsujiKenji
en-aut-sei=Tsuji
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

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

affil-num=2
en-affil=Pathology, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Nephrology, Okayama University Hospital
kn-affil=
en-keyword=acute posterior multifocal placoid pigment epitheliopathy
kn-keyword=acute posterior multifocal placoid pigment epitheliopathy
en-keyword=choroidopathy
kn-keyword=choroidopathy
en-keyword=uveitis
kn-keyword=uveitis
en-keyword=lacrimal gland tumor
kn-keyword=lacrimal gland tumor
en-keyword=igg4-related disease
kn-keyword=igg4-related disease
END

start-ver=1.4
cd-journal=joma
no-vol=115
cd-vols=
no-issue=11
article-no=
start-page=3660
end-page=3671
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240922
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Identification of ENO-1 positive extracellular vesicles as a circulating biomarker for monitoring of Ewing sarcoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The lack of circulating biomarkers for tumor monitoring is a major problem in Ewing sarcoma management. The development of methods for accurate tumor monitoring is required, considering the high recurrence rate of drug- resistant Ewing sarcoma. Here, we describe a sensitive analytical technique for tumor monitoring of Ewing sarcoma by detecting circulating extracellular vesicles secreted from Ewing sarcoma cells. Proteomic analysis of Ewing sarcoma cell-derived extracellular vesicles identi-fied 564 proteins prominently observed in extracellular vesicles from three Ewing sarcoma cell lines. Among these, CD99, SLC1A5, and ENO-1 were identified on extra-cellular vesicles purified from sera of patients with Ewing sarcoma before treatment but not on extracellular vesicles from those after treatment and healthy individuals. Notably, not only Ewing sarcoma-derived extracellular vesicles but also Ewing sar-coma cells demonstrated proteomic expression of CD99 and ENO-1 on their surface membranes. ENO-1(+)CD6(3+) extracellular vesicle detection was reduced after tumor resection while both CD99+CD63+ and ENO-1(+)CD6(3+) extracellular vesicles were detected in serum from Ewing sarcoma- bearing mice. Finally, the accuracy of liquid biopsy targeting these candidates was assessed using extracellular vesicles from the sera of patients with Ewing sarcoma. Elevated ENO-1+CD81+ extracellular vesicles in the serum of patients before treatments distinguished patients with Ewing sarcoma from healthy individuals with an area under the curve value of 0.92 (P< 0.001) and reflected the tumor burden in patients with Ewing sarcoma during multidisciplinary treatments. Collectively, circulating ENO-1(+)CD81(+) extracellular vesicle detection could represent a novel tool for tumor monitoring of Ewing sarcoma.
en-copyright=
kn-copyright=

en-aut-name=UotaniKoji
en-aut-sei=Uotani
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujiwaraTomohiro
en-aut-sei=Fujiwara
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UedaKoji
en-aut-sei=Ueda
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=IwataShintaro
en-aut-sei=Iwata
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MoritaTakuya
en-aut-sei=Morita
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KiyonoMasahiro
en-aut-sei=Kiyono
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KunisadaToshiyuki
en-aut-sei=Kunisada
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TakedaKen
en-aut-sei=Takeda
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HaseiJoe
en-aut-sei=Hasei
en-aut-mei=Joe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YoshiokaYusuke
en-aut-sei=Yoshioka
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OchiyaTakahiro
en-aut-sei=Ochiya
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=13
ORCID=

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

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

affil-num=3
en-affil=Cancer Precision Medicine Center, Japanese Foundation for Cancer Research
kn-affil=

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

affil-num=5
en-affil=Department of Musculoskeletal Oncology, National Cancer Center Hospital
kn-affil=

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

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

affil-num=8
en-affil=Department of Medical Materials for Musculoskeletal Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

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

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

affil-num=11
en-affil=Department of Molecular and Cellular Medicine, Institute of Medical Science, Tokyo Medical University
kn-affil=

affil-num=12
en-affil=Department of Molecular and Cellular Medicine, Institute of Medical Science, Tokyo Medical University
kn-affil=

affil-num=13
en-affil=Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=circulating biomarker
kn-keyword=circulating biomarker
en-keyword=Ewing sarcoma
kn-keyword=Ewing sarcoma
en-keyword=extracellular vesicles
kn-keyword=extracellular vesicles
en-keyword=liquid biopsy
kn-keyword=liquid biopsy
en-keyword=proteome
kn-keyword=proteome
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=5
article-no=
start-page=763
end-page=779
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240223
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=GRP78 Contributes to the Beneficial Effects of SGLT2 Inhibitor on Proximal Tubular Cells in DKD
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The beneficial effects of sodium?glucose cotransporter 2 (SGLT2) inhibitors on kidney function are well-known; however, their molecular mechanisms are not fully understood. We focused on 78-kDa glucose-regulated protein (GRP78) and its interaction with SGLT2 and integrin-β1 beyond the chaperone property of GRP78. In streptozotocin (STZ)-induced diabetic mouse kidneys, GRP78, SGLT2, and integrin-β1 increased in the plasma membrane fraction, while they were suppressed by canagliflozin. The altered subcellular localization of GRP78/integrin-β1 in STZ mice promoted epithelial mesenchymal transition (EMT) and fibrosis, which were mitigated by canagliflozin. High-glucose conditions reduced intracellular GRP78, increased its secretion, and caused EMT-like changes in cultured HK2 cells, which were again inhibited by canagliflozin. Urinary GRP78 increased in STZ mice, and in vitro experiments with recombinant GRP78 suggested that inflammation spread to surrounding tubular cells and that canagliflozin reversed this effect. Under normal glucose culture, canagliflozin maintained sarco/endoplasmic reticulum (ER) Ca2+-ATPase (SERCA) activity, promoted ER robustness, reduced ER stress response impairment, and protected proximal tubular cells. In conclusion, canagliflozin restored subcellular localization of GRP78, SGLT2, and integrin-β1 and inhibited EMT and fibrosis in DKD. In nondiabetic chronic kidney disease, canagliflozin promoted ER robustness by maintaining SERCA activity and preventing ER stress response failure, and it contributed to tubular protection.
en-copyright=
kn-copyright=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamaguchiSatoshi
en-aut-sei=Yamaguchi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

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

affil-num=1
en-affil=Division of Kidney, Diabetes and Endocrine Diseases, Okayama University Hospital
kn-affil=

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

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

start-ver=1.4
cd-journal=joma
no-vol=65
cd-vols=
no-issue=11
article-no=
start-page=1769
end-page=1786
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240824
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Nutrient Requirements Shape the Preferential Habitat of Allorhizobium vitis VAR03-1, a Commensal Bacterium, in the Rhizosphere of Arabidopsis thaliana
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A diverse range of commensal bacteria inhabit the rhizosphere, influencing host plant growth and responses to biotic and abiotic stresses. While root-released nutrients can define soil microbial habitats, the bacterial factors involved in plant?microbe interactions are not well characterized. In this study, we investigated the colonization patterns of two plant disease biocontrol agents, Allorhizobium vitis VAR03-1 and Pseudomonas protegens Cab57, in the rhizosphere of Arabidopsis thaliana using Murashige and Skoog (MS) agar medium. VAR03-1 formed colonies even at a distance from the roots, preferentially in the upper part, while Cab57 colonized only the root surface. The addition of sucrose to the agar medium resulted in excessive proliferation of VAR03-1, similar to its pattern without sucrose, whereas Cab57 formed colonies only near the root surface. Overgrowth of both bacterial strains upon nutrient supplementation inhibited host growth, independent of plant immune responses. This inhibition was reduced in the VAR03-1 ΔrecA mutant, which exhibited increased biofilm formation, suggesting that some activities associated with the free-living lifestyle rather than the sessile lifestyle may be detrimental to host growth. VAR03-1 grew in liquid MS medium with sucrose alone, while Cab57 required both sucrose and organic acids. Supplementation of sugars and organic acids allowed both bacterial strains to grow near and away from Arabidopsis roots in MS agar. These results suggest that nutrient requirements for bacterial growth may determine their growth habitats in the rhizosphere, with nutrients released in root exudates potentially acting as a limiting factor in harnessing microbiota.
en-copyright=
kn-copyright=

en-aut-name=HemeldaNiarsi Merry
en-aut-sei=Hemelda
en-aut-mei=Niarsi Merry
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=BaoJiyuan
en-aut-sei=Bao
en-aut-mei=Jiyuan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WatanabeMegumi
en-aut-sei=Watanabe
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MatsuiHidenori
en-aut-sei=Matsui
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ToyodaKazuhiro
en-aut-sei=Toyoda
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IchinoseYuki
en-aut-sei=Ichinose
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NoutoshiYoshiteru
en-aut-sei=Noutoshi
en-aut-mei=Yoshiteru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Commensal bacteria
kn-keyword=Commensal bacteria
en-keyword=Nutrient requirements
kn-keyword=Nutrient requirements
en-keyword=Organic acids
kn-keyword=Organic acids
en-keyword=Plant-microbe interactions
kn-keyword=Plant-microbe interactions
en-keyword=Rhizosphere
kn-keyword=Rhizosphere
en-keyword=Sugars
kn-keyword=Sugars
END

start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=1
article-no=
start-page=1099
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240916
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Histological differences related to autophagy in the minor salivary gland between primary and secondary types of Sj?gren's syndrome
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Some forms of Sj?gren’s syndrome (SS) follow a clinical course accompanied by systemic symptoms caused by lymphocyte infiltration and proliferation in the liver, kidneys, and other organs. To better understand the clinical outcomes of SS, here we used minor salivary gland tissues from patients and examine their molecular, biological, and pathological characteristics. A retrospective study was performed, combining clinical data and formalin-fixed paraffin-embedded (FFPE) samples from female patients over 60 years of age who underwent biopsies at Okayama University Hospital. We employed direct digital RNA counting with nCounter? and multiplex immunofluorescence analysis with a PhenoCycler? on the labial gland biopsies. We compared FFPE samples from SS patients who presented with other connective tissue diseases (secondary SS) with those from stable SS patients with symptoms restricted to the exocrine glands (primary SS). Secondary SS tissues showed enhanced epithelial damage and lymphocytic infiltration accompanied by elevated expression of autophagy marker genes in the immune cells of the labial glands. The close intercellular distance between helper T cells and B cells positive for autophagy-associated molecules suggests accelerated autophagy in these lymphocytes and potential B cell activation by helper T cells. These findings indicate that examination of FFPE samples from labial gland biopsies can be an effective tool for evaluating molecular histological differences between secondary and primary SS through multiplexed analysis of gene expression and tissue imaging.
en-copyright=
kn-copyright=

en-aut-name=Ono-MinagiHitomi
en-aut-sei=Ono-Minagi
en-aut-mei=Hitomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NohnoTsutomu
en-aut-sei=Nohno
en-aut-mei=Tsutomu
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=TanakaTakehiro
en-aut-sei=Tanaka
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KatsuyamaTakayuki
en-aut-sei=Katsuyama
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyawakiKohta
en-aut-sei=Miyawaki
en-aut-mei=Kohta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
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=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=YoshinoTadashi
en-aut-sei=Yoshino
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
ORCID=

en-aut-name=SakaiTakayoshi
en-aut-sei=Sakai
en-aut-mei=Takayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OhuchiHideyo
en-aut-sei=Ohuchi
en-aut-mei=Hideyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

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

affil-num=2
en-affil=Department of Cytology and Histology, Okayama University Medical School
kn-affil=

affil-num=3
en-affil=Department of Oral Pathology and Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Pathology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Division of Precision Medicine, Kyushu University School of Medicine
kn-affil=

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

affil-num=8
en-affil=Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Oral and Maxillofacial Reconstructive Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

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

affil-num=11
en-affil=Department of Oral Pathology and Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Rehabilitation for Orofacial Disorders, Osaka University Graduate School of Dentistry
kn-affil=

affil-num=13
en-affil=Department of Cytology and Histology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Autoimmune disease
kn-keyword=Autoimmune disease
en-keyword=Xerostomia
kn-keyword=Xerostomia
en-keyword=Multiplex immunostaining
kn-keyword=Multiplex immunostaining
en-keyword=Spatial analysis
kn-keyword=Spatial analysis
en-keyword=Autophagy
kn-keyword=Autophagy
END

start-ver=1.4
cd-journal=joma
no-vol=21
cd-vols=
no-issue=5
article-no=
start-page=464
end-page=473
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240827
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Terrein Exhibits Anti-tumor Activity by Suppressing Angiogenin Expression in Malignant Melanoma Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/Aim: Malignant melanoma is a tumor with a poor prognosis that can metastasize distally at an early stage. Terrein, a metabolite produced by Aspergillus terreus, suppresses the expression of angiogenin, an angiogenic factor. However, the pharmacological effects of natural terrein have not been elucidated, because only a small amount of terrein can be extracted from large fungal cultures. In this study, we investigated the antineoplastic effects of terrein on human malignant melanoma cells and its underlying mechanisms. Materials and methods: Human malignant melanoma cell lines were cultured in the presence of terrein and analyzed. Angiogenin production was evaluated using ELISA. Ribosome biosynthesis was evaluated using silver staining of the nucleolar organizer region. Intracellular signaling pathways were analyzed using western blotting. Malignant melanoma cells were transplanted subcutaneously into the backs of nude mice. The tumors were removed at 5 weeks and analyzed histopathologically. Results: Terrein inhibited angiogenin expression, proliferation, migration, invasion, and ribosome biosynthesis in malignant melanoma cells. Terrein was shown to inhibit tumor growth and angiogenesis in animal models. Conclusion: This study demonstrated that terrein has anti-tumor effects against malignant melanoma. Furthermore, chemically synthesized non-natural terrein can be mass-produced and serve as a novel potential anti-tumor drug candidate.
en-copyright=
kn-copyright=

en-aut-name=HIROSETAIRA
en-aut-sei=HIROSE
en-aut-mei=TAIRA
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KUNISADAYUKI
en-aut-sei=KUNISADA
en-aut-mei=YUKI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KADOYAKOICHI
en-aut-sei=KADOYA
en-aut-mei=KOICHI
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=SAKAMOTOYUMI
en-aut-sei=SAKAMOTO
en-aut-mei=YUMI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OBATAKYOICHI
en-aut-sei=OBATA
en-aut-mei=KYOICHI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ONOKISHO
en-aut-sei=ONO
en-aut-mei=KISHO
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TAKAKURAHIROAKI
en-aut-sei=TAKAKURA
en-aut-mei=HIROAKI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
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=10
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=11
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=12
ORCID=

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

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

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

affil-num=4
en-affil=Department of Pharmacy, Faculty of Pharmacy, Gifu University of Medical Science
kn-affil=

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

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

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

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

affil-num=9
en-affil=Department of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Division of Applied Chemistry, Graduate School of Natural Sciences and Technology, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=Head and neck cancer
kn-keyword=Head and neck cancer
en-keyword=oral cancer
kn-keyword=oral cancer
en-keyword=malignant melanoma
kn-keyword=malignant melanoma
en-keyword=angiogenin
kn-keyword=angiogenin
en-keyword=terrein
kn-keyword=terrein
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=20521
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240903
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Suppression of PTBP1 in hippocampal astrocytes promotes neurogenesis and ameliorates recognition memory in mice with cerebral ischemia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The therapeutic potential of suppressing polypyrimidine tract-binding protein 1 (Ptbp1) messenger RNA by viral transduction in a post-stroke dementia mouse model has not yet been examined. In this study, 3 days after cerebral ischemia, we injected a viral vector cocktail containing adeno-associated virus (AAV)-pGFAP-mCherry and AAV-pGFAP-CasRx (control vector) or a cocktail of AAV-pGFAP-mCherry and AAV-pGFAP-CasRx-SgRNA-(Ptbp1) (1:5, 1.0 x 1011 viral genomes) into post-stroke mice via the tail vein. We observed new mCherry/NeuN double-positive neuron-like cells in the hippocampus 56 days after cerebral ischemia. A portion of mCherry/GFAP double-positive astrocyte-like glia could have been converted into new mCherry/NeuN double-positive neuron-like cells with morphological changes. The new neuronal cells integrated into the dentate gyrus and recognition memory was significantly ameliorated. These results demonstrated that the in vivo conversion of hippocampal astrocyte-like glia into functional new neurons by the suppression of Ptbp1 might be a therapeutic strategy for post-stroke dementia.
en-copyright=
kn-copyright=

en-aut-name=FukuiYusuke
en-aut-sei=Fukui
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=HuXinran
en-aut-sei=Hu
en-aut-mei=Xinran
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=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=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

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

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

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

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

affil-num=8
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=CasRx
kn-keyword=CasRx
en-keyword=Hippocampal neurogenesis
kn-keyword=Hippocampal neurogenesis
en-keyword=In vivo direct reprogramming
kn-keyword=In vivo direct reprogramming
en-keyword=Ischemic stroke
kn-keyword=Ischemic stroke
en-keyword=PHP.eB
kn-keyword=PHP.eB
en-keyword=Ptbp1
kn-keyword=Ptbp1
en-keyword=Recognition memory
kn-keyword=Recognition memory
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=8
article-no=
start-page=1835
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240812
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Surface Pre-Reacted Glass-Ionomer Eluate Suppresses Osteoclastogenesis through Downregulation of the MAPK Signaling Pathway
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Surface pre-reacted glass-ionomer (S-PRG) is a new bioactive filler utilized for the restoration of decayed teeth by its ability to release six bioactive ions that prevent the adhesion of dental plaque to the tooth surface. Since ionic liquids are reported to facilitate transepithelial penetration, we reasoned that S-PRG applied to root caries could impact the osteoclasts (OCs) in the proximal alveolar bone. Therefore, this study aimed to investigate the effect of S-PRG eluate solution on RANKL-induced OC-genesis and mineral dissolution in vitro. Using RAW264.7 cells as OC precursor cells (OPCs), TRAP staining and pit formation assays were conducted to monitor OC-genesis and mineral dissolution, respectively, while OC-genesis-associated gene expression was measured using quantitative real-time PCR (qPCR). Expression of NFATc1, a master regulator of OC differentiation, and the phosphorylation of MAPK signaling molecules were measured using Western blotting. S-PRG eluate dilutions at 1/200 and 1/400 showed no cytotoxicity to RAW264.7 cells but did significantly suppress both OC-genesis and mineral dissolution. The same concentrations of S-PRG eluate downregulated the RANKL-mediated induction of OCSTAMP and CATK mRNAs, as well as the expression of NFATc1 protein and the phosphorylation of ERK, JNK, and p38. These results demonstrate that S-PRG eluate can downregulate RANKL-induced OC-genesis and mineral dissolution, suggesting that its application to root caries might prevent alveolar bone resorption.
en-copyright=
kn-copyright=

en-aut-name=ChandraJanaki
en-aut-sei=Chandra
en-aut-mei=Janaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraShin
en-aut-sei=Nakamura
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShindoSatoru
en-aut-sei=Shindo
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=LeonElizabeth
en-aut-sei=Leon
en-aut-mei=Elizabeth
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=CastellonMaria
en-aut-sei=Castellon
en-aut-mei=Maria
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=PastoreMaria Rita
en-aut-sei=Pastore
en-aut-mei=Maria Rita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HeidariAlireza
en-aut-sei=Heidari
en-aut-mei=Alireza
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WitekLukasz
en-aut-sei=Witek
en-aut-mei=Lukasz
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=CoelhoPaulo G.
en-aut-sei=Coelho
en-aut-mei=Paulo G.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakatsukaToshiyuki
en-aut-sei=Nakatsuka
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KawaiToshihisa
en-aut-sei=Kawai
en-aut-mei=Toshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

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

affil-num=3
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=4
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=5
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=6
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=7
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=8
en-affil=Biomaterials Division, NYU Dentistry
kn-affil=

affil-num=9
en-affil=Department of Biochemistry and Molecular Biology, Miller School of Medicine, University of Miami
kn-affil=

affil-num=10
en-affil=R&D Department, Shofu Inc.
kn-affil=

affil-num=11
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=
en-keyword=S-PRG
kn-keyword=S-PRG
en-keyword=osteoclast
kn-keyword=osteoclast
en-keyword=hydroxyapatite
kn-keyword=hydroxyapatite
en-keyword=TRAP staining
kn-keyword=TRAP staining
en-keyword=bioactive filler
kn-keyword=bioactive filler
END

start-ver=1.4
cd-journal=joma
no-vol=51
cd-vols=
no-issue=
article-no=
start-page=102104
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=2024
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Protracted coronavirus disease 2019 after chimeric antigen receptor-T cell therapy successfully treated with sequential multidrug therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A 56-year-old woman who received CD19 chimeric antigen receptor-T cell therapy for refractory diffuse large B-cell lymphoma developed severe coronavirus disease 2019 (COVID-19) and was treated with nirmatrelvir/ritonavir in April 2022. However, she experienced persistent fatigue and cough and fever in June. Computed tomography revealed bilateral ground-glass opacities (GGO), and the patient was treated with corticosteroids for organizing pneumonia after COVID19. Partial improvement was observed, but new GGO appeared despite corticosteroid therapy. Genome analysis of severe acute respiratory syndrome coronavirus 2 detected Omicron variant BA.1.1.2, which was prevalent at the time of initial infection. The patient was diagnosed with protracted COVID-19 and was treated with remdesivir, molnupiravir, nirmatrelvir/ritonavir, and tixagevimab/cilgavimab. These treatments appeared to contribute to the improvement of protracted COVID-19.
en-copyright=
kn-copyright=

en-aut-name=YamashitaMasahiro
en-aut-sei=Yamashita
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HigoHisao
en-aut-sei=Higo
en-aut-mei=Hisao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
ORCID=

en-aut-name=MatsumotoChiaki
en-aut-sei=Matsumoto
en-aut-mei=Chiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
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=6
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=7
ORCID=

en-aut-name=RaiKammei
en-aut-sei=Rai
en-aut-mei=Kammei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
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=10
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=11
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=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=MiyaharaNobuaki
en-aut-sei=Miyahara
en-aut-mei=Nobuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

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

affil-num=4
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Center for Clinical Oncology, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

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

affil-num=12
en-affil=Center for Clinical Oncology, Okayama University 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=
en-keyword=Chimeric antigen receptor-T cell therapy
kn-keyword=Chimeric antigen receptor-T cell therapy
en-keyword=Coronavirus disease 2019
kn-keyword=Coronavirus disease 2019
en-keyword=Multidrug therapy
kn-keyword=Multidrug therapy
en-keyword=Organizing pneumonia
kn-keyword=Organizing pneumonia
END

start-ver=1.4
cd-journal=joma
no-vol=357
cd-vols=
no-issue=
article-no=
start-page=114601
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241001
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Revisiting the hormonal control of sexual dimorphism in chicken feathers
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sexual dimorphism in plumage is widespread among avian species. In chickens, adult females exhibit countershading, characterized by dull-colored round feathers lacking fringe on the saddle, while adult males display vibrant plumage with deeply fringed bright feathers. This dimorphism is estrogen-dependent, and administering estrogen to males transforms their showy plumage into cryptic female-like plumage. Extensive studies have shown that estrogen’s role in female plumage formation requires thyroid hormone; however, the precise mechanisms of their interaction remain unclear. In this study, we investigated the roles of estrogen and thyroid hormone in creating sexual dimorphism in the structure and coloration of saddle feathers by administering each hormone to adult males and observing the resulting changes in regenerated feathers induced by plucking. RT-PCR analysis revealed that the expression of type 3 deiodinase (DIO3), responsible for thyroid hormone inactivation, correlates with fringing. Estrogen suppressed DIO3 and agouti signaling protein (ASIP) expression while stimulating BlSK1, a marker of barbule cells, resulting in female-like feathers with mottled patterns and lacking fringes. Administration of thyroxine (T4) stimulated BlSK1 and proopiomelanocortin (POMC) expression, with no effect on ASIP, leading to the formation of solid black feathers lacking fringes. Triiodothyronine (T3) significantly increased POMC expression in pulp cells in culture. Taken together, these findings suggest that estrogen promotes the formation of solid vanes by suppressing DIO3 expression, while also inducing the formation of mottled patterns through inhibition of ASIP expression and indirect stimulation of melanocortin expression via changes in local T3 concentration. This is the first report describing molecular mechanism underlying hormonal crosstalk in creating sexual dimorphism in feathers.
en-copyright=
kn-copyright=

en-aut-name=YouLi
en-aut-sei=You
en-aut-mei=Li
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishioKaori
en-aut-sei=Nishio
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KowataKinue
en-aut-sei=Kowata
en-aut-mei=Kinue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HorikawaMinaru
en-aut-sei=Horikawa
en-aut-mei=Minaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FukuchiHibiki
en-aut-sei=Fukuchi
en-aut-mei=Hibiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OgoshiMaho
en-aut-sei=Ogoshi
en-aut-mei=Maho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AizawaSayaka
en-aut-sei=Aizawa
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Biology, Faculty of Science, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Melanocortin
kn-keyword=Melanocortin
en-keyword=Thyroid hormone
kn-keyword=Thyroid hormone
en-keyword=ASIP
kn-keyword=ASIP
en-keyword=Estrogen
kn-keyword=Estrogen
en-keyword=Deiodinase
kn-keyword=Deiodinase
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=16
article-no=
start-page=1373
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240817
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Direct Binding of Synaptopodin 2-Like Protein to Alpha-Actinin Contributes to Actin Bundle Formation in Cardiomyocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Synaptopodin 2-like protein (SYNPO2L) is localized in the sarcomere of cardiomyocytes and is involved in heart morphogenesis. However, the molecular function of SYNPO2L in the heart is not fully understood. We investigated the interaction of SYNPO2L with sarcomeric alpha-actinin and actin filaments in cultured mouse cardiomyocytes. Immunofluorescence studies showed that SYNPO2L colocalized with alpha-actinin and actin filaments at the Z-discs of the sarcomere. Recombinant SYNPO2La or SYNPO2Lb caused a bundling of the actin filaments in the absence of alpha-actinin and enhanced the alpha-actinin-dependent formation of actin bundles. In addition, high-speed atomic force microscopy revealed that SYNPO2La directly bound to alpha-actinin via its globular ends. The interaction between alpha-actinin and SYNPO2La fixed the movements of the two proteins on the actin filaments. These results strongly suggest that SYNPO2L cooperates with alpha-actinin during actin bundle formation to facilitate sarcomere formation and maintenance.
en-copyright=
kn-copyright=

en-aut-name=YamadaHiroshi
en-aut-sei=Yamada
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OsakaHirona
en-aut-sei=Osaka
en-aut-mei=Hirona
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TatsumiNanami
en-aut-sei=Tatsumi
en-aut-mei=Nanami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ArakiMiu
en-aut-sei=Araki
en-aut-mei=Miu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AbeTadashi
en-aut-sei=Abe
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KaiharaKeiko
en-aut-sei=Kaihara
en-aut-mei=Keiko
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=TakashimaEizo
en-aut-sei=Takashima
en-aut-mei=Eizo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UchihashiTakayuki
en-aut-sei=Uchihashi
en-aut-mei=Takayuki
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=TakeiKohji
en-aut-sei=Takei
en-aut-mei=Kohji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

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

affil-num=2
en-affil=Graduate School of Science, Nagoya University
kn-affil=

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

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

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

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

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

affil-num=8
en-affil=Division of Malaria Research, Proteo-Science Center, Ehime University
kn-affil=

affil-num=9
en-affil=Graduate School of Science, Nagoya University
kn-affil=

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

affil-num=11
en-affil=Department of Neuroscience, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=SYNPO2L
kn-keyword=SYNPO2L
en-keyword=actinin
kn-keyword=actinin
en-keyword=actin
kn-keyword=actin
en-keyword=sarcomere
kn-keyword=sarcomere
en-keyword=cardiomyocyte
kn-keyword=cardiomyocyte
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=16
article-no=
start-page=9038
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240820
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Quercetin Attenuates Acetaldehyde-Induced Cytotoxicity via the Heme Oxygenase-1-Dependent Antioxidant Mechanism in Hepatocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=It is still unclear whether or how quercetin influences the toxic events induced by acetaldehyde in hepatocytes, though quercetin has been reported to mitigate alcohol-induced mouse liver injury. In this study, we evaluated the modulating effect of quercetin on the cytotoxicity induced by acetaldehyde in mouse hepatoma Hepa1c1c7 cells, the frequently used cellular hepatocyte model. The pretreatment with quercetin significantly inhibited the cytotoxicity induced by acetaldehyde. The treatment with quercetin itself had an ability to enhance the total ALDH activity, as well as the ALDH1A1 and ALDH3A1 gene expressions. The acetaldehyde treatment significantly enhanced the intracellular reactive oxygen species (ROS) level, whereas the quercetin pretreatment dose-dependently inhibited it. Accordingly, the treatment with quercetin itself significantly up-regulated the representative intracellular antioxidant-related gene expressions, including heme oxygenase-1 (HO-1), glutamate-cysteine ligase, catalytic subunit (GCLC), and cystine/glutamate exchanger (xCT), that coincided with the enhancement of the total intracellular glutathione (GSH) level. Tin protoporphyrin IX (SNPP), a typical HO-1 inhibitor, restored the quercetin-induced reduction in the intracellular ROS level, whereas buthionine sulphoximine, a representative GSH biosynthesis inhibitor, did not. SNPP also cancelled the quercetin-induced cytoprotection against acetaldehyde. These results suggest that the low-molecular-weight antioxidants produced by the HO-1 enzymatic reaction are mainly attributable to quercetin-induced cytoprotection.
en-copyright=
kn-copyright=

en-aut-name=LiKexin
en-aut-sei=Li
en-aut-mei=Kexin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KidawaraMinori
en-aut-sei=Kidawara
en-aut-mei=Minori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ChenQiguang
en-aut-sei=Chen
en-aut-mei=Qiguang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MunemasaShintaro
en-aut-sei=Munemasa
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MurataYoshiyuki
en-aut-sei=Murata
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakamuraToshiyuki
en-aut-sei=Nakamura
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=7
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=quercetin
kn-keyword=quercetin
en-keyword=acetaldehyde
kn-keyword=acetaldehyde
en-keyword=glutathione
kn-keyword=glutathione
en-keyword=aldehyde dehydrogenase
kn-keyword=aldehyde dehydrogenase
en-keyword=heme oxygenase-1
kn-keyword=heme oxygenase-1
END

start-ver=1.4
cd-journal=joma
no-vol=17
cd-vols=
no-issue=16
article-no=
start-page=4108
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240819
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of Scaffold Geometrical Structure on Macrophage Polarization during Bone Regeneration Using Honeycomb Tricalcium Phosphate
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The polarization balance of M1/M2 macrophages with different functions is important in osteogenesis and bone repair processes. In a previous study, we succeeded in developing honeycomb tricalcium phosphate (TCP), which is a cylindrical scaffold with a honeycomb arrangement of straight pores, and we demonstrated that TCP with 300 and 500 mu m pore diameters (300TCP and 500TCP) induced bone formation within the pores. However, the details of the influence of macrophage polarization on bone formation using engineered biomaterials, especially with respect to the geometric structure of the artificial biomaterials, are unknown. In this study, we examined whether differences in bone tissue formation due to differences in TCP geometry were due to the polarity of the assembling macrophages. Immunohistochemistry for IBA-1, iNOS, and CD163 single staining was performed. The 300TCP showed a marked infiltration of iNOS-positive cells, which are thought to be M1 macrophages, during the osteogenesis process, while no involvement of CD163-positive cells, which are thought to be M2 macrophages, was observed in the TCP pores. In addition, 500TCP showed a clustering of iNOS-positive cells and CD163-positive cells at 2 weeks, suggesting the involvement of M2 macrophages in the formation of bone tissue in the TCP pores. In conclusion, we demonstrated for the first time that the geometrical structure of the artificial biomaterial, i.e., the pore size of honeycomb TCP, affects the polarization of M1/2 macrophages and bone tissue formation in TCP pores.
en-copyright=
kn-copyright=

en-aut-name=TakabatakeKiyofumi
en-aut-sei=Takabatake
en-aut-mei=Kiyofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TsujigiwaHidetsugu
en-aut-sei=Tsujigiwa
en-aut-mei=Hidetsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
ORCID=

en-aut-name=ChangAnqi
en-aut-sei=Chang
en-aut-mei=Anqi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=PiaoTianyan
en-aut-sei=Piao
en-aut-mei=Tianyan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=InadaYasunori
en-aut-sei=Inada
en-aut-mei=Yasunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ArashimaTakuma
en-aut-sei=Arashima
en-aut-mei=Takuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MorimatsuAyumi
en-aut-sei=Morimatsu
en-aut-mei=Ayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
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=10
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=11
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 Life Science, Faculty of Science, Okayama University of Science
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=

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

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

affil-num=11
en-affil=Department of Oral Pathology and Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=honeycomb TCP
kn-keyword=honeycomb TCP
en-keyword=bone formation
kn-keyword=bone formation
en-keyword=macrophages
kn-keyword=macrophages
en-keyword=polarization
kn-keyword=polarization
END

start-ver=1.4
cd-journal=joma
no-vol=476
cd-vols=
no-issue=11
article-no=
start-page=1761
end-page=1775
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240829
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The role of GABA in modulation of taste signaling within the taste bud
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Taste buds contain 2 types of GABA-producing cells: sour-responsive Type III cells and glial-like Type I cells. The physiological role of GABA, released by Type III cells is not fully understood. Here, we investigated the role of GABA released from Type III cells using transgenic mice lacking the expression of GAD67 in taste bud cells (Gad67-cKO mice). Immunohistochemical experiments confirmed the absence of GAD67 in Type III cells of Gad67-cKO mice. Furthermore, no difference was observed in the expression and localization of cell type markers, ectonucleoside triphosphate diphosphohydrolase 2 (ENTPD2), gustducin, and carbonic anhydrase 4 (CA4) in taste buds between wild-type (WT) and Gad67-cKO mice. Short-term lick tests demonstrated that both WT and Gad67-cKO mice exhibited normal licking behaviors to each of the five basic tastants. Gustatory nerve recordings from the chorda tympani nerve demonstrated that both WT and Gad67-cKO mice similarly responded to five basic tastants when they were applied individually. However, gustatory nerve responses to sweet?sour mixtures were significantly smaller than the sum of responses to each tastant in WT mice but not in Gad67-cKO mice. In summary, elimination of GABA signalling by sour-responsive Type III taste cells eliminates the inhibitory cell?cell interactions seen with application of sour?sweet mixtures.
en-copyright=
kn-copyright=

en-aut-name=MikamiAyaka
en-aut-sei=Mikami
en-aut-mei=Ayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HuangHai
en-aut-sei=Huang
en-aut-mei=Hai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HyodoAiko
en-aut-sei=Hyodo
en-aut-mei=Aiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HorieKengo
en-aut-sei=Horie
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YasumatsuKeiko
en-aut-sei=Yasumatsu
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NinomiyaYuzo
en-aut-sei=Ninomiya
en-aut-mei=Yuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MitohYoshihiro
en-aut-sei=Mitoh
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

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

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

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

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

affil-num=5
en-affil=Tokyo Dental Junior College
kn-affil=

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

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

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

affil-num=9
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Gamma-aminobutyric acid
kn-keyword=Gamma-aminobutyric acid
en-keyword=Taste buds
kn-keyword=Taste buds
en-keyword=Glutamate decarboxylase
kn-keyword=Glutamate decarboxylase
en-keyword=Taste mixture
kn-keyword=Taste mixture
en-keyword=Sour
kn-keyword=Sour
en-keyword=Sweet
kn-keyword=Sweet
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=14543
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240624
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cervical spinal cord stimulation exerts anti-epileptic effects in a rat model of epileptic seizure through the suppression of CCL2-mediated cascades
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Epidural spinal cord stimulation (SCS) is indicated for the treatment of intractable pain and is widely used in clinical practice. In previous basic research, the therapeutic effects of SCS have been demonstrated for epileptic seizure. However, the mechanism has not yet been elucidated. In this study, we investigated the therapeutic effect of SCS and the influence of epileptic seizure. First, SCS in the cervical spine was performed. The rats were divided into four groups: control group and treatment groups with SCS conducted at 2, 50, and 300 Hz frequency. Two days later, convulsions were induced by the intraperitoneal administration of kainic acid, followed by video monitoring to assess seizures. We also evaluated glial cells in the hippocampus by fluorescent immunostaining, electroencephalogram measurements, and inflammatory cytokines such as C-C motif chemokine ligand 2 (CCL2) by quantitative real-time polymerase chain reaction. Seizure frequency and the number of glial cells were significantly lower in the 300 Hz group than in the control group. SCS at 300 Hz decreased gene expression level of CCL2, which induces monocyte migration. SCS has anti-seizure effects by inhibiting CCL2-mediated cascades. The suppression of CCL2 and glial cells may be associated with the suppression of epileptic seizure.
en-copyright=
kn-copyright=

en-aut-name=OkazakiYosuke
en-aut-sei=Okazaki
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SasakiTatsuya
en-aut-sei=Sasaki
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HosomotoKakeru
en-aut-sei=Hosomoto
en-aut-mei=Kakeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TanimotoShun
en-aut-sei=Tanimoto
en-aut-mei=Shun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KawaiKoji
en-aut-sei=Kawai
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NagaseTakayuki
en-aut-sei=Nagase
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SugaharaChiaki
en-aut-sei=Sugahara
en-aut-mei=Chiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YabunoSatoru
en-aut-sei=Yabuno
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KinKyohei
en-aut-sei=Kin
en-aut-mei=Kyohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SasadaSusumu
en-aut-sei=Sasada
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YasuharaTakao
en-aut-sei=Yasuhara
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TanakaShota
en-aut-sei=Tanaka
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

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

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

affil-num=3
en-affil=Department of Neurosurgery, Kure Kyosai Hospital
kn-affil=

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

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

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

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

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

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

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

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

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

affil-num=13
en-affil=Department of Neurosurgery, Okayama Rosai Hospital
kn-affil=
en-keyword=Epileptic seizure
kn-keyword=Epileptic seizure
en-keyword=Glial cells
kn-keyword=Glial cells
en-keyword=Spinal cord stimulation
kn-keyword=Spinal cord stimulation
en-keyword=C-C motif chemokine ligand 2
kn-keyword=C-C motif chemokine ligand 2
END

start-ver=1.4
cd-journal=joma
no-vol=64
cd-vols=
no-issue=10
article-no=
start-page=382
end-page=386
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=2024
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Important Notes for Preventing Entrapment of Distal Filter-based Embolic Protection Device in Carotid Artery Stenting
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Failure to retrieve a distal filter-based embolic protection device (EPD) is a potential complication of carotid artery stenting. This may be caused by trapping of the proximal marker of the EPD within the stent tip marker. Maintaining an adequate distance between the two can prevent this. We examined the behavior of several stent-filter-based EPD combinations, focusing on their propensity to become trapped or disengage in vitro. Four physicians subjectively rated the force required to result in trapping using a 5-point scale. Moreover, the force required to disengage trapped devices was evaluated. The Casper stent & horbar;Spider FX EPD combination was difficult to disengage when entrapment occurred, which suggested that this phenomenon tended to occur with this combination. The stent tip marker of the closed-cell stents advanced as they shortened, which may be a unique feature of closed-cell stents. Although trapping is uncommon, it can cause serious complications. To prevent these complications, device characteristics should be well understood before they are used in patients.
en-copyright=
kn-copyright=

en-aut-name=FUJITAJuntaro
en-aut-sei=FUJITA
en-aut-mei=Juntaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HIROTSUNENobuyuki
en-aut-sei=HIROTSUNE
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MATSUDAYuki
en-aut-sei=MATSUDA
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HAMASAKIOsamu
en-aut-sei=HAMASAKI
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FUKUDAShoichi
en-aut-sei=FUKUDA
en-aut-mei=Shoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OKADAYoshihiro
en-aut-sei=OKADA
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KOBASHIAiko
en-aut-sei=KOBASHI
en-aut-mei=Aiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NISHIGAKIShohei
en-aut-sei=NISHIGAKI
en-aut-mei=Shohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MAKINOKeigo
en-aut-sei=MAKINO
en-aut-mei=Keigo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TOMITAYusuke
en-aut-sei=TOMITA
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KIDANINaoya
en-aut-sei=KIDANI
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MURAOKAKenichiro
en-aut-sei=MURAOKA
en-aut-mei=Kenichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=NISHINOShigeki
en-aut-sei=NISHINO
en-aut-mei=Shigeki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

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

affil-num=2
en-affil=Department of Neurosurgery and Neuroendovascular Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=3
en-affil=Department of Neurosurgery, Miyoshi Central Hospital
kn-affil=

affil-num=4
en-affil= Department of Neurosurgery, Miyoshi Central Hospital
kn-affil=

affil-num=5
en-affil=Department of Neurosurgery and Neuroendovascular Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=6
en-affil=Department of Neurosurgery and Neuroendovascular Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=7
en-affil=Department of Neurosurgery and Neuroendovascular Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=8
en-affil=Department of Neurosurgery and Neuroendovascular Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=9
en-affil=Department of Neurosurgery and Neuroendovascular Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=10
en-affil=Department of Neurosurgery and Neuroendovascular Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=11
en-affil=Department of Neurosurgery and Neuroendovascular Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=12
en-affil=Department of Neurosurgery and Neuroendovascular Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=13
en-affil=Department of Neurosurgery and Neuroendovascular Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=
en-keyword=carotid artery stenting
kn-keyword=carotid artery stenting
en-keyword=distal filter-based embolic protection device
kn-keyword=distal filter-based embolic protection device
en-keyword=complication
kn-keyword=complication
END

start-ver=1.4
cd-journal=joma
no-vol=62
cd-vols=
no-issue=5
article-no=
start-page=897
end-page=900
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202409
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A randomized, open-label phase II study on the preventive effect of goshajinkigan against peripheral neuropathy induced by paclitaxel-containing chemotherapy: The OLCSG2101 study protocol
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Paclitaxel (PTX) is an essential cytotoxic anticancer agent and a standard treatment regimen component for various malignant tumors, including advanced unresectable non-small cell lung cancer, thymic cancer, and primary unknown cancers. However, chemotherapy-induced peripheral neuropathy (CIPN) caused by PTX is a significant adverse event that may lead to chemotherapy discontinuation and deterioration of the quality of life (QOL). Although treatment modalities such as goshajinkigan (GJG), pregabalin, and duloxetine are empirically utilized for CIPN, there is no established evidence for an agent as a preventive measure. We designed a randomized phase II trial (OLCSG2101) to investigate whether prophylactic GJG administration can prevent the onset of CIPN induced by PTX.<br>
Methods: This study was designed as a two-arm, prospective, randomized, multicenter phase II trial. The patients will be randomly assigned to either the GJG prophylaxis arm (Arm A) or the GJG non-prophylaxis arm (Arm B), using cancer type (lung cancer or not) and age (<70 years or not) as adjustment factors. A total of 66 patients (33 in each arm) will be enrolled.<br>
Discussion: The results of this study may contribute to better management of CIPN, which can enable the continuation of chemotherapy and maintenance of the patient's QOL.<br>
Ethics and dissemination: Ethical approval was obtained from the certified review board of Okayama University (approval no. CRB21-005) on September 28, 2021. Results will be published in peer-reviewed journals and presented at national and international conferences.<br>
Trial registration: Japan Registry of Clinical Trials (registration number jRCTs061210047).
en-copyright=
kn-copyright=

en-aut-name=NakamuraNaoki
en-aut-sei=Nakamura
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=TanakaTakaaki
en-aut-sei=Tanaka
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KatoYuka
en-aut-sei=Kato
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OzeIsao
en-aut-sei=Oze
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KozukiToshiyuki
en-aut-sei=Kozuki
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YokoyamaToshihide
en-aut-sei=Yokoyama
en-aut-mei=Toshihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

en-aut-name=KuyamaShoichi
en-aut-sei=Kuyama
en-aut-mei=Shoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
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=11
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=12
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=Center of Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Division of Cancer Epidemiology and Prevention, Aichi Cancer Center Research Institute
kn-affil=

affil-num=6
en-affil=Department of Respiratory Medicine, Shikoku Cancer Center
kn-affil=

affil-num=7
en-affil=Department of Respiratory Medicine, Kurashiki Central Hospital
kn-affil=

affil-num=8
en-affil=Department of Respiratory Medicine, KKR Takamatsu Hospital
kn-affil=

affil-num=9
en-affil=Department of Respiratory Medicine, Iwakuni Clinical Center
kn-affil=

affil-num=10
en-affil=Department of Respiratory Medicine, Okayama Rosai Hospital
kn-affil=

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

affil-num=12
en-affil=Center of Innovative Clinical Medicine, Okayama University Hospital
kn-affil=
en-keyword=Kampo
kn-keyword=Kampo
en-keyword=CIPN
kn-keyword=CIPN
en-keyword=prophylaxis
kn-keyword=prophylaxis
en-keyword=neuropathy
kn-keyword=neuropathy
en-keyword=taxane
kn-keyword=taxane
END

start-ver=1.4
cd-journal=joma
no-vol=38
cd-vols=
no-issue=2
article-no=
start-page=394
end-page=408
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200221
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The neurotoxicity of psychoactive phenethylamines “2C series” in cultured monoaminergic neuronal cell lines
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose The aim of this study was to evaluate the neurotoxicity of psychoactive abused 2,5-dimethoxy-substituted phenethylamines “2C series” in monoaminergic neurons.<br>
Methods After the exposure to “2C series”, 2,5-dimethoxy-4-propylthiophenethylamine (2C-T-7), 2,5-dimethoxy-4-isopropylthiophenethylamine (2C-T-4), 2,5-dimethoxy-4-ethylthiophenthylamine (2C-T-2), 2,5-dimethoxy-4-iodophenethylamine (2C-I) or 2,5-dimethoxy-4-chlorophenethylamine (2C-C), we examined their neurotoxicity, morphological changes, and effects of concomitant exposure to 3,4-methylenedioxymethamphetamine (MDMA) or methamphetamine (METH), using cultured neuronal dopaminergic CATH.a cells and serotonin-containing B65 cells.<br>
Results Single dose exposure to “2C series” for 24 h showed significant cytotoxicity as increase in lactate dehydrogenase (LDH) release from both monoaminergic neurons: 2C-T-7, 2C-C (EC50; 100 ?M)?>?2C-T-2 (150 ?M), 2C-T-4 (200 ?M)?>?2C-I (250 ?M) in CATH.a cells and 2C-T-7, 2C-I (150 ?M)?>?2C-T-2 (250 ?M)?>?2C-C, 2C-T-4 (300 ?M) in B65 cells. The “2C series”-induced neurotoxicity in both cells was higher than that of MDMA or METH (EC50:???1?2 mM). In addition, apoptotic morphological changes were observed at relatively lower concentrations of “2C series”. The concomitant exposure to non-toxic dose of MDMA or METH synergistically enhanced 2C series drugs-induced LDH release and apoptotic changes in B65 cells, but to a lesser extent in CATH.a cells. In addition, the lower dose of 2C-T-7, 2C-T-2 or 2C-I promoted reactive oxygen species production in the mitochondria of B65 cells, even at the early stages (3 h) without apparent morphological changes.<br>
Conclusion The 2,5-dimethoxy-substitution of “2C series” induced severe neurotoxicity in both dopaminergic and serotonin-containing neurons. The non-toxic dose of MDMA or METH synergistically enhanced its neurotoxicity in serotonergic neurons.
en-copyright=
kn-copyright=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
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=FunadaMasahiko
en-aut-sei=Funada
en-aut-mei=Masahiko
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=Division of Drug Dependence, National Institute of Mental Health, National Center of Neurology and Psychiatry
kn-affil=
en-keyword=Psychoactive drugs
kn-keyword=Psychoactive drugs
en-keyword=2,5-Dimethoxy-substituted phenethylamines
kn-keyword=2,5-Dimethoxy-substituted phenethylamines
en-keyword=Neurotoxicity
kn-keyword=Neurotoxicity
en-keyword=Serotonin-containing  neurons
kn-keyword=Serotonin-containing  neurons
en-keyword=Dopamine neurons
kn-keyword=Dopamine neurons
en-keyword=Reactive oxygen species
kn-keyword=Reactive oxygen species
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=18063
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240808
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Human heart-on-a-chip microphysiological system comprising endothelial cells, fibroblasts, and iPSC-derived cardiomyocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In recent years, research on organ-on-a-chip technology has been flourishing, particularly for drug screening and disease model development. Fibroblasts and vascular endothelial cells engage in crosstalk through paracrine signaling and direct cell-cell contact, which is essential for the normal development and function of the heart. Therefore, to faithfully recapitulate cardiac function, it is imperative to incorporate fibroblasts and vascular endothelial cells into a heart-on-a-chip model. Here, we report the development of a human heart-on-a-chip composed of induced pluripotent stem cell (iPSC)-derived cardiomyocytes, fibroblasts, and vascular endothelial cells. Vascular endothelial cells cultured on microfluidic channels responded to the flow of culture medium mimicking blood flow by orienting themselves parallel to the flow direction, akin to in vivo vascular alignment in response to blood flow. Furthermore, the flow of culture medium promoted integrity among vascular endothelial cells, as evidenced by CD31 staining and lower apparent permeability. The tri-culture condition of iPSC-derived cardiomyocytes, fibroblasts, and vascular endothelial cells resulted in higher expression of the ventricular cardiomyocyte marker IRX4 and increased contractility compared to the bi-culture condition with iPSC-derived cardiomyocytes and fibroblasts alone. Such tri-culture-derived cardiac tissues exhibited cardiac responses similar to in vivo hearts, including an increase in heart rate upon noradrenaline administration. In summary, we have achieved the development of a heart-on-a-chip composed of cardiomyocytes, fibroblasts, and vascular endothelial cells that mimics in vivo cardiac behavior.
en-copyright=
kn-copyright=

en-aut-name=LiuYun
en-aut-sei=Liu
en-aut-mei=Yun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KamranRumaisa
en-aut-sei=Kamran
en-aut-mei=Rumaisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HanXiaoxia
en-aut-sei=Han
en-aut-mei=Xiaoxia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WangMengxue
en-aut-sei=Wang
en-aut-mei=Mengxue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=LiQiang
en-aut-sei=Li
en-aut-mei=Qiang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=LaiDaoyue
en-aut-sei=Lai
en-aut-mei=Daoyue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
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=8
ORCID=

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

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

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

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

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

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

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

affil-num=8
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Induced pluripotent stem cells
kn-keyword=Induced pluripotent stem cells
en-keyword=Fibroblasts
kn-keyword=Fibroblasts
en-keyword=Endothelial cells
kn-keyword=Endothelial cells
en-keyword=Heart
kn-keyword=Heart
en-keyword=Heart-on-a-chip
kn-keyword=Heart-on-a-chip
en-keyword=Organ-on-a-chip
kn-keyword=Organ-on-a-chip
END

start-ver=1.4
cd-journal=joma
no-vol=136
cd-vols=
no-issue=2
article-no=
start-page=69
end-page=73
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=A case of immune checkpoint inhibitor-associated colitis treated with infliximab
kn-title=インフリキシマブが著効した免疫関連有害事象大腸炎の１例
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=　A 52-year-old Japanese man diagnosed with non-small cell lung cancer initiated chemotherapy with tremelimumab, durvalumab, nanoparticle albumin-bound paclitaxel, and carboplatin. On the fourth day of the first treatment course, he developed a fever, followed by watery diarrhea exceeding 10 episodes per day and bloody stools the next day. Immunotherapy-related adverse event colitis was diagnosed through CT scans and colonoscopy examinations. Despite the ineffectiveness of systemic steroid administration, prompt alleviation of symptoms was achieved through the administration of infliximab. In our case, the patient developed Grade 3 diarrhea, prompting the initiation of intravenous prednisolone at 80mg/day in accordance with guidelines. However, symptom improvement was not attained. In situations where symptoms persist beyond three days despite systemic steroid administration, the consideration of adjunctive infliximab use at a dosage of 5mg/kg becomes necessary.
en-copyright=
kn-copyright=

en-aut-name=IwamuroMasaya
en-aut-sei=Iwamuro
en-aut-mei=Masaya
kn-aut-name=岩室雅也
kn-aut-sei=岩室
kn-aut-mei=雅也
aut-affil-num=1
ORCID=

en-aut-name=HiraokaSakiko
en-aut-sei=Hiraoka
en-aut-mei=Sakiko
kn-aut-name=平岡佐規子
kn-aut-sei=平岡
kn-aut-mei=佐規子
aut-affil-num=2
ORCID=

en-aut-name=OtsukaMotoyuki
en-aut-sei=Otsuka
en-aut-mei=Motoyuki
kn-aut-name=大塚基之
kn-aut-sei=大塚
kn-aut-mei=基之
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Gastroenterology and Hepatology, Okayama University Hospital
kn-affil=岡山大学病院　消化器内科

affil-num=2
en-affil=Inflammatory Bowel Disease Center, Okayama University Hospital
kn-affil=岡山大学病院　炎症性腸疾患センター

affil-num=3
en-affil=Department of Gastroenterology and Hepatology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学学術研究院医歯薬学域　消化器・肝臓内科学
en-keyword=インフリキシマブ（infliximab）
kn-keyword=インフリキシマブ（infliximab）
en-keyword=免疫関連有害事象（immune-related adverse events）
kn-keyword=免疫関連有害事象（immune-related adverse events）
en-keyword=大腸炎（colitis）
kn-keyword=大腸炎（colitis）
END

start-ver=1.4
cd-journal=joma
no-vol=136
cd-vols=
no-issue=2
article-no=
start-page=51
end-page=53
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The 2023 Incentive Award of the Okayama Medical Association in Neuroscience (2023 Niimi Prize)
kn-title=令和５年度岡山医学会賞　脳神経研究奨励賞（新見賞）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=YabunoSatoru
en-aut-sei=Yabuno
en-aut-mei=Satoru
kn-aut-name=藪野諭
kn-aut-sei=藪野
kn-aut-mei=諭
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Neurological Surgery, 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　脳神経外科学
END

start-ver=1.4
cd-journal=joma
no-vol=149
cd-vols=
no-issue=
article-no=
start-page=13
end-page=16
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2018
dt-pub=201809
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Functional analysis of N-terminal propeptide in the precursor of Vibrio vulnificus metalloprotease by using cell-free translational system
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Vibrio vulnificus is a human pathogen causing fatal septicemia with edematous and hemorrhagic skin damage. Among multiple virulence factors, an extracellular metalloprotease termed as V. vulnificus protease (VVP) is known to play a crucial role in eliciting the skin damage. The mature VVP (413 aa) is composed of two domains, the N-terminal core domain with proteolytic activity and the C-terminal domain mediates efficient attachment to protein substrates. However, VVP is produced as an inactive precursor (609 aa) with a signal peptide (24 aa) and propeptide (172 aa). In order to clarify the function of propeptide, a series of DNA fragments encoding the VVP precursor and its various domains were designed and the proteins were expressed in vitro by using cell-free translational system. The results indicated that the propeptide might function as an intramolecular chaperon to promote the proper folding of both N-terminal and C-terminal domains. The obtained results also suggest that the propeptide, itself was unstable and thus digested easily by the enzymes present in cell lysate used for cell-free system. Additionally, the C-terminal domain in VVP found to inhibit the folding of the N-terminal domain in absence of propeptide.
en-copyright=
kn-copyright=

en-aut-name=KawaseTomoka
en-aut-sei=Kawase
en-aut-mei=Tomoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiuraFumi
en-aut-sei=Miura
en-aut-mei=Fumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=DebnathAnusuya
en-aut-sei=Debnath
en-aut-mei=Anusuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ImakuraKinuyo
en-aut-sei=Imakura
en-aut-mei=Kinuyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyoshiShin-ichi
en-aut-sei=Miyoshi
en-aut-mei=Shin-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

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

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

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

affil-num=5
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Vibrio vulnificus
kn-keyword=Vibrio vulnificus
en-keyword=Protease
kn-keyword=Protease
en-keyword=Propeptide
kn-keyword=Propeptide
en-keyword=Domain
kn-keyword=Domain
en-keyword=Cell-free translational system
kn-keyword=Cell-free translational system
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=
article-no=
start-page=1329162
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240809
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Vaccine and antiviral drug promise for preventing post-acute sequelae of COVID-19, and their combination for its treatment
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction: Most healthy individuals recover from acute SARS-CoV-2 infection, whereas a remarkable number continues to suffer from unexplained symptoms, known as Long COVID or post-acute COVID-19 syndrome (PACS). It is therefore imperative that methods for preventing and treating the onset of PASC be investigated with the utmost urgency.<br>
Methods: A mathematical model of the immune response to vaccination and viral infection with SARS-CoV-2, incorporating immune memory cells, was developed.<br>
Results and discussion: Similar to our previous model, persistent infection was observed by the residual virus in the host, implying the possibility of chronic inflammation and delayed recovery from tissue injury. Pre-infectious vaccination and antiviral medication administered during onset can reduce the acute viral load; however, they show no beneficial effects in preventing persistent infection. Therefore, the impact of these treatments on the PASC, which has been clinically observed, is mainly attributed to their role in preventing severe tissue damage caused by acute viral infections. For PASC patients with persistent infection, vaccination was observed to cause an immediate rapid increase in viral load, followed by a temporary decrease over approximately one year. The former was effectively suppressed by the coadministration of antiviral medications, indicating that this combination is a promising treatment for PASC.
en-copyright=
kn-copyright=

en-aut-name=SumiTomonari
en-aut-sei=Sumi
en-aut-mei=Tomonari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HaradaKouji
en-aut-sei=Harada
en-aut-mei=Kouji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Computer Science and Engineering, Toyohashi University of Technology
kn-affil=
en-keyword=post-acute sequelae of SARS-CoV-2 infection
kn-keyword=post-acute sequelae of SARS-CoV-2 infection
en-keyword=PASC
kn-keyword=PASC
en-keyword=long Covid
kn-keyword=long Covid
en-keyword=persistent viruses
kn-keyword=persistent viruses
en-keyword=vaccine
kn-keyword=vaccine
en-keyword=antiviral drug
kn-keyword=antiviral drug
en-keyword=mathematical model
kn-keyword=mathematical model
en-keyword=immune response
kn-keyword=immune response
END

start-ver=1.4
cd-journal=joma
no-vol=115
cd-vols=
no-issue=10
article-no=
start-page=3231
end-page=3247
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240809
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Overcoming immunotherapy resistance and inducing abscopal effects with boron neutron immunotherapy (B-NIT)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Immune checkpoint inhibitors (ICIs) are effective against many advanced malignancies. However, many patients are nonresponders to immunotherapy, and overcoming this resistance to treatment is important. Boron neutron capture therapy (BNCT) is a local chemoradiation therapy with the combination of boron drugs that accumulate selectively in cancer and the neutron irradiation of the cancer site. Here, we report the first boron neutron immunotherapy (B-NIT), combining BNCT and ICI immunotherapy, which was performed on a radioresistant and immunotherapy-resistant advanced-stage B16F10 melanoma mouse model. The BNCT group showed localized tumor suppression, but the anti-PD-1 antibody immunotherapy group did not show tumor suppression. Only the B-NIT group showed strong tumor growth inhibition at both BNCT-treated and shielded distant sites. Intratumoral CD8+ T-cell infiltration and serum high mobility group box 1 (HMGB1) levels were higher in the B-NIT group. Analysis of CD8(+) T cells in tumor-infiltrating lymphocytes (TILs) showed that CD62L- CD44(+) effector memory T cells and CD69(+) early-activated T cells were predominantly increased in the B-NIT group. Administration of CD8-depleting mAb to the B-NIT group completely suppressed the augmented therapeutic effects. This indicated that B-NIT has a potent immune-induced abscopal effect, directly destroying tumors with BNCT, inducing antigen-spreading effects, and protecting normal tissue. B-NIT, immunotherapy combined with BNCT, is the first treatment to overcome immunotherapy resistance in malignant melanoma. In the future, as its therapeutic efficacy is demonstrated not only in melanoma but also in other immunotherapy-resistant malignancies, B-NIT can become a new treatment candidate for advanced-stage cancers.
en-copyright=
kn-copyright=

en-aut-name=FujimotoTakuya
en-aut-sei=Fujimoto
en-aut-mei=Takuya
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=KanehiraNoriyuki
en-aut-sei=Kanehira
en-aut-mei=Noriyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MatsushitaHirokazu
en-aut-sei=Matsushita
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakuraiYoshinori
en-aut-sei=Sakurai
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KenmotsuNaoya
en-aut-sei=Kenmotsu
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MizutaRyo
en-aut-sei=Mizuta
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KondoNatsuko
en-aut-sei=Kondo
en-aut-mei=Natsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TakataTakushi
en-aut-sei=Takata
en-aut-mei=Takushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KitamatsuMizuki
en-aut-sei=Kitamatsu
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=IgawaKazuyo
en-aut-sei=Igawa
en-aut-mei=Kazuyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=FujimuraAtsushi
en-aut-sei=Fujimura
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OtaniYoshihiro
en-aut-sei=Otani
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=ShirakawaMakoto
en-aut-sei=Shirakawa
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=ShigeyasuKunitoshi
en-aut-sei=Shigeyasu
en-aut-mei=Kunitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
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=16
ORCID=

en-aut-name=TogashiYosuke
en-aut-sei=Togashi
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=SuzukiMinoru
en-aut-sei=Suzuki
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
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=19
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=20
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 Dermatology, 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=Division of Translational Oncoimmunology, Aichi Cancer Center Research Institute
kn-affil=

affil-num=5
en-affil=Institute for Integrated Radiation and Nuclear Science, Kyoto University
kn-affil=

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

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

affil-num=8
en-affil=Institute for Integrated Radiation and Nuclear Science, Kyoto University
kn-affil=

affil-num=9
en-affil=Institute for Integrated Radiation and Nuclear Science, Kyoto University
kn-affil=

affil-num=10
en-affil=Faculty of Science and Engineering, Kindai University
kn-affil=

affil-num=11
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=12
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

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

affil-num=14
en-affil=Neutron Therapy Research Center, Okayama University
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=

affil-num=17
en-affil=Department of Tumor Microenvironment, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=18
en-affil=Institute for Integrated Radiation and Nuclear Science, Kyoto University
kn-affil=

affil-num=19
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=20
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=
en-keyword=abscopal effect
kn-keyword=abscopal effect
en-keyword=advanced melanoma
kn-keyword=advanced melanoma
en-keyword=boron neutron capture therapy
kn-keyword=boron neutron capture therapy
en-keyword=boron-neutron immunotherapy
kn-keyword=boron-neutron immunotherapy
en-keyword=immune combination therapy
kn-keyword=immune combination therapy
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=4
article-no=
start-page=337
end-page=343
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202408
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pneumocephalus with Inverted Papilloma in the Frontoethmoidal Sinus: Case Report and Literature Review
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Here, we describe the unique case of a pneumocephalus originating from an inverted papilloma (IP) in the frontoethmoidal sinus. A 71-year-old man with diabetes presented with headaches and altered consciousness. Imaging revealed the pneumocephalus together with bone destruction in the left frontal sinus. He underwent simultaneous endoscopic endonasal and transcranial surgery using an ORBEYE exoscope. Pathological diagnosis of the tumor confirmed IP. Post-surgery, the pneumocephalus was significantly resolved and the squamous cell carcinoma antigen level, which had been elevated, decreased. This case underscores the importance of a multidisciplinary approach and innovative surgical methods in treating complex sinonasal pathologies.
en-copyright=
kn-copyright=

en-aut-name=MakiharaSeiichiro
en-aut-sei=Makihara
en-aut-mei=Seiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OtaniYoshihiro
en-aut-sei=Otani
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
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=4
ORCID=

en-aut-name=ShimizuAiko
en-aut-sei=Shimizu
en-aut-mei=Aiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IkemachiRyosuke
en-aut-sei=Ikemachi
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OkazakiYosuke
en-aut-sei=Okazaki
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OtaTomoyuki
en-aut-sei=Ota
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MatsumotoHiroshi
en-aut-sei=Matsumoto
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MiyamotoShotaro
en-aut-sei=Miyamoto
en-aut-mei=Shotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TsumuraMunechika
en-aut-sei=Tsumura
en-aut-mei=Munechika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=HayashiSeiya
en-aut-sei=Hayashi
en-aut-mei=Seiya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=UmakoshiMichiari
en-aut-sei=Umakoshi
en-aut-mei=Michiari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=HirashitaKoji
en-aut-sei=Hirashita
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=AndoMizuo
en-aut-sei=Ando
en-aut-mei=Mizuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

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

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

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

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

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

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

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

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

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

affil-num=10
en-affil=Department of Otolaryngology-Head & Neck Surgery, Kagawa Rosai Hospital
kn-affil=

affil-num=11
en-affil=Department of Otolaryngology-Head & Neck Surgery, Kagawa Rosai Hospital
kn-affil=

affil-num=12
en-affil=Department of Neurosurgery, Kagawa Rosai Hospital
kn-affil=

affil-num=13
en-affil=Department of Neurosurgery, Kagawa Rosai Hospital
kn-affil=

affil-num=14
en-affil=Department of Neurosurgery, Kagawa Rosai Hospital
kn-affil=

affil-num=15
en-affil=Department of Otolaryngology-Head & Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=pneumocephalus
kn-keyword=pneumocephalus
en-keyword=inverted papilloma
kn-keyword=inverted papilloma
en-keyword=frontoethmoidal sinus
kn-keyword=frontoethmoidal sinus
en-keyword=endoscopic endonasal and transcranial surgery
kn-keyword=endoscopic endonasal and transcranial surgery
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=zbae092
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240716
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cytosolic acidification and oxidation are the toxic mechanisms of SO2 in Arabidopsis guard cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=SO2/H2SO3 can damage plants. However, its toxic mechanism has still been controversial. Two models have been proposed, cytosolic acidification model and cellular oxidation model. Here, we assessed the toxic mechanism of H2SO3 in three cell types of Arabidopsis thaliana, mesophyll cells, guard cells (GCs), and petal cells. The sensitivity of GCs of Chloride channel a (CLCa)-knockout mutants to H2SO3 was significantly lower than those of wildtype plants. Expression of other CLC genes in mesophyll cells and petal cells were different from GCs. Treatment with antioxidant, disodium 4,5-dihydroxy-1,3-benzenedisulfonate (tiron), increased the median lethal concentration (LC50) of H2SO3 in GCs indicating the involvement of cellular oxidation, while the effect was negligible in mesophyll cells and petal cells. These results indicate that there are two toxic mechanisms of SO2 to Arabidopsis cells: cytosolic acidification and cellular oxidation, and the toxic mechanism may vary among cell types.
en-copyright=
kn-copyright=

en-aut-name=MozhganiMahdi
en-aut-sei=Mozhgani
en-aut-mei=Mahdi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OoiLia
en-aut-sei=Ooi
en-aut-mei=Lia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EspagneChristelle
en-aut-sei=Espagne
en-aut-mei=Christelle
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FilleurSophie
en-aut-sei=Filleur
en-aut-mei=Sophie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MoriIzumi C
en-aut-sei=Mori
en-aut-mei=Izumi C
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=2
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=3
en-affil=Universit? Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC)
kn-affil=

affil-num=4
en-affil=Universit? Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC)
kn-affil=

affil-num=5
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=cytosolic acidification
kn-keyword=cytosolic acidification
en-keyword=Arabidopsis
kn-keyword=Arabidopsis
en-keyword=cellular oxidation
kn-keyword=cellular oxidation
en-keyword=chloride channel a
kn-keyword=chloride channel a
en-keyword=sulfur dioxide
kn-keyword=sulfur dioxide
END

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=4
article-no=
start-page=253
end-page=256
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230614
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A case of mucosal-associated lymphoid tissue lymphoma of the urachus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction: Urachus carcinoma is a rare malignancy with an aggressive potential and a poor prognosis, and evidence is limited for its diagnosis and treatment.<br>
Case presentation: A 75-year-old man underwent fluorodeoxyglucose positron emission tomography/computed tomography for staging prostate cancer, and a mass (standardized uptake value max 9.5) was observed on the outside of the urinary bladder dome. T2-weighted magnetic resonance imaging showed the urachus and a low-intensity tumor, which suggested a malignant tumor. We suspected urachal carcinoma and performed total resection of the urachus and partial cystectomy. Pathological examination revealed mucosa-associated lymphoid tissue lymphoma with cells positive for CD20 and negative for CD3, CD5, and cyclin D1. After the surgery, no recurrence has been observed for more than 2 years.<br>
Conclusion: We encountered an extremely rare case of mucosa-associated lymphoid tissue lymphoma of the urachus. Surgical resection of the tumor provided an accurate diagnosis and good disease control.
en-copyright=
kn-copyright=

en-aut-name=TsuboiKazuma
en-aut-sei=Tsuboi
en-aut-mei=Kazuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=BekkuKensuke
en-aut-sei=Bekku
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HaisaKohei
en-aut-sei=Haisa
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KajiharaYuta
en-aut-sei=Kajihara
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TsugawaTakuji
en-aut-sei=Tsugawa
en-aut-mei=Takuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=InoueYosuke
en-aut-sei=Inoue
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakoTomoko
en-aut-sei=Sako
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MuraoWataru
en-aut-sei=Murao
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=EbaraShin
en-aut-sei=Ebara
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Urology, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

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

affil-num=3
en-affil=Department of Urology, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=4
en-affil=Department of Urology, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=5
en-affil=Department of Urology, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=6
en-affil=Department of Urology, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=7
en-affil=Department of Urology, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=8
en-affil=Department of Urology, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=9
en-affil=Department of Urology, Hiroshima City Hiroshima Citizens Hospital
kn-affil=
en-keyword=bladder cancer
kn-keyword=bladder cancer
en-keyword=malignant lymphoma
kn-keyword=malignant lymphoma
en-keyword=MALT lymphoma
kn-keyword=MALT lymphoma
en-keyword=urachal cancer
kn-keyword=urachal cancer
en-keyword=urachal remnant
kn-keyword=urachal remnant
END

start-ver=1.4
cd-journal=joma
no-vol=5
cd-vols=
no-issue=9
article-no=
start-page=884
end-page=890
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240731
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Novel strategy for activating gene expression through triplex DNA formation targeting epigenetically suppressed genes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Triplex DNA formation is a useful genomic targeting tool that is expected to have a wide range of applications, including the antigene method; however, there are fundamental limitations in its forming sequence. We recently extended the triplex DNA-forming sequence to methylated DNA sequences containing 5mCG base pairs by developing guanidino-dN, which is capable of recognizing a 5mCG base pair with high affinity. We herein investigated the effect of triplex DNA formation using TFOs with guanidino-dN on methylated DNA sequences at the promoter of the RASSF1A gene, whose expression is epigenetically suppressed by DNA methylation in MCF-7 cells, on gene expression. Interestingly, triplex DNA formation increased the expression of the RASSF1A gene at the transcript and protein levels. Furthermore, RASSF1A-activated MCF-7 cells exhibited cell growth suppressing activity. Changes in the expression of various genes associated with the promotion of apoptosis and breast cancer survival accompanied the activation of RASSF1A in cells exhibited antiproliferative activity. These results suggest the potential of increases in gene expression through triplex DNA formation as a new genomic targeting tool.
en-copyright=
kn-copyright=

en-aut-name=NotomiRyotaro
en-aut-sei=Notomi
en-aut-mei=Ryotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SasakiShigeki
en-aut-sei=Sasaki
en-aut-mei=Shigeki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TaniguchiYosuke
en-aut-sei=Taniguchi
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Graduate School of Pharmaceutical Sciences, Kyushu University
kn-affil=

affil-num=2
en-affil= Graduate School of Pharmaceutical Sciences, Nagasaki International University
kn-affil=

affil-num=3
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=8
article-no=
start-page=ziae085
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240704
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Macrophages modulate mesenchymal stem cell function via tumor necrosis factor alpha in tooth extraction model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Mesenchymal stem cells (MSCs) and macrophages collaboratively contribute to bone regeneration after injury. However, detailed mechanisms underlying the interaction between MSCs and inflammatory macrophages (M1) remain unclear. A macrophage-depleted tooth extraction model was generated in 5-wk-old female C57BL/6J mice using clodronate liposome (12.5 mg/kg/mouse, intraperitoneally) or saline injection (control) before maxillary first molar extraction. Mice were sacrificed on days 1, 3, 5, 7, and 10 after tooth extraction (n?=?4). Regenerated bone volume evaluation of tooth extraction socket (TES) and histochemical analysis of CD80+M1, CD206+M2 (anti-inflammatory macrophages), PDGFRα+MSC, and TNF-α+ cells were performed. In vitro, isolated MSCs with or without TNF-α stimulation (10 ng/mL, 24 h, n?=?3) were bulk RNA-sequenced (RNA-Seq) to identify TNF-α stimulation-specific MSC transcriptomes. Day 7 micro-CT and HE staining revealed significantly lower mean bone volume (clodronate vs control: 0.01 mm3 vs 0.02 mm3, p<.0001) and mean percentage of regenerated bone area per total TES in clodronate group (41.97% vs 54.03%, p<.0001). Clodronate group showed significant reduction in mean number of CD80+, TNF-α+, PDGFRα+, and CD80+TNF-α+ cells on day 5 (306.5 vs 558.8, p<.0001; 280.5 vs 543.8, p<.0001; 365.0 vs 633.0, p<.0001, 29.0 vs 42.5, p<.0001), while these cells recovered significantly on day 7 (493.3 vs 396.0, p=.0004; 479.3 vs 384.5, p=.0008; 593.0 vs 473.0, p=.0010, 41.0 vs 32.5, p=.0003). RNA-Seq analysis showed that 15 genes (|log2FC|?>?5.0, log2TPM?>?5) after TNF-α stimulation were candidates for regulating MSC’s immunomodulatory capacity. In vivo, Clec4e and Gbp6 are involved in inflammation and bone formation. Clec4e, Gbp6, and Cxcl10 knockdown increased osteogenic differentiation of MSCs in vitro. Temporal reduction followed by apparent recovery of TNF-α-producing M1 macrophages and MSCs after temporal macrophage depletion suggests that TNF-α activated MSCs during TES healing. In vitro mimicking the effect of TNF-α on MSCs indicated that there are 15 candidate MSC genes for regulation of immunomodulatory capacity.
en-copyright=
kn-copyright=

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=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=WangZiyi
en-aut-sei=Wang
en-aut-mei=Ziyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ZhangJiewen
en-aut-sei=Zhang
en-aut-mei=Jiewen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KitagawaWakana
en-aut-sei=Kitagawa
en-aut-mei=Wakana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
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=7
ORCID=

en-aut-name=IshibashiKei
en-aut-sei=Ishibashi
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
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=10
ORCID=

en-aut-name=OnoMitsuaki
en-aut-sei=Ono
en-aut-mei=Mitsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
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=12
ORCID=

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

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

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

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

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

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

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

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

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

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

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

affil-num=12
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=cytokines
kn-keyword=cytokines
en-keyword=dental biology
kn-keyword=dental biology
en-keyword=injury healing
kn-keyword=injury healing
en-keyword=osteoimmunology
kn-keyword=osteoimmunology
en-keyword=stem cells
kn-keyword=stem cells
END

start-ver=1.4
cd-journal=joma
no-vol=45
cd-vols=
no-issue=11
article-no=
start-page=1596
end-page=1601
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20221101
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Investigation of the Expression of Serine Protease in Vibrio vulnificus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Vibrio vulnificus is a Gram-negative estuarine bacterium that causes infection in immuno-compromised patients, eels, and shrimp. V. vulnificus NCIMB2137, a metalloprotease-negative strain isolated from a diseased eel, produces a 45-kDa chymotrypsin-like alkaline serine protease known as VvsA. The gene encoding vvsA also includes another gene, vvsB with an unknown function; however, it is assumed to be an essential molecular chaperone for the maturation of VvsA. In the present study, we used an in vitro cell-free translation system to examine the maturation pathway of VvsA. We individually expressed the vvsA and vvsB genes and detected their mRNAs. However, the sample produced from vvsA did not exhibit protease activity. A sodium dodecyl sulfate (SDS) analysis detected the VvsB protein, but not the VvsA protein. A Western blotting analysis using a histidine (His)-tag at the amino terminus of proteins also showed no protein production by vvsA. These results suggested the translation, but not the transcription of vvsA. Factors derived from Escherichia coli were used in the in vitro cell-free translation system employed in the present study. The operon of the serine protease gene containing vvsA and vvsB was expressed in E. coli. Although serine proteases were produced, they were cleaved at different sites and no active mature forms were detected. These results indicate that the operon encoding vvsA and vvsB is a gene constructed to be specifically expressed in V. vulnificus.
en-copyright=
kn-copyright=

en-aut-name=KawaseTomoka
en-aut-sei=Kawase
en-aut-mei=Tomoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=DebnathAnusuya
en-aut-sei=Debnath
en-aut-mei=Anusuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MizunoTamaki
en-aut-sei=Mizuno
en-aut-mei=Tamaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyakeYui
en-aut-sei=Miyake
en-aut-mei=Yui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

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

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

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

affil-num=4
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Vibrio vulnificus serine protease
kn-keyword=Vibrio vulnificus serine protease
en-keyword=intermolecular chaperone
kn-keyword=intermolecular chaperone
en-keyword=cell-free translation system
kn-keyword=cell-free translation system
END

start-ver=1.4
cd-journal=joma
no-vol=371
cd-vols=
no-issue=
article-no=
start-page=fnae053
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=2024
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Regulatory role of VvsB protein on serine protease activity of VvsA in Vibrio vulnificus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background:Vibrio vulnificus NCIMB2137, a Gram-negative, metalloprotease negative estuarine strain was isolated from a diseased eel. A 45 kDa chymotrypsin-like alkaline serine protease known as VvsA has been recently reported as one of the major virulence factor responsible for the pathogenesis of this strain. The vvsA gene along with a downstream gene vvsB, whose function is still unknown constitute an operon designated as vvsAB. Objective: This study examines the contribution of VvsB to the functionality of VvsA. Method: In this study, VvsB was individually expressed using Rapid Translation System (RTS system), followed by an analysis of its role in regulating the serine protease activity of VvsA. Result: The proteolytic activity of VvsA increased upon the addition of purified VvsB to the culture supernatant of V. vulnificus. However, the attempts of protein expression using an E. coli system revealed a noteworthy observation that protein expression from the vvsA gene exhibited higher protease activity compared to that from the vvsAB gene within the cytoplasmic fraction. These findings suggest an intricate interplay between VvsB and VvsA, where VvsB potentially interacts with VvsA inside the bacterium and suppress the proteolytic activity. While outside the bacterial milieu, VvsB appears to stimulate the activation of inactive VvsA. Conclusion: The findings suggest that Vibrio vulnificus regulates VvsA activity through the action of VvsB, both intracellularly and extracellularly, to ensure its survival.
en-copyright=
kn-copyright=

en-aut-name=KawaseTomoka
en-aut-sei=Kawase
en-aut-mei=Tomoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=DebnathAnusuya
en-aut-sei=Debnath
en-aut-mei=Anusuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OkamotoKeinosuke
en-aut-sei=Okamoto
en-aut-mei=Keinosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

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

affil-num=2
en-affil=Department of Biotechnology, Brainware University
kn-affil=

affil-num=3
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=RTS system
kn-keyword=RTS system
en-keyword=in vitro cell-free translation system, PU
kn-keyword=in vitro cell-free translation system, PU
en-keyword=Proteinase unit, VvsA
kn-keyword=Proteinase unit, VvsA
en-keyword=Vibrio vulnificus serine protease, SD
kn-keyword=Vibrio vulnificus serine protease, SD
en-keyword=Shine-Dalgarno sequence
kn-keyword=Shine-Dalgarno sequence
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=6
article-no=
start-page=1119
end-page=1122
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240605
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Epigenetic Regulation of Carbonic Anhydrase 9 Expression by Nitric Oxide in Human Small Airway Epithelial Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=DNA methylation is a crucial epigenetic modification that regulates gene expression and determines cell fate; however, the triggers that alter DNA methylation levels remain unclear. Recently, we showed that S-nitrosylation of DNA methyltransferase (DNMT) induces DNA hypomethylation and alters gene expression. Furthermore, we identified DBIC, a specific inhibitor of S-nitrosylation of DNMT3B, to suppress nitric oxide (NO)-induced gene alterations. However, it remains unclear how NO-induced DNA hypomethylation regulates gene expression and whether this mechanism is maintained in normal cells and triggers disease-related changes. To address these issues, we focused on carbonic anhydrase 9 (CA9), which is upregulated under nitrosative stress in cancer cells. We pharmacologically evaluated its regulatory mechanisms using human small airway epithelial cells (SAECs) and DBIC. We demonstrated that nitrosative stress promotes the recruitment of hypoxia-inducible factor 1 alpha to the CA9 promoter region and epigenetically induces CA9 expression in SAECs. Our results suggest that nitrosative stress is a key epigenetic regulator that may cause diseases by altering normal cell function.
en-copyright=
kn-copyright=

en-aut-name=MoriyaYuto
en-aut-sei=Moriya
en-aut-mei=Yuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KubotaSho
en-aut-sei=Kubota
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IijimaYuta
en-aut-sei=Iijima
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

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

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

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

affil-num=5
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=nitric oxide
kn-keyword=nitric oxide
en-keyword=human small airway epithelial cell
kn-keyword=human small airway epithelial cell
en-keyword=epigenetics
kn-keyword=epigenetics
en-keyword=DNA methylation
kn-keyword=DNA methylation
en-keyword=carbonic anhydrase 9
kn-keyword=carbonic anhydrase 9
en-keyword=hypoxia-inducible factor 1 alpha
kn-keyword=hypoxia-inducible factor 1 alpha
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=8
article-no=
start-page=208
end-page=214
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202408
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Anterior Uveitis After Discontinuation of Janus Kinase Inhibitor, Ruxolitinib
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Primary myelofibrosis shows widespread fibrosis in the bone marrow and is part of myeloproliferative neoplasms in which gene mutations in hematopoietic stem cells lead to abnormal clonal expansion of one or more lineage of myeloid and erythroid cells and megakaryocytes. Janus kinase (JAK) inhibitors are the main therapeutic regimen for primary myelofibrosis which harbors gene mutations, resulting in continuous activation of JAK-STAT signaling pathway. Since JAK inhibitors modulate immunological state, the administration would have a potential for uveitis. A 67-year-old patient presented with weight loss of 10 kg in the past 2 years after his retirement. He showed normocytic anemia with anisocytosis and abnormal shape, as well as hepatosplenomegaly. Suspected of hematological malignancy, bone marrow biopsy led to the diagnosis of primary myelofibrosis (grade 2) with bizarre megakaryocytes and relative maintenance of myeloid and erythroid lineage. He started to have blood transfusion. Genomic DNA analysis of the peripheral blood showed a pathogenic variant in the exon 9 of calreticulin (CALR) gene while pathogenic variants in Janus kinase-2 (JAK2), and myeloproliferative leukemia virus oncogene (MPL) were absent. He began to have oral ruxolitinib 10 mg daily at the timepoint of 5 months after the initial visit and the dose was increased to 20 mg daily 8 months later but was discontinued further 4 months later because he showed the limited effect of ruxolitinib. He had blood transfusion every week or every 2 weeks in the following 2 months until he noticed blurred vision in the right eye. The right eye showed thick fibrin membrane formation in the anterior chamber in front of the pupil which prevented the fundus from visualization. The left eye showed no inflammation and optic nerve atrophy, sequel to tuberculous meningitis in childhood. The patient started to use 0.1% betamethasone six times daily and 1% atropine once daily as eye drops. A week later, fibrin membrane disappeared and the pupillary area with total iris posterior synechia was visible in the right eye. He regained the vision in the right eye and did not show relapse of uveitis only with topical 0.1% betamethasone. Uveitis might be related with the administration and discontinuation of ruxolitinib.
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=IkedaNaoto
en-aut-sei=Ikeda
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MonobeYasumasa
en-aut-sei=Monobe
en-aut-mei=Yasumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=Department of Internal Medicine, Kaneda Hospital
kn-affil=

affil-num=3
en-affil=Department of Pathology, General Medical Center, Kawasaki Medical School
kn-affil=

affil-num=4
en-affil=Department of Pathology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Janus kinase inhibitor
kn-keyword=Janus kinase inhibitor
en-keyword=Ruxolitinib
kn-keyword=Ruxolitinib
en-keyword=Anemia
kn-keyword=Anemia
en-keyword=Myelofibrosis
kn-keyword=Myelofibrosis
en-keyword=Anterior uveitis
kn-keyword=Anterior uveitis
END

start-ver=1.4
cd-journal=joma
no-vol=39
cd-vols=
no-issue=5
article-no=
start-page=463
end-page=483
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240731
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Detailed Re-Examination of the Period Gene Rescue Experiments Shows That Four to Six Cryptochrome-Positive Posterior Dorsal Clock Neurons (DN1p) of Drosophila melanogaster Can Control Morning and Evening Activity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Animal circadian clocks play a crucial role in regulating behavioral adaptations to daily environmental changes. The fruit fly Drosophila melanogaster exhibits 2 prominent peaks of activity in the morning and evening, known as morning (M) and evening (E) peaks. These peaks are controlled by 2 distinct circadian oscillators located in separate groups of clock neurons in the brain. To investigate the clock neurons responsible for the M and E peaks, a cell-specific gene expression system, the GAL4-UAS system, has been commonly employed. In this study, we re-examined the two-oscillator model for the M and E peaks of Drosophila by utilizing more than 50 Gal4 lines in conjunction with the UAS-period16 line, which enables the restoration of the clock function in specific cells in the period (per) null mutant background. Previous studies have indicated that the group of small ventrolateral neurons (s-LNv) is responsible for controlling the M peak, while the other group, consisting of the 5th ventrolateral neuron (5th LNv) and the three cryptochrome (CRY)-positive dorsolateral neurons (LNd), is responsible for the E peak. Furthermore, the group of posterior dorsal neurons 1 (DN1p) is thought to also contain M and E oscillators. In this study, we found that Gal4 lines directed at the same clock neuron groups can lead to different results, underscoring the fact that activity patterns are influenced by many factors. Nevertheless, we were able to confirm previous findings that the entire network of circadian clock neurons controls M and E peaks, with the lateral neurons playing a dominant role. In addition, we demonstrate that 4 to 6 CRY-positive DN1p cells are sufficient to generate M and E peaks in light-dark cycles and complex free-running rhythms in constant darkness. Ultimately, our detailed screening could serve as a catalog to choose the best Gal4 lines that can be used to rescue per in specific clock neurons.
en-copyright=
kn-copyright=

en-aut-name=SekiguchiManabu
en-aut-sei=Sekiguchi
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ReinhardNils
en-aut-sei=Reinhard
en-aut-mei=Nils
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FukudaAyumi
en-aut-sei=Fukuda
en-aut-mei=Ayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KatohShun
en-aut-sei=Katoh
en-aut-mei=Shun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=RiegerDirk
en-aut-sei=Rieger
en-aut-mei=Dirk
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=Helfrich-F?rsterCharlotte
en-aut-sei=Helfrich-F?rster
en-aut-mei=Charlotte
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshiiTaishi
en-aut-sei=Yoshii
en-aut-mei=Taishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Neurobiology and Genetics, Theodor-Boveri Institute, Biocenter, University of W?rzburg
kn-affil=

affil-num=3
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Neurobiology and Genetics, Theodor-Boveri Institute, Biocenter, University of W?rzburg
kn-affil=

affil-num=6
en-affil=Neurobiology and Genetics, Theodor-Boveri Institute, Biocenter, University of W?rzburg
kn-affil=

affil-num=7
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=period
kn-keyword=period
en-keyword=GAL4-UAS
kn-keyword=GAL4-UAS
en-keyword=clock neuron
kn-keyword=clock neuron
en-keyword=activity rhythm
kn-keyword=activity rhythm
en-keyword=two-oscillator model
kn-keyword=two-oscillator model
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=7
article-no=
start-page=e70003
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240719
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Rare case of rectal carcinoid with synchronous primary carcinoid tumors of the lung misdiagnosed as lung metastases
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A 68-year-old woman was referred to our hospital for rectal surgery after a pathological diagnosis of rectal carcinoid with venous invasion following endoscopic submucosal dissection of a 5?mm-sized submucosal tumor in the lower rectum. Chest CT showed nodules in the left upper lobe and right lower lobe, but positron emission tomography and somatostatin receptor scintigraphy showed no hyperaccumulation in the lung nodules. CT-guided needle biopsy was performed on the nodular lesion in the left upper lobe, which showed focal growth of tumor cells with a high N/C ratio and positive synaptophysin, leading to a diagnosis of pulmonary metastasis of rectal carcinoid. Since the patient was asymptomatic and did not wish to undergo surgery or chemotherapy, she was followed up strictly with sufficient informed consent. Three years have passed since the diagnosis, and there is no tendency for the lung metastasis to increase, and no other new lesions have been observed. The disease had not progressed and remained stable. Therefore, immunohistological analysis of the lung biopsy specimen was performed again, which was positive for TTF-1 and negative for CDX2. Consequently, the diagnosis was changed to primary lung carcinoid tumors, and the patient remains under follow-up with no disease progression.
en-copyright=
kn-copyright=

en-aut-name=TeraishiFuminori
en-aut-sei=Teraishi
en-aut-mei=Fuminori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShojiRhohei
en-aut-sei=Shoji
en-aut-mei=Rhohei
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=

affil-num=1
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School
kn-affil=

affil-num=2
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School
kn-affil=

affil-num=3
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School
kn-affil=
en-keyword=lung metastases
kn-keyword=lung metastases
en-keyword=neuroendocrine tumor
kn-keyword=neuroendocrine tumor
en-keyword=rectal carcinoid
kn-keyword=rectal carcinoid
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=13
article-no=
start-page=7398
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240705
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mechanisms and Functions of Sweet Reception in Oral and Extraoral Organs
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The oral detection of sugars relies on two types of receptor systems. The first is the G-protein-coupled receptor TAS1R2/TAS1R3. When activated, this receptor triggers a downstream signaling cascade involving gustducin, phospholipase C beta 2 (PLC beta 2), and transient receptor potential channel M5 (TRPM5). The second type of receptor is the glucose transporter. When glucose enters the cell via this transporter, it is metabolized to produce ATP. This ATP inhibits the opening of KATP channels, leading to cell depolarization. Beside these receptor systems, sweet-sensitive taste cells have mechanisms to regulate their sensitivity to sweet substances based on internal and external states of the body. Sweet taste receptors are not limited to the oral cavity; they are also present in extraoral organs such as the gastrointestinal tract, pancreas, and brain. These extraoral sweet receptors are involved in various functions, including glucose absorption, insulin release, sugar preference, and food intake, contributing to the maintenance of energy homeostasis. Additionally, sweet receptors may have unique roles in certain organs like the trachea and bone. This review summarizes past and recent studies on sweet receptor systems, exploring the molecular mechanisms and physiological functions of sweet (sugar) detection in both oral and extraoral organs.
en-copyright=
kn-copyright=

en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NinomiyaYuzo
en-aut-sei=Ninomiya
en-aut-mei=Yuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

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

affil-num=2
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=sweet taste
kn-keyword=sweet taste
en-keyword=energy homeostasis
kn-keyword=energy homeostasis
en-keyword=T1R3
kn-keyword=T1R3
en-keyword=GLUT
kn-keyword=GLUT
en-keyword=SGLT
kn-keyword=SGLT
en-keyword=sugar
kn-keyword=sugar
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=13
article-no=
start-page=2326
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240625
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Efficacy of Cisplatin-CXCR4 Antagonist Combination Therapy in Oral Cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cisplatin is a platinum-based compound that is widely used for treating inoperable oral squamous cell carcinoma (OSCC) in Japan; however, resistance to cisplatin presents a challenge and innovative approaches are required. We aimed to investigate the therapeutic potential of targeting the chemokine receptor CXCR4, which is involved in angiogenesis and tumor progression, using the CXCR4 inhibitor AMD3100, in combination with cisplatin. AMD3100 induced necrosis and bleeding in OSCC xenografts by inhibiting angiogenesis. We investigated the combined ability of AMD3100 plus cisplatin to enhance the antitumor effect in cisplatin-resistant OSCC. An MTS assay identified HSC-2 cells as cisplatin-resistant cells in vitro. Mice treated with the cisplatin-AMD combination exhibited the most significant reduction in tumor volume, accompanied by extensive hemorrhage and necrosis. Histological examination indicated thin and short tumor vessels in the AMD and cisplatin?AMD groups. These results indicated that cisplatin and AMD3100 had synergistic antitumor effects, highlighting their potential for vascular therapy of refractory OSCC. Antitumor vascular therapy using cisplatin combined with a CXCR4 inhibitor provides a novel strategy for addressing cisplatin-resistant OSCC.
en-copyright=
kn-copyright=

en-aut-name=YoshidaSaori
en-aut-sei=Yoshida
en-aut-mei=Saori
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=SoeYamin
en-aut-sei=Soe
en-aut-mei=Yamin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=SanouSho
en-aut-sei=Sanou
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

en-aut-name=TakeshitaYohei
en-aut-sei=Takeshita
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HisatomiMiki
en-aut-sei=Hisatomi
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
ORCID=

en-aut-name=AsaumiJunichi
en-aut-sei=Asaumi
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YanagiYoshinobu
en-aut-sei=Yanagi
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Preliminary Examination Room, Okayama University Hospital
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 and Maxillofacial Surgery, 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 and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Hospital
kn-affil=

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

affil-num=10
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Preliminary Examination Room, Okayama University Hospital
kn-affil=
en-keyword=oral squamous cell carcinoma
kn-keyword=oral squamous cell carcinoma
en-keyword=CXCR4
kn-keyword=CXCR4
en-keyword=cisplatin
kn-keyword=cisplatin
en-keyword=antitumor vascular therapy
kn-keyword=antitumor vascular therapy
END

start-ver=1.4
cd-journal=joma
no-vol=137
cd-vols=
no-issue=11
article-no=
start-page=jcs261977
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240612
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Toxicity of the model protein 3×GFP arises from degradation overload, not from aggregate formation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Although protein aggregation can cause cytotoxicity, such aggregates can also form to mitigate cytotoxicity from misfolded proteins, although the nature of these contrasting aggregates remains unclear. We previously found that overproduction (op) of a three green fluorescent protein-linked protein (3×GFP) induces giant aggregates and is detrimental to growth. Here, we investigated the mechanism of growth inhibition by 3×GFP-op using non-aggregative 3×MOX-op as a control in Saccharomyces cerevisiae. The 3×GFP aggregates were induced by misfolding, and 3×GFP-op had higher cytotoxicity than 3×MOX-op because it perturbed the ubiquitin-proteasome system. Static aggregates formed by 3×GFP-op dynamically trapped Hsp70 family proteins (Ssa1 and Ssa2 in yeast), causing the heat-shock response. Systematic analysis of mutants deficient in the protein quality control suggested that 3×GFP-op did not cause a critical Hsp70 depletion and aggregation functioned in the direction of mitigating toxicity. Artificial trapping of essential cell cycle regulators into 3×GFP aggregates caused abnormalities in the cell cycle. In conclusion, the formation of the giant 3×GFP aggregates itself is not cytotoxic, as it does not entrap and deplete essential proteins. Rather, it is productive, inducing the heat-shock response while preventing an overload to the degradation system.
en-copyright=
kn-copyright=

en-aut-name=NambaShotaro
en-aut-sei=Namba
en-aut-mei=Shotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MoriyaHisao
en-aut-sei=Moriya
en-aut-mei=Hisao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Faculty of Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Aggregation
kn-keyword=Aggregation
en-keyword=Fluorescent protein
kn-keyword=Fluorescent protein
en-keyword=Hsp70
kn-keyword=Hsp70
en-keyword=Overproduction
kn-keyword=Overproduction
en-keyword=Toxicity
kn-keyword=Toxicity
en-keyword=Yeast
kn-keyword=Yeast
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=13
article-no=
start-page=e34206
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240715
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Resolvin D2-induced reparative dentin and pulp stem cells after pulpotomy in a rat model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction: Vital pulp therapy (VPT) is performed to preserve dental pulp. However, the biocompatibility of the existing materials is of concern. Therefore, novel materials that can induce pulp healing without adverse effects need to be developed. Resolvin D2 (RvD2), one of specialized pro-resolving mediators, can resolve inflammation and promote the healing of periapical lesions. Therefore, RvD2 may be suitable for use in VPT. In the present study, we evaluated the efficacy of RvD2 against VPT using in vivo and in vitro models.<br>
Methods: First molars of eight-week-old male Sprague?Dawley rats were used for pulpotomy. They were then divided into three treatment groups: RvD2, phosphate-buffered saline, and calcium hydroxide groups. Treatment results were assessed using radiological, histological, and immunohistochemical (GPR18, TNF-α, Ki67, VEGF, TGF-β, CD44, CD90, and TRPA1) analyses. Dental pulp-derived cells were treated with RvD2 in vitro and analyzed using cell-proliferation and cell-migration assays, real-time PCR (Gpr18, Tnf-α, Il-1β, Tgf-β, Vegf, Nanog, and Trpa1), ELISA (VEGF and TGF-β), immunocytochemistry (TRPA1), and flow cytometry (dental pulp stem cells: DPSCs).<br>
Results: The formation of calcified tissue in the pulp was observed in the RvD2 and calcium hydroxide groups. RvD2 inhibited inflammation in dental pulp cells. RvD2 promoted cell proliferation and migration and the expression of TGF-β and VEGF in vitro and in vivo. RvD2 increased the number of DPSCs. In addition, RvD2 suppressed TRPA1 expression as a pain receptor.<br>
Conclusion: RvD2 induced the formation of reparative dentin, anti-inflammatory effects, and decreased pain, along with the proliferation of DPSCs via the expression of VEGF and TGF-β, on the pulp surface in pulpotomy models.
en-copyright=
kn-copyright=

en-aut-name=YonedaMitsuhiro
en-aut-sei=Yoneda
en-aut-mei=Mitsuhiro
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=NakamuraShin
en-aut-sei=Nakamura
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AriasZulema
en-aut-sei=Arias
en-aut-mei=Zulema
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OnoMitsuaki
en-aut-sei=Ono
en-aut-mei=Mitsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
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=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 Periodontics and Endodontics, Division of Dentistry, Okayama University Hospital
kn-affil=

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

affil-num=3
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

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

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

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

affil-num=7
en-affil=The Center for Graduate Medical Education (Dental Division), Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Dental pulp
kn-keyword=Dental pulp
en-keyword=Regeneration
kn-keyword=Regeneration
en-keyword=Pulp-capping agents
kn-keyword=Pulp-capping agents
en-keyword=Specialized pro-resolving mediators
kn-keyword=Specialized pro-resolving mediators
en-keyword=Resolvin D2
kn-keyword=Resolvin D2
en-keyword=Calcification
kn-keyword=Calcification
en-keyword=Cytokine
kn-keyword=Cytokine
en-keyword=TRPA1
kn-keyword=TRPA1
en-keyword=Animal model
kn-keyword=Animal model
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=10
article-no=
start-page=1138
end-page=1149
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240606
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=S100A11 is involved in the progression of colorectal cancer through the desmosome-catenin-TCF signaling?pathway
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Compiling evidence has indicated that S100A11 expression at high levels is closely associated with various cancer species. Consistent with the results reported elsewhere, we have also revealed that S100A11 is highly expressed in squamous cell carcinoma, mesothelioma, and pancreatic cancers and plays a crucial role in cancer progression when secreted into extracellular fluid. Those studies are all focused on the extracellular role of S100A11. However, most of S100A11 is still present within cancer cells, although the intracellular role of S100A11 in cancer cells has not been fully elucidated. Thus, we aimed to investigate S100A11 functions within cancer cells, primarily focusing on colorectal cancer cells, whose S100A11 is abundantly present in cells and still poorly studied cancer for the protein. Our efforts revealed that overexpression of S100A11 promotes proliferation and migration, and downregulation inversely dampens those cancer behaviors. To clarify how intracellular S100A11 aids cancer cell activation, we tried to identify S100A11 binding proteins, resulting in novel binding partners in the inner membrane, many of which are desmosome proteins. Our molecular approach defined that S100A11 regulates the expression level of DSG1, a component protein of desmosome, by which S100A11 activates the TCF pathway via promoting nuclear translocation of γ-catenin from the desmosome. The identified new pathway greatly helps to comprehend S100A11’s nature in colorectal cancers and others.
en-copyright=
kn-copyright=

en-aut-name=ZhouJin
en-aut-sei=Zhou
en-aut-mei=Jin
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=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MizutaNaoko
en-aut-sei=Mizuta
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamakawaAtsuko
en-aut-sei=Yamakawa
en-aut-mei=Atsuko
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=S100A11
kn-keyword=S100A11
en-keyword=Desmosome
kn-keyword=Desmosome
en-keyword=TCF signaling
kn-keyword=TCF signaling
en-keyword=Colorectal cancer
kn-keyword=Colorectal cancer
END

start-ver=1.4
cd-journal=joma
no-vol=128
cd-vols=
no-issue=27
article-no=
start-page=6509
end-page=6517
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240701
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Bidirectional Optical Control of Proton Motive Force in Escherichia coli Using Microbial Rhodopsins
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Proton (H+) motive force (PMF) serves as the energy source for the flagellar motor rotation, crucial for microbial motility. Here, to control PMF using light, we introduced light-driven inward and outward proton pump rhodopsins, RmXeR and AR3, into Escherichia coli. The motility of E. coli cells expressing RmXeR and AR3 significantly decreased and increased upon illumination, respectively. Tethered cell experiments revealed that, upon illumination, the torque of the flagellar motor decreased to nearly zero (28 pN nm) with RmXeR, while it increased to 1170 pN nm with AR3. These alterations in PMF correspond to +146 mV (RmXeR) and ?140 mV (AR3), respectively. Thus, bidirectional optical control of PMF in E. coli was successfully achieved by using proton pump rhodopsins. This system holds a potential for enhancing our understanding of the roles of PMF in various biological functions.
en-copyright=
kn-copyright=

en-aut-name=NakanishiKotaro
en-aut-sei=Nakanishi
en-aut-mei=Kotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KojimaKeiichi
en-aut-sei=Kojima
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SowaYoshiyuki
en-aut-sei=Sowa
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SudoYuki
en-aut-sei=Sudo
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

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

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

affil-num=3
en-affil=Department of Frontier Bioscience and Research Center for Micro-Nano Technology, Hosei University
kn-affil=

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

start-ver=1.4
cd-journal=joma
no-vol=65
cd-vols=
no-issue=4
article-no=
start-page=491
end-page=499
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240628
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Comparison of mutation spectra induced by gamma-rays and carbon ion beams
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The ionizing radiation with high linear energy transfer (LET), such as a heavy ion beam, induces more serious biological effects than low LET ones, such as gamma- and X-rays. This indicates a difference in the DNA damage produced by low and high LET radiations and their biological effects. We have been studying the differences in DNA damage produced by gamma-rays and carbon ion beams. Therefore, we analyze mutations induced by both ionizing radiations to discuss the differences in their biological effects in this study. pUC19 plasmid DNA was irradiated by carbon ion beams in the solution containing 1M dimethyl sulfoxide to mimic a cellular condition. The irradiated DNA was cloned in competent cells of Escherichia coli. The clones harboring some mutations in the region of lacZ alpha were selected, and the sequence alterations were analyzed. A one-deletion mutation is significant in the carbon-irradiated DNA, and the C:G <-> T:A transition is minor. On the other hand, the gamma-irradiated DNA shows mainly G:C <-> T:A transversion. These results suggest that carbon ion beams produce complex DNA damage, and gamma-rays are prone to single oxidative base damage, such as 8-oxoguanine. Carbon ion beams can also introduce oxidative base damage, and the damage species is 5-hydroxycytosine. This was consistent with our previous results of DNA damage caused by heavy ion beams. We confirmed the causal DNA damage by mass spectrometry for these mutations.
en-copyright=
kn-copyright=

en-aut-name=TokuyamaYuka
en-aut-sei=Tokuyama
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MoriKanae
en-aut-sei=Mori
en-aut-mei=Kanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IsobeMidori
en-aut-sei=Isobe
en-aut-mei=Midori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TeratoHiroaki
en-aut-sei=Terato
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Analytical Research Center for Experimental Science, Saga University
kn-affil=

affil-num=2
en-affil=Analytical Research Center for Experimental Science, Saga University
kn-affil=

affil-num=3
en-affil=Advanced Science Research Center, Okayama University
kn-affil=

affil-num=4
en-affil=Advanced Science Research Center, Okayama University
kn-affil=
en-keyword=base damage
kn-keyword=base damage
en-keyword=mutation
kn-keyword=mutation
en-keyword=gamma-rays
kn-keyword=gamma-rays
en-keyword=heavy ion beam
kn-keyword=heavy ion beam
END

start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=11
article-no=
start-page=1419
end-page=1432
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202411
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Inverse genetics tracing the differentiation pathway of human chondrocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective: Mammalian somatic cells can be reprogrammed into induced pluripotent stem cells (iPSCs) via the forced expression of Yamanaka reprogramming factors. However, only a limited population of the cells that pass through a particular pathway can metamorphose into iPSCs, while the others do not. This study aimed to clarify the pathways that chondrocytes follow during the reprogramming process.<br>
Design: The fate of human articular chondrocytes under reprogramming was investigated through a time-coursed single-cell transcriptomic analysis, which we termed an inverse genetic approach. The iPS interference technique was also employed to verify that chondrocytes inversely return to pluripotency following the proper differentiation pathway.<br>
Results: We confirmed that human chondrocytes could be converted into cells with an iPSC phenotype. Moreover, it was clarified that a limited population that underwent the silencing of SOX9, a master gene for chondrogenesis, at a specific point during the proper transcriptome transition pathway, could eventually become iPSCs. Interestingly, the other cells, which failed to be reprogrammed, followed a distinct pathway toward cells with a surface zone chondrocyte phenotype. The critical involvement of cellular communication network factors (CCNs) in this process was indicated. The idea that chondrocytes, when reprogrammed into iPSCs, follow the differentiation pathway backward was supported by the successful iPS interference using SOX9.<br>
Conclusions: This inverse genetic strategy may be useful for seeking candidates for the master genes for the differentiation of various somatic cells. The utility of CCNs in articular cartilage regeneration is also supported.
en-copyright=
kn-copyright=

en-aut-name=DoH.T.
en-aut-sei=Do
en-aut-mei=H.T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OnoM.
en-aut-sei=Ono
en-aut-mei=M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WangZ.
en-aut-sei=Wang
en-aut-mei=Z.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KitagawaW.
en-aut-sei=Kitagawa
en-aut-mei=W.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=DangA.T.
en-aut-sei=Dang
en-aut-mei=A.T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YonezawaT.
en-aut-sei=Yonezawa
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KubokiT.
en-aut-sei=Kuboki
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OohashiT.
en-aut-sei=Oohashi
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KubotaS.
en-aut-sei=Kubota
en-aut-mei=S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

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

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

affil-num=9
en-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Cartilage
kn-keyword=Cartilage
en-keyword=Chondrocyte
kn-keyword=Chondrocyte
en-keyword=Differentiation
kn-keyword=Differentiation
en-keyword=Reprogramming
kn-keyword=Reprogramming
en-keyword=CCN family
kn-keyword=CCN family
END

start-ver=1.4
cd-journal=joma
no-vol=820
cd-vols=
no-issue=
article-no=
start-page=137598
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240118
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neurogenesis impairment with glial activation in the hippocampus-connected regions of intracerebroventricular streptozotocin-injected mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Adult neurogenesis in the hippocampus and subventricular zone (SVZ) is impaired by intracerebroventricular administration of streptozotocin (icv-STZ) to rodents. Although neural cells in the several brain regions which connect with the hippocampus or SVZ is thought to be involved in the adult neurogenesis, few studies have investigated morphological alterations of glial cells in these areas. The present study revealed that icv-STZ induces reduction of neural progenitor cells and a dramatic increase in reactive astrocytes and microglia especially in the hippocampus and various hippocampus-connected brain areas. In contrast, there was no significant neuronal damage excluding demyelination of the stria medullaris. The results indicate the hippocampal neurogenesis impairment of this model might be occurred by activated glial cells in the hippocampus, or hippocampus-connected regions.
en-copyright=
kn-copyright=

en-aut-name=MasaiKaori
en-aut-sei=Masai
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakayamaYuta
en-aut-sei=Nakayama
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShinKotaro
en-aut-sei=Shin
en-aut-mei=Kotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SugaharaChiaki
en-aut-sei=Sugahara
en-aut-mei=Chiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=

en-aut-name=YasuharaTakao
en-aut-sei=Yasuhara
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
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 Medical School
kn-affil=

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

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

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

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

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

affil-num=8
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Streptozotocin
kn-keyword=Streptozotocin
en-keyword=Adult neurogenesis
kn-keyword=Adult neurogenesis
en-keyword=Astrocyte
kn-keyword=Astrocyte
en-keyword=Microglia
kn-keyword=Microglia
END

start-ver=1.4
cd-journal=joma
no-vol=208
cd-vols=
no-issue=
article-no=
start-page=145-
end-page=154
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240627
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Comparison of proportions and prognostic impact of pathological complete response between evaluations of representative specimen and total specimen in primary breast cancer after neoadjuvant chemoradiotherapy: an ancillary study of JCOG0306
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background In JCOG0306 trial, a phase II study to examine the efficacy of neoadjuvant chemotherapy followed by radiation therapy (NAC-RT) to primary breast cancer, pathological complete response (pCR) was evaluated from specimens of the representative cross-section including the tumor center that had been accurately marked [representative specimen (RS) method]. In this ancillary study, we examined if the RS method was comparable to the conventional total specimen (TS) method, which is widely employed in Japan, to identify the pCR group showing excellent prognosis.<br>
Methods We obtained long-term follow-up data of 103 patients enrolled in JCOG0306 trial. As histological therapeutic effect, pCR (ypT0 and ypT0/is) and quasi-pCR [QpCR, ypT0/is plus Grade 2b (only a few remaining invasive cancer cells)] were evaluated with RS and TS methods. Concordance of pCR between these two methods and associations of the pCR with prognosis were examined.<br>
Results ypT0, ypT0/is, and QpCR were observed in 28 (27.2%), 39 (37.9%), and 45 (43.7%) patients with RS method, whereas these were 20 (19.4%), 25 (24.3%) and 40 (38.9%) with TS method, respectively. Between RS and TS methods, concordance proportions of ypT0 and ypTis were 92.2% and 86.4%, respectively. Risk of recurrence of ypT0/is group was lower than that of non-ypT0/is group (HR 0.408, 95% CI [0.175?0.946], P?=?0.037) and risk of death of ypT0/is group was lower than that of non-ypT0/is group (HR 0.251, 95% CI [0.073?0.857], P?=?0.027). The ypT0 and ypT0/is groups with RS method showed excellent prognosis similarly with those with TS method, and RS method was able to differentiate the OS and RFS between pCR and non-pCR than TS method significantly even if pCR was classified ypT0 or ypT0/is. With TS method, QpCR criteria stratified patients into the better and worse prognosis groupsmore clearly than pCR criteria of ypT0 or ypT0/is.<br>
Conclusions RS method was comparable to TS method for the evaluation of pCR in the patients who received NAC-RT to primary breast cancer provided the tumor center was accurately marked. As pCR criteria with RS method, ypT0/is appeared more appropriate than ypT0.
en-copyright=
kn-copyright=

en-aut-name=ShienTadahiko
en-aut-sei=Shien
en-aut-mei=Tadahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TsudaHitoshi
en-aut-sei=Tsuda
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SasakiKeita
en-aut-sei=Sasaki
en-aut-mei=Keita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MizusawaJunki
en-aut-sei=Mizusawa
en-aut-mei=Junki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AkiyamaFutoshi
en-aut-sei=Akiyama
en-aut-mei=Futoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KurosumiMasafumi
en-aut-sei=Kurosumi
en-aut-mei=Masafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SawakiMasataka
en-aut-sei=Sawaki
en-aut-mei=Masataka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TamuraNobuko
en-aut-sei=Tamura
en-aut-mei=Nobuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TanakaKiyo
en-aut-sei=Tanaka
en-aut-mei=Kiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KogawaTakahiro
en-aut-sei=Kogawa
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakahashiMina
en-aut-sei=Takahashi
en-aut-mei=Mina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=HayashiNaoki
en-aut-sei=Hayashi
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MukaiHirofumi
en-aut-sei=Mukai
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MasudaNorikazu
en-aut-sei=Masuda
en-aut-mei=Norikazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=HaraFumikata
en-aut-sei=Hara
en-aut-mei=Fumikata
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=IwataHiroji
en-aut-sei=Iwata
en-aut-mei=Hiroji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

affil-num=1
en-affil=Department of Breast and Endocrine Surgery, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Basic Pathology, National Defense Medical College
kn-affil=

affil-num=3
en-affil=JCOG Data Center/Operations Office, National Cancer Center Hospital
kn-affil=

affil-num=4
en-affil=JCOG Data Center/Operations Office, National Cancer Center Hospital
kn-affil=

affil-num=5
en-affil=Department of Pathology, Cancer Institute Hospital
kn-affil=

affil-num=6
en-affil=Department of Diagnostic Pathology, Kameda Kyobashi Clinic
kn-affil=

affil-num=7
en-affil=Department of Breast Oncology, Aichi Cancer Center Hospital
kn-affil=

affil-num=8
en-affil=Department of Breast Surgery, Toranomon Hospital
kn-affil=

affil-num=9
en-affil=Department of Breast Surgery, Toranomon Hospital
kn-affil=

affil-num=10
en-affil=Department of Breast Medical Oncology, Cancer Institute Hospital
kn-affil=

affil-num=11
en-affil=Department of Breast Oncology, National Hospital Organization Shikoku Cancer Center
kn-affil=

affil-num=12
en-affil=Department of Breast Surgery Oncology, St Lukes International Hospital
kn-affil=

affil-num=13
en-affil=Department of Breast and Medical Oncology, National Cancer Center Hospital East
kn-affil=

affil-num=14
en-affil=Department of Surgery, Breast Oncology, National Hospital Organization Osaka National Hospital
kn-affil=

affil-num=15
en-affil=Department of Breast Medical Oncology, Cancer Institute Hospital
kn-affil=

affil-num=16
en-affil=Department of Breast Oncology, Aichi Cancer Center Hospital
kn-affil=
en-keyword=Breast cancer
kn-keyword=Breast cancer
en-keyword=Neoadjuvant chemoradiotherapy
kn-keyword=Neoadjuvant chemoradiotherapy
en-keyword=Pathological therapeutic effect
kn-keyword=Pathological therapeutic effect
en-keyword=Specimen sampling method
kn-keyword=Specimen sampling method
END

start-ver=1.4
cd-journal=joma
no-vol=121
cd-vols=
no-issue=25
article-no=
start-page=e2318150121
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240612
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Replication of single viruses across the kingdoms, Fungi, Plantae, and Animalia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=It is extremely rare that a single virus crosses host barriers across multiple kingdoms. Based on phylogenetic and paleovirological analyses, it has previously been hypothesized that single members of the family Partitiviridae could cross multiple kingdoms. Partitiviridae accommodates members characterized by their simple bisegmented double-stranded RNA genome; asymptomatic infections of host organisms; the absence of an extracellular route for entry in nature; and collectively broad host range. Herein, we show the replicability of single fungal partitiviruses in three kingdoms of host organisms: Fungi, Plantae, and Animalia. Betapartitiviruses of the phytopathogenic fungusRosellinia necatrix could replicate in protoplasts of the carrot (Daucus carota), Nicotiana benthamiana and Nicotiana tabacum, in some cases reaching a level detectable by agarose gel electrophoresis. Moreover, betapartitiviruses showed more robust replication than the tested alphapartitiviruses. One of the fungal betapartitiviruses, RnPV18, could persistently and stably infect carrot plants regenerated from virion-transfected protoplasts. Both alpha- and betapartitiviruses, although with different host preference, could replicate in two insect cell lines derived from the fall armyworm Spodoptera frugiperda and the fruit fly Drosophila melanogaster. Our results indicate the replicability of single partitiviruses in members of three kingdoms and provide insights into virus adaptation, host jumping, and evolution.
en-copyright=
kn-copyright=

en-aut-name=TelengechPaul
en-aut-sei=Telengech
en-aut-mei=Paul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HyodoKiwamu
en-aut-sei=Hyodo
en-aut-mei=Kiwamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IchikawaHiroaki
en-aut-sei=Ichikawa
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KuwataRyusei
en-aut-sei=Kuwata
en-aut-mei=Ryusei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KondoHideki
en-aut-sei=Kondo
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SuzukiNobuhiro
en-aut-sei=Suzuki
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=2
en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=3
en-affil=Institute of Agrobiological Sciences, National Agriculture and Food Research Organization
kn-affil=

affil-num=4
en-affil=Faculty of Veterinary Medicine, Okayama University of Science
kn-affil=

affil-num=5
en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=6
en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=cross- kingdom infection
kn-keyword=cross- kingdom infection
en-keyword=partitivirus
kn-keyword=partitivirus
en-keyword=fungal virus
kn-keyword=fungal virus
en-keyword=Plantae
kn-keyword=Plantae
en-keyword=Animalia
kn-keyword=Animalia
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=5
cd-vols=
no-issue=4
article-no=
start-page=810
end-page=814
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240619
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Combination of reduced post-transplant cyclophosphamide and early tacrolimus initiation increases the incidence of chronic graft-versus-host disease in human leukocyte antigen-haploidentical peripheral blood stem-cell transplantation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We evaluated the clinical impacts of the concurrent modification of post-transplant cyclophosphamide (PTCy) dose and tacrolimus (Tac)-initiation timing in 61 patients with human leukocyte antigen-haploidentical transplantation. Reduced-dose PTCy (80 mg/kg) was associated with a higher incidence of moderate-to-severe chronic graft-versus-host disease (GVHD) than standard-dose PTCy (100 mg/kg) (35.0% vs. 26.6%, p = 0.053). Notably, early-initiation Tac (day -1) increased moderate-to-severe chronic GVHD than standard-initiation Tac (day 5) in the reduced-dose PTCy group (p = 0.032), whereas Tac-initiation timing did not impact chronic GVHD in the standard-dose PTCy group. These data indicate that the combination of reduced-dose PTCy and early-initiation Tac can amplify chronic GVHD.
en-copyright=
kn-copyright=

en-aut-name=TeraoToshiki
en-aut-sei=Terao
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
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=3
ORCID=

en-aut-name=TakasukaHiroki
en-aut-sei=Takasuka
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
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=6
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=7
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=8
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=9
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=10
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=11
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=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 Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Hematology and Oncology, 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=
en-keyword=chronic GVHD
kn-keyword=chronic GVHD
en-keyword=haploidentical
kn-keyword=haploidentical
en-keyword=hematopoietic stem-cell transplantation
kn-keyword=hematopoietic stem-cell transplantation
en-keyword=PTCy
kn-keyword=PTCy
en-keyword=tacrolimus
kn-keyword=tacrolimus
END

start-ver=1.4
cd-journal=joma
no-vol=29
cd-vols=
no-issue=11
article-no=
start-page=2632
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240603
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=In Vitro Study of Tumor-Homing Peptide-Modified Magnetic Nanoparticles for Magnetic Hyperthermia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cancer cells have higher heat sensitivity compared to normal cells; therefore, hyperthermia is a promising approach for cancer therapy because of its ability to selectively kill cancer cells by heating them. However, the specific and rapid heating of tumor tissues remains challenging. This study investigated the potential of magnetic nanoparticles (MNPs) modified with tumor-homing peptides (THPs), specifically PL1 and PL3, for tumor-specific magnetic hyperthermia therapy. The synthesis of THP-modified MNPs involved the attachment of PL1 and PL3 peptides to the surface of the MNPs, which facilitated enhanced tumor cell binding and internalization. Cell specificity studies revealed an increased uptake of PL1- and PL3-MNPs by tumor cells compared to unmodified MNPs, indicating their potential for targeted delivery. In vitro hyperthermia experiments demonstrated the efficacy of PL3-MNPs in inducing tumor cell death when exposed to an alternating magnetic field (AMF). Even without exposure to an AMF, an additional ferroptotic pathway was suggested to be mediated by the nanoparticles. Thus, this study suggests that THP-modified MNPs, particularly PL3-MNPs, hold promise as a targeted approach for tumor-specific magnetic hyperthermia therapy.
en-copyright=
kn-copyright=

en-aut-name=ZhouShengli
en-aut-sei=Zhou
en-aut-mei=Shengli
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TsutsumiuchiKaname
en-aut-sei=Tsutsumiuchi
en-aut-mei=Kaname
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ImaiRitsuko
en-aut-sei=Imai
en-aut-mei=Ritsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MikiYukiko
en-aut-sei=Miki
en-aut-mei=Yukiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KondoAnna
en-aut-sei=Kondo
en-aut-mei=Anna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakagawaHiroshi
en-aut-sei=Nakagawa
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=WatanabeKazunori
en-aut-sei=Watanabe
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

affil-num=2
en-affil=College of Bioscience and Biotechnology, Chubu University
kn-affil=

affil-num=3
en-affil=College of Bioscience and Biotechnology, Chubu University
kn-affil=

affil-num=4
en-affil=College of Bioscience and Biotechnology, Chubu University
kn-affil=

affil-num=5
en-affil=College of Bioscience and Biotechnology, Chubu University
kn-affil=

affil-num=6
en-affil=College of Bioscience and Biotechnology, Chubu University
kn-affil=

affil-num=7
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=tumor-homing peptide
kn-keyword=tumor-homing peptide
en-keyword=magnetic hyperthermia
kn-keyword=magnetic hyperthermia
en-keyword=magnetic nanoparticles
kn-keyword=magnetic nanoparticles
en-keyword=ferroptosis
kn-keyword=ferroptosis
en-keyword=tumor-specific delivery
kn-keyword=tumor-specific delivery
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=5
article-no=
start-page=e0300644
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240517
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=PAI-1 mediates acquired resistance to MET-targeted therapy in non-small cell lung cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Mechanisms underlying primary and acquired resistance to MET tyrosine kinase inhibitors (TKIs) in managing non-small cell lung cancer remain unclear. In this study, we investigated the possible mechanisms acquired for crizotinib in MET-amplified lung carcinoma cell lines. Two MET-amplified lung cancer cell lines, EBC-1 and H1993, were established for acquired resistance to MET-TKI crizotinib and were functionally elucidated. Genomic and transcriptomic data were used to assess the factors contributing to the resistance mechanism, and the alterations hypothesized to confer resistance were validated. Multiple mechanisms underlie acquired resistance to crizotinib in MET-amplified lung cancer cell lines. In EBC-1-derived resistant cells, the overexpression of SERPINE1, the gene encoding plasminogen activator inhibitor-1 (PAI-1), mediated the drug resistance mechanism. Crizotinib resistance was addressed by combination therapy with a PAI-1 inhibitor and PAI-1 knockdown. Another mechanism of resistance in different subline cells of EBC-1 was evaluated as epithelial-to-mesenchymal transition with the upregulation of antiapoptotic proteins. In H1993-derived resistant cells, MEK inhibitors could be a potential therapeutic strategy for overcoming resistance with downstream mitogen-activated protein kinase pathway activation. In this study, we revealed the different mechanisms of acquired resistance to the MET inhibitor crizotinib with potential therapeutic application in patients with MET-amplified lung carcinoma.
en-copyright=
kn-copyright=

en-aut-name=ThuYin Min
en-aut-sei=Thu
en-aut-mei=Yin Min
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SuzawaKen
en-aut-sei=Suzawa
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TomidaShuta
en-aut-sei=Tomida
en-aut-mei=Shuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OchiKosuke
en-aut-sei=Ochi
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TsudakaShimpei
en-aut-sei=Tsudaka
en-aut-mei=Shimpei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakatsuFumiaki
en-aut-sei=Takatsu
en-aut-mei=Fumiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=DateKeiichi
en-aut-sei=Date
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MatsudaNaoki
en-aut-sei=Matsuda
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IwataKazuma
en-aut-sei=Iwata
en-aut-mei=Kazuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakataKentaro
en-aut-sei=Nakata
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=ShienKazuhiko
en-aut-sei=Shien
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=YamamotoHiromasa
en-aut-sei=Yamamoto
en-aut-mei=Hiromasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=13
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=14
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=15
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=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=4
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=5
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=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 Surgery, Division of Cardiovascular and Thoracic Surgery, Duke University School of Medicine
kn-affil=

affil-num=11
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=12
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=13
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=14
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=15
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological 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=
article-no=
start-page=1371307
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=Dissection of the signal transduction machinery responsible for the lysyl oxidase-like 4-mediated increase in invasive motility in triple-negative breast cancer cells: mechanistic insight into the integrin-β1-NF-κB-MMP9 axis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Triple-negative breast cancer (TNBC) cells are a highly formidable cancer to treat. Nonetheless, by continued investigation into the molecular biology underlying the complex regulation of TNBC cell activity, vulnerabilities can be exposed as potential therapeutic targets at the molecular level. We previously revealed that lysyl oxidase-like 4 (LOXL4) promotes the invasiveness of TNBC cells via cell surface annexin A2 as a novel binding substrate of LOXL4, which promotes the abundant localization of integrin-beta 1 at the cancer plasma membrane. However, it has yet to be uncovered how the LOXL4-mediated abundance of integrin-beta 1 hastens the invasive outgrowth of TNBC cells at the molecular level.<br>
Methods LOXL4-overexpressing stable clones were established from MDA-MB-231 cells and subjected to molecular analyses, real-time qPCR and zymography to clarify their invasiveness, signal transduction, and matrix metalloprotease (MMP) activity, respectively.<br>
Results Our results show that LOXL4 potently promotes the induction of matrix metalloprotease 9 (MMP9) via activation of nuclear factor-kappa B (NF-kappa B). Our molecular analysis revealed that TNF receptor-associated factor 4 (TRAF4) and TGF-beta activated kinase 1 (TAK1) were required for the activation of NF-kappa B through I kappa beta kinase kinase (IKK alpha/beta) phosphorylation.<br>
Conclusion Our results demonstrate that the newly identified LOXL4-mediated axis, integrin-beta 1-TRAF4-TAK1-IKK alpha/beta-I kappa beta alpha-NF-kappa B-MMP9, is crucial for TNBC cell invasiveness.
en-copyright=
kn-copyright=

en-aut-name=JiangFan
en-aut-sei=Jiang
en-aut-mei=Fan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ChenYouyi
en-aut-sei=Chen
en-aut-mei=Youyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
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=4
ORCID=

en-aut-name=KomalasariNi Luh Gede Yoni
en-aut-sei=Komalasari
en-aut-mei=Ni Luh Gede Yoni
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=Kasano-CamonesCarlos Ichiro
en-aut-sei=Kasano-Camones
en-aut-mei=Carlos Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NinomiyaKazumi
en-aut-sei=Ninomiya
en-aut-mei=Kazumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
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=9
ORCID=

en-aut-name=GoharaYuma
en-aut-sei=Gohara
en-aut-mei=Yuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
ORCID=

en-aut-name=RumaI. Made Winarsa
en-aut-sei=Ruma
en-aut-mei=I. Made Winarsa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=SumardikaI. Wayan
en-aut-sei=Sumardika
en-aut-mei=I. Wayan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=ZhouJin
en-aut-sei=Zhou
en-aut-mei=Jin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=HonjoTomoko
en-aut-sei=Honjo
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=SakaguchiYoshihiko
en-aut-sei=Sakaguchi
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=YamauchiAkira
en-aut-sei=Yamauchi
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=KuribayashiFutoshi
en-aut-sei=Kuribayashi
en-aut-mei=Futoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=FutamiJunichiro
en-aut-sei=Futami
en-aut-mei=Junichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=KondoEisaku
en-aut-sei=Kondo
en-aut-mei=Eisaku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=InoueYusuke
en-aut-sei=Inoue
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
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=22
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=23
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 Breast Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine
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=Faculty of Medicine, Udayana University
kn-affil=

affil-num=6
en-affil=Faculty of Science and Technology, Division of Molecular Science, Gunma University
kn-affil=

affil-num=7
en-affil=Faculty of Science and Technology, Division of Molecular Science, Gunma University
kn-affil=

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

affil-num=9
en-affil=Department of Cell Biology, 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=

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

affil-num=12
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=13
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=14
en-affil=Medical Oncology Department of Gastrointestinal Tumors, Liaoning Cancer Hospital & Institute, Cancer Hospital of the Dalian University of Technology
kn-affil=

affil-num=15
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=16
en-affil=Department of Microbiology, Tokushima Bunri University
kn-affil=

affil-num=17
en-affil=Department of Biochemistry, Kawasaki Medical School
kn-affil=

affil-num=18
en-affil=Department of Biochemistry, Kawasaki Medical School
kn-affil=

affil-num=19
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=20
en-affil=Division of Tumor Pathology, Near InfraRed Photo-Immuno-Therapy Research Institute, Kansai Medical University
kn-affil=

affil-num=21
en-affil=Faculty of Science and Technology, Division of Molecular Science, Gunma University
kn-affil=

affil-num=22
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=23
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=breast cancer
kn-keyword=breast cancer
en-keyword=invasion
kn-keyword=invasion
en-keyword=lysyl oxidase
kn-keyword=lysyl oxidase
en-keyword=NF-κB
kn-keyword=NF-κB
en-keyword=MMP9
kn-keyword=MMP9
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=11
article-no=
start-page=6269
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240606
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=SPRED2 Is a Novel Regulator of Autophagy in Hepatocellular Carcinoma Cells and Normal Hepatocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sprouty-related enabled/vasodilator-stimulated phosphoprotein homology 1 domain containing 2 (SPRED2) is an inhibitor of the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway and has been shown to promote autophagy in several cancers. Here, we aimed to determine whether SPRED2 plays a role in autophagy in hepatocellular carcinoma (HCC) cells. The Cancer Genome Atlas (TCGA) Liver Cancer Database showed a negative association between the level of SPRED2 and p62, a ubiquitin-binding scaffold protein that accumulates when autophagy is inhibited. Immunohistochemically, accumulation of p62 was detected in human HCC tissues with low SPRED2 expression. Overexpression of SPRED2 in HCC cells increased the number of autophagosomes and autophagic vacuoles containing damaged mitochondria, decreased p62 levels, and increased levels of light-chain-3 (LC3)-II, an autophagy marker. In contrast, SPRED2 deficiency increased p62 levels and decreased LC3-II levels. SPRED2 expression levels were negatively correlated with translocase of outer mitochondrial membrane 20 (TOM20) expression levels, suggesting its role in mitophagy. Mechanistically, SPRED2 overexpression reduced ERK activation followed by the mechanistic or mammalian target of rapamycin complex 1 (mTORC1)-mediated signaling pathway, and SPRED2 deficiency showed the opposite pattern. Finally, hepatic autophagy was impaired in the liver of SPRED2-deficient mice with hepatic lipid droplet accumulation in response to starvation. These results indicate that SPRED2 is a critical regulator of autophagy not only in HCC cells, but also in hepatocytes, and thus the manipulation of this process may provide new insights into liver pathology.
en-copyright=
kn-copyright=

en-aut-name=WangTianyi
en-aut-sei=Wang
en-aut-mei=Tianyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=GaoTong
en-aut-sei=Gao
en-aut-mei=Tong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FujisawaMasayoshi
en-aut-sei=Fujisawa
en-aut-mei=Masayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=5
ORCID=

en-aut-name=YoshimuraTeizo
en-aut-sei=Yoshimura
en-aut-mei=Teizo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsukawaAkihiro
en-aut-sei=Matsukawa
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

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

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

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

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

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

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

affil-num=7
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=autophagy
kn-keyword=autophagy
en-keyword=mitophagy
kn-keyword=mitophagy
en-keyword=SPRED proteins
kn-keyword=SPRED proteins
en-keyword=MAPK/ERK
kn-keyword=MAPK/ERK
en-keyword=mTOR
kn-keyword=mTOR
en-keyword=hepatocellular carcinoma
kn-keyword=hepatocellular carcinoma
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=4610
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240530
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=An NLR paralog Pit2 generated from tandem duplication of Pit1 fine-tunes Pit1 localization and function
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=NLR family proteins act as intracellular receptors. Gene duplication amplifies the number of NLR genes, and subsequent mutations occasionally provide modifications to the second gene that benefits immunity. However, evolutionary processes after gene duplication and functional relationships between duplicated NLRs remain largely unclear. Here, we report that the rice NLR protein Pit1 is associated with its paralogue Pit2. The two are required for the resistance to rice blast fungus but have different functions: Pit1 induces cell death, while Pit2 competitively suppresses Pit1-mediated cell death. During evolution, the suppression of Pit1 by Pit2 was probably generated through positive selection on two fate-determining residues in the NB-ARC domain of Pit2, which account for functional differences between Pit1 and Pit2. Consequently, Pit2 lost its plasma membrane localization but acquired a new function to interfere with Pit1 in the cytosol. These findings illuminate the evolutionary trajectory of tandemly duplicated NLR genes after gene duplication.
en-copyright=
kn-copyright=

en-aut-name=LiYuying
en-aut-sei=Li
en-aut-mei=Yuying
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WangQiong
en-aut-sei=Wang
en-aut-mei=Qiong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=JiaHuimin
en-aut-sei=Jia
en-aut-mei=Huimin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshikawaKazuya
en-aut-sei=Ishikawa
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=

en-aut-name=UebaTakahiro
en-aut-sei=Ueba
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TsujimotoAtsumi
en-aut-sei=Tsujimoto
en-aut-mei=Atsumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamanakaMiki
en-aut-sei=Yamanaka
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YabumotoYasuyuki
en-aut-sei=Yabumoto
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
ORCID=

en-aut-name=SasakiEriko
en-aut-sei=Sasaki
en-aut-mei=Eriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=FukaoYoichiro
en-aut-sei=Fukao
en-aut-mei=Yoichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=FujiwaraMasayuki
en-aut-sei=Fujiwara
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=Kaneko-KawanoTakako
en-aut-sei=Kaneko-Kawano
en-aut-mei=Takako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=TanLi
en-aut-sei=Tan
en-aut-mei=Li
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=KojimaChojiro
en-aut-sei=Kojima
en-aut-mei=Chojiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=WingRod A.
en-aut-sei=Wing
en-aut-mei=Rod A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=SebastianAlfino
en-aut-sei=Sebastian
en-aut-mei=Alfino
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=NishimuraHideki
en-aut-sei=Nishimura
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=FukadaFumi
en-aut-sei=Fukada
en-aut-mei=Fumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=NiuQingfeng
en-aut-sei=Niu
en-aut-mei=Qingfeng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=ShimizuMotoki
en-aut-sei=Shimizu
en-aut-mei=Motoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=YoshidaKentaro
en-aut-sei=Yoshida
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=TerauchiRyohei
en-aut-sei=Terauchi
en-aut-mei=Ryohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=ShimamotoKo
en-aut-sei=Shimamoto
en-aut-mei=Ko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
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=26
ORCID=

affil-num=1
en-affil=Shenzhen Branch, Guangdong Laboratory of Lingnan Modern Agriculture, Key Laboratory of Synthetic Biology, Ministry of Agriculture and Rural Affairs, Agricultural Genomics Institute at Shenzhen, Chinese Academy of Agricultural Sciences
kn-affil=

affil-num=2
en-affil=Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=3
en-affil=College of Agronomy, Jiangxi Agricultural University
kn-affil=

affil-num=4
en-affil=Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=5
en-affil=Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=6
en-affil=Laboratory of Plant Molecular Genetics, Nara Institute of Science and Technology
kn-affil=

affil-num=7
en-affil=Laboratory of Plant Molecular Genetics, Nara Institute of Science and Technology
kn-affil=

affil-num=8
en-affil=Laboratory of Plant Molecular Genetics, Nara Institute of Science and Technology
kn-affil=

affil-num=9
en-affil=Laboratory of Plant Molecular Genetics, Nara Institute of Science and Technology
kn-affil=

affil-num=10
en-affil=Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=11
en-affil=Faculty of Science, Kyushu University
kn-affil=

affil-num=12
en-affil=Department of Bioinformatics, Ritsumeikan University
kn-affil=

affil-num=13
en-affil=YANMAR HOLDINGS Co., Ltd.
kn-affil=

affil-num=14
en-affil=College of Pharmaceutical Sciences, Ritsumeikan University
kn-affil=

affil-num=15
en-affil=Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=16
en-affil=Graduate School of Engineering Science, Yokohama National University
kn-affil=

affil-num=17
en-affil=Arizona Genomics Institute, School of Plant Sciences, University of Arizona
kn-affil=

affil-num=18
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=19
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=20
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=21
en-affil=Advanced Academy, Anhui Agricultural University, Research Centre for Biological Breeding Technology
kn-affil=

affil-num=22
en-affil=Iwate Biotechnology Research Center
kn-affil=

affil-num=23
en-affil=Graduate School of Agriculture, Kyoto University 
kn-affil=

affil-num=24
en-affil=Iwate Biotechnology Research Center
kn-affil=

affil-num=25
en-affil=Laboratory of Plant Molecular Genetics, Nara Institute of Science and Technology
kn-affil=

affil-num=26
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=3
article-no=
start-page=291
end-page=294
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=A Case of Gallbladder Metastasis of Malignant Melanoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In the clinical course of malignant melanoma, which can metastasize to multiple organs, gallbladder metastases are rarely detected. A 69-year-old man who underwent resection of a primary malignant melanoma was subsequently treated with nivolumab for lung metastases and achieved complete response. Seven years after surgery, multiple nodules were found in the gallbladder, and he underwent laparoscopic cholecystectomy. The postoperative diagnosis was metastases of malignant melanoma. He has been recurrence-free 8 months after surgery. If radical resection is possible, such surgery should be performed for gallbladder metastases found in patients with other controlled lesions of malignant melanoma.
en-copyright=
kn-copyright=

en-aut-name=MinagiHitoshi
en-aut-sei=Minagi
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AokiHideki
en-aut-sei=Aoki
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=DoitaSusumu
en-aut-sei=Doita
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyakeEiki
en-aut-sei=Miyake
en-aut-mei=Eiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OgawaToshihiro
en-aut-sei=Ogawa
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TaniguchiFumitaka
en-aut-sei=Taniguchi
en-aut-mei=Fumitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=WatanabeMegumi
en-aut-sei=Watanabe
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ArataTakashi
en-aut-sei=Arata
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KatsudaKoh
en-aut-sei=Katsuda
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TanakayaKohji
en-aut-sei=Tanakaya
en-aut-mei=Kohji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Surgery, National Hospital Organization, Iwakuni Clinical Center
kn-affil=

affil-num=2
en-affil=Department of Surgery, National Hospital Organization, Iwakuni Clinical Center
kn-affil=

affil-num=3
en-affil=Department of Surgery, National Hospital Organization, Iwakuni Clinical Center
kn-affil=

affil-num=4
en-affil=Department of Surgery, National Hospital Organization, Iwakuni Clinical Center
kn-affil=

affil-num=5
en-affil=Department of Surgery, National Hospital Organization, Iwakuni Clinical Center
kn-affil=

affil-num=6
en-affil=Department of Surgery, National Hospital Organization, Iwakuni Clinical Center
kn-affil=

affil-num=7
en-affil=Department of Surgery, National Hospital Organization, Iwakuni Clinical Center
kn-affil=

affil-num=8
en-affil=Department of Surgery, National Hospital Organization, Iwakuni Clinical Center
kn-affil=

affil-num=9
en-affil=Department of Surgery, National Hospital Organization, Iwakuni Clinical Center
kn-affil=

affil-num=10
en-affil=Department of Surgery, National Hospital Organization, Iwakuni Clinical Center
kn-affil=
en-keyword=malignant melanoma
kn-keyword=malignant melanoma
en-keyword=gallbladder metastasis
kn-keyword=gallbladder metastasis
en-keyword=laparoscopic cholecystectomy
kn-keyword=laparoscopic cholecystectomy
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=3
article-no=
start-page=281
end-page=284
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=Spontaneous Bilateral Pneumothorax in a Patient with Anorexia Nervosa: The Management of Prolonged Postoperative Air Leakage
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A 24-year-old Japanese female with anorexia nervosa presented to our hospital for bilateral pneumothorax, and 12-Fr thoracostomy catheters were inserted into the bilateral pleural cavities. On hospital day 9, a thoracoscopic bullectomy was performed. However, air leakage relapsed on both sides on postoperative day 1. The air leakage on the right side was particularly persistent, and we switched the drainage to a Heimlich valve. Both lungs expanded gradually and the chest tube was removed on postoperative day 19. Passive pleural drainage might be an option for prolonged air leakage after a bullectomy in patients with anorexia nervosa.
en-copyright=
kn-copyright=

en-aut-name=OkadaKazuhiro
en-aut-sei=Okada
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MakiYuho
en-aut-sei=Maki
en-aut-mei=Yuho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MatsubaraKei
en-aut-sei=Matsubara
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HiranoYutaka
en-aut-sei=Hirano
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FujiwaraToshiya
en-aut-sei=Fujiwara
en-aut-mei=Toshiya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsuuraMotoki
en-aut-sei=Matsuura
en-aut-mei=Motoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Thoracic Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=2
en-affil=Department of Thoracic Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=3
en-affil=Department of Thoracic Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=4
en-affil=Department of Thoracic Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=5
en-affil=Department of Thoracic Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=

affil-num=6
en-affil=Department of Thoracic Surgery, Hiroshima City Hiroshima Citizens Hospital
kn-affil=
en-keyword=spontaneous pneumothorax
kn-keyword=spontaneous pneumothorax
en-keyword=anorexia nervosa
kn-keyword=anorexia nervosa
en-keyword=Heimlich valve
kn-keyword=Heimlich valve
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=259
end-page=270
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=The Role of the Lipid Profile and Oxidative Stress in Fatigue, Sleep Disorders and Cognitive Impairment in Patients with Multiple Sclerosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The aim of this study is to investigate the relationship of the lipid profile, dysfunctional high-density lipoprotein, ischaemia-modified albumin and thiol?disulfide homeostasis with cognitive impairment, fatigue and sleep disorders in patients with multiple sclerosis. The cognitive functions of patients were evaluated with the Brief International Cognitive Assessment for Multiple Sclerosis battery. Fatigue was evaluated with the Fatigue Severity Scale and the Fatigue Impact Scale. The Pittsburgh Sleep Quality Index and the Epworth Sleepiness Scale were used to assess patients’ sleep disturbance. Peripheral blood samples were collected, and lipid levels and myeloperoxidase and paraoxonase activity were measured. The myeloperoxidase/paraoxonase ratio, which indicates dysfunctional high-density lipoprotein, was calculated. Thiol?disulfide homeostasis and ischaemia-modified albumin were measured.<br>
We did not identify any relationship between dysfunctional high-density lipoprotein and the physical disability, cognitive decline, fatigue and sleep problems of multiple sclerosis. Thiol?disulfide homeostasis was associated with cognitive scores. The shift of the balance towards disulfide was accompanied by a decrease in cognitive scores. On the other hand, we did not detect any relationship between fatigue and sleep disorders and thiol?disulfide homeostasis. Our findings revealed a possible correlation between cognitive dysfunction and thiol?disulfide homeostasis in multiple sclerosis patients.
en-copyright=
kn-copyright=

en-aut-name=VuralGonul
en-aut-sei=Vural
en-aut-mei=Gonul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=DemirEsra
en-aut-sei=Demir
en-aut-mei=Esra
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=GumusyaylaSadiye
en-aut-sei=Gumusyayla
en-aut-mei=Sadiye
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ErenFunda
en-aut-sei=Eren
en-aut-mei=Funda
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=BarakliSerdar
en-aut-sei=Barakli
en-aut-mei=Serdar
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NeseliogluSalim
en-aut-sei=Neselioglu
en-aut-mei=Salim
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ErelOzcan
en-aut-sei=Erel
en-aut-mei=Ozcan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Neurology, Faculty of Medicine, Ankara Yildirim Beyazit University
kn-affil=

affil-num=2
en-affil=Department of Neurology, Ankara City Hospital
kn-affil=

affil-num=3
en-affil=Department of Neurology, Faculty of Medicine, Ankara Yildirim Beyazit University
kn-affil=

affil-num=4
en-affil=Department of Clinical Biochemistry, Ankara City Hospital
kn-affil=

affil-num=5
en-affil=Department of Neurology, Ankara City Hospital
kn-affil=

affil-num=6
en-affil=Department of Clinical Biochemistry, Ankara City Hospital
kn-affil=

affil-num=7
en-affil=Department of Clinical Biochemistry, Ankara City Hospital
kn-affil=
en-keyword=multiple sclerosis
kn-keyword=multiple sclerosis
en-keyword=dysfunctional HDL
kn-keyword=dysfunctional HDL
en-keyword=thiol?disulfide homeostasis
kn-keyword=thiol?disulfide homeostasis
en-keyword=cognitive decline
kn-keyword=cognitive decline
END

start-ver=1.4
cd-journal=joma
no-vol=74
cd-vols=
no-issue=7
article-no=
start-page=394
end-page=407
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=The specific shapes of capillaries are associated with worse prognosis in patients with invasive breast cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Angiogenesis is considered essential for tumor progression; however, whether histological counting of blood vessel numbers, expressed as microvessel density (MVD), can be a prognostic factor in breast cancer remains controversial. It has been suggested that the specific morphology of blood vessels such as glomeruloid microvascular proliferation (GMP) is associated with clinical parameters. Here, we aimed to clarify the significance of MVD with revised immunohistochemistry and to identify new blood vessel shapes that predict prognosis in breast cancer. Four hundred and eleven primary breast cancer specimens were collected, and the sections were immunohistochemically stained with CD31 (single staining) and CD31 and Collagen IV (double staining). The prognosis of patients was examined based on the MVD value, and the presence of GMP and other blood vessels with other specific shapes. As a result, high MVD value and the presence of GMP were not associated with worse prognosis. By contrast, patients with deep-curved capillaries surrounding tumor cell nests (C-shaped) or excessively branched capillaries near tumor cell nests showed a significantly poor prognosis. The presence of these capillaries was also correlated with clinicopathological parameters such as Ki-67 index. Thus, the morphology of capillaries rather than MVD can be a better indicator of tumor aggressiveness.
en-copyright=
kn-copyright=

en-aut-name=SweHnin‐Wint‐Wint
en-aut-sei=Swe
en-aut-mei=Hnin‐Wint‐Wint
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujisawaMasayoshi
en-aut-sei=Fujisawa
en-aut-mei=Masayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
ORCID=

en-aut-name=KomatsubaraYu
en-aut-sei=Komatsubara
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YoshimuraTeizo
en-aut-sei=Yoshimura
en-aut-mei=Teizo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShienTadahiko
en-aut-sei=Shien
en-aut-mei=Tadahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsukawaAkihiro
en-aut-sei=Matsukawa
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

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

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

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

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

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

affil-num=6
en-affil=Department of Breast and Endocrine Surgery, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=angiogenesis
kn-keyword=angiogenesis
en-keyword=blood vessels
kn-keyword=blood vessels
en-keyword=breast cancer
kn-keyword=breast cancer
en-keyword=CD31 antigen
kn-keyword=CD31 antigen
en-keyword=immunohistochemistry
kn-keyword=immunohistochemistry
en-keyword=microvessel density
kn-keyword=microvessel density
en-keyword=survival analysis
kn-keyword=survival analysis
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=5
article-no=
start-page=e0302537
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240521
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The use of artificial intelligence in induced pluripotent stem cell-based technology over 10-year period: A systematic scoping review
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background <br>
Stem cell research, particularly in the domain of induced pluripotent stem cell (iPSC) technology, has shown significant progress. The integration of artificial intelligence (AI), especially machine learning (ML) and deep learning (DL), has played a pivotal role in refining iPSC classification, monitoring cell functionality, and conducting genetic analysis. These enhancements are broadening the applications of iPSC technology in disease modelling, drug screening, and regenerative medicine. This review aims to explore the role of AI in the advancement of iPSC research.<br>
Methods <br>
In December 2023, data were collected from three electronic databases (PubMed, Web of Science, and Science Direct) to investigate the application of AI technology in iPSC processing.<br>
Results <br>
This systematic scoping review encompassed 79 studies that met the inclusion criteria. The number of research studies in this area has increased over time, with the United States emerging as a leading contributor in this field. AI technologies have been diversely applied in iPSC technology, encompassing the classification of cell types, assessment of disease-specific phenotypes in iPSC-derived cells, and the facilitation of drug screening using iPSC. The precision of AI methodologies has improved significantly in recent years, creating a foundation for future advancements in iPSC-based technologies.<br>
Conclusions <br>
Our review offers insights into the role of AI in regenerative and personalized medicine, highlighting both challenges and opportunities. Although still in its early stages, AI technologies show significant promise in advancing our understanding of disease progression and development, paving the way for future clinical applications.
en-copyright=
kn-copyright=

en-aut-name=VoQuan Duy
en-aut-sei=Vo
en-aut-mei=Quan Duy
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=IdaToshihiro
en-aut-sei=Ida
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=YuasaShinsuke
en-aut-sei=Yuasa
en-aut-mei=Shinsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

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

affil-num=3
en-affil=Faculty of Medicine, Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Faculty of Medicine, Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Faculty of Medicine, Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=10
article-no=
start-page=807
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240509
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Exploring the Regulators of Keratinization: Role of BMP-2 in Oral Mucosa
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The oral mucosa functions as a physico-chemical and immune barrier to external stimuli, and an adequate width of the keratinized mucosa around the teeth or implants is crucial to maintaining them in a healthy and stable condition. In this study, for the first time, bulk RNA-seq analysis was performed to explore the gene expression of laser microdissected epithelium and lamina propria from mice, aiming to investigate the differences between keratinized and non-keratinized oral mucosa. Based on the differentially expressed genes (DEGs) and Gene Ontology (GO) Enrichment Analysis, bone morphogenetic protein 2 (BMP-2) was identified to be a potential regulator of oral mucosal keratinization. Monoculture and epithelial-mesenchymal cell co-culture models in the air-liquid interface (ALI) indicated that BMP-2 has direct and positive effects on epithelial keratinization and proliferation. We further performed bulk RNA-seq of the ALI monoculture stimulated with BMP-2 in an attempt to identify the downstream factors promoting epithelial keratinization and proliferation. Analysis of the DEGs identified, among others, IGF2, ID1, LTBP1, LOX, SERPINE1, IL24, and MMP1 as key factors. In summary, these results revealed the involvement of a well-known growth factor responsible for bone development, BMP-2, in the mechanism of oral mucosal keratinization and proliferation, and pointed out the possible downstream genes involved in this mechanism.
en-copyright=
kn-copyright=

en-aut-name=MuXindi
en-aut-sei=Mu
en-aut-mei=Xindi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OnoMitsuaki
en-aut-sei=Ono
en-aut-mei=Mitsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NguyenHa Thi Thu
en-aut-sei=Nguyen
en-aut-mei=Ha Thi Thu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=ZhaoKun
en-aut-sei=Zhao
en-aut-mei=Kun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KomoriTaishi
en-aut-sei=Komori
en-aut-mei=Taishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=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=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

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

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

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

affil-num=8
en-affil=Department of Oral Rehabilitation and Implantology, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=cell differentiation
kn-keyword=cell differentiation
en-keyword=epithelia
kn-keyword=epithelia
en-keyword=growth factor(s)
kn-keyword=growth factor(s)
en-keyword=bioinformatics
kn-keyword=bioinformatics
en-keyword=extracellular matrix (ECM)
kn-keyword=extracellular matrix (ECM)
en-keyword=mucocutaneous disorders
kn-keyword=mucocutaneous disorders
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=1
article-no=
start-page=128
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240522
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Subtotal esophagectomy and concurrent reconstruction with free jejunal flap for primary esophageal cancer after pancreatoduodenectomy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Pancreatoduodenectomy and subtotal esophagectomy are widely considered the most invasive and difficult surgical procedures in gastrointestinal surgery. Subtotal esophagectomy after pancreatoduodenectomy is expected to be extremely difficult due to complicated anatomical changes, and selecting an appropriate intestinal reconstruction method will also be a difficult task. Therefore, perhaps because the method is considered impossible, there have been few reports of subtotal esophagectomy after pancreatoduodenectomy.<br>
Case presentation A 73-year-old man with a history of pancreatoduodenectomy was diagnosed with superficial thoracic esophageal squamous cell carcinoma. Definitive chemoradiation therapy was recommended at another hospital; however, he visited our department to undergo surgery. We performed the robot-assisted thoracoscopic subtotal esophagectomy. There were some difficulties with the reconstruction: the gastric tube could not be used, the reconstruction was long, and the organs reconstructed in the previous surgery had to be preserved. However, the concurrent reconstruction was achieved with the help of a free jejunal flap and vascular reconstruction. All reconstructions from the previous surgery, including the remnant stomach, were preserved via regional abdominal lymph node dissection. After reconstruction, intravenous indocyanine green showed that circulation in the reconstructed intestines was preserved. On postoperative day 1, no recurrent nerve paralysis was observed during laryngoscopy. The patient could start oral intake smoothly 2 weeks after surgery and did not exhibit any postoperative complications related to the reconstruction. The patient was transferred to another hospital on postoperative day 21.<br>
Conclusions Owing to the free jejunal flap interposition method, we safely performed one stage subtotal esophagectomy and concurrent reconstruction, preservation of the remnant stomach, and pancreaticobiliary reconstruction in patients with a history of pancreatoduodenectomy. We believe that this method is acceptable and useful for patients undergoing complicated reconstruction.
en-copyright=
kn-copyright=

en-aut-name=MoriwakeKazuya
en-aut-sei=Moriwake
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=KawasakiKento
en-aut-sei=Kawasaki
en-aut-mei=Kento
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MatsumotoTasuku
en-aut-sei=Matsumoto
en-aut-mei=Tasuku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HashimotoMasashi
en-aut-sei=Hashimoto
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KatoTakuya
en-aut-sei=Kato
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MaedaNaoaki
en-aut-sei=Maeda
en-aut-mei=Naoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TanabeShunsuke
en-aut-sei=Tanabe
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShirakawaYasuhiro
en-aut-sei=Shirakawa
en-aut-mei=Yasuhiro
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=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=
en-keyword=Reconstruction with the free jejunum flap
kn-keyword=Reconstruction with the free jejunum flap
en-keyword=Subtotal esophagectomy
kn-keyword=Subtotal esophagectomy
en-keyword=After pancreatoduodenectomy
kn-keyword=After pancreatoduodenectomy
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=10
article-no=
start-page=e174618
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240522
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Double-faced CX3CL1 enhances lymphangiogenesis-dependent metastasis in an aggressive subclone of oral squamous cell carcinoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Because cancer cells have a genetically unstable nature, they give rise to genetically different variant subclones inside a single tumor. Understanding cancer heterogeneity and subclone characteristics is crucial for developing more efficacious therapies. Oral squamous cell carcinoma (OSCC) is characterized by high heterogeneity and plasticity. On the other hand, CX3C motif ligand 1 (CX3CL1) is a double-faced chemokine with anti- and pro -tumor functions. Our study reported that CX3CL1 functioned differently in tumors with different cancer phenotypes, both in vivo and in vitro. Mouse OSCC 1 (MOC1) and MOC2 cells responded similarly to CX3CL1 in vitro. However, in vivo, CX3CL1 increased keratinization in indolent MOC1 cancer, while CX3CL1 promoted cervical lymphatic metastasis in aggressive MOC2 cancer. These outcomes were due to double-faced CX3CL1 effects on different immune microenvironments indolent and aggressive cancer created. Furthermore, we established that CX3CL1 promoted cancer metastasis via the lymphatic pathway by stimulating lymphangiogenesis and transendothelial migration of lymph -circulating tumor cells. CX3CL1 enrichment in lymphatic metastasis tissues was observed in aggressive murine and human cell lines. OSCC patient samples with CX3CL1 enrichment exhibited a strong correlation with lower overall survival rates and higher recurrence and distant metastasis rates. In conclusion, CX3CL1 is a pivotal factor that stimulates the metastasis of aggressive cancer subclones within the heterogeneous tumors to metastasize, and our study demonstrates the prognostic value of CX3CL1 enrichment in long-term monitoring in OSCC.
en-copyright=
kn-copyright=

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=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=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=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=OharaToshiaki
en-aut-sei=Ohara
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FukuharaYoko
en-aut-sei=Fukuhara
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=

en-aut-name=ShanQuisheng
en-aut-sei=Shan
en-aut-mei=Quisheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SoeYamin
en-aut-sei=Soe
en-aut-mei=Yamin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OnoKisho
en-aut-sei=Ono
en-aut-mei=Kisho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
ORCID=

en-aut-name=MizukawaNobuyoshi
en-aut-sei=Mizukawa
en-aut-mei=Nobuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=13
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=14
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 Microbiology, 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 Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama Universit
kn-affil=

affil-num=6
en-affil=Department of Oral Morphology, 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=

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

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

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

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

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

affil-num=14
en-affil=Department of Oral Pathology and Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=63
cd-vols=
no-issue=9
article-no=
start-page=1261
end-page=1267
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240501
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Severe Cytokine Release Syndrome and Immune Effector Cell-associated Neurotoxicity Syndrome in a Man Receiving Immune Checkpoint Inhibitors for Lung Cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A 55-year-old man with stage IV lung adenocarcinoma was treated with cisplatin, pemetrexed, nivolumab, and ipilimumab. Approximately 100 days after treatment initiation, he became disoriented and presented to the emergency department with a high fever. Blood tests revealed liver and kidney dysfunctions. Subsequently, the patient developed generalized convulsions that required intensive care. He was clinically diagnosed with cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS). Organ damage was gradually controlled with immunosuppressive drugs, including steroids, and the patient was discharged. Successful treatment is rare in patients with CRS, including ICANS, during immune checkpoint inhibitor treatment for solid tumors.
en-copyright=
kn-copyright=

en-aut-name=TanakaTakaaki
en-aut-sei=Tanaka
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TaokaMasataka
en-aut-sei=Taoka
en-aut-mei=Masataka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
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=4
ORCID=

en-aut-name=HigoHisao
en-aut-sei=Higo
en-aut-mei=Hisao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
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=7
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=8
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=9
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=10
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=11
ORCID=

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

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

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

affil-num=4
en-affil=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Respiratory Medicine, Okayama University Hospital
kn-affil=

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

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

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

affil-num=9
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Center for Clinical Oncology, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=immune checkpoint inhibitor
kn-keyword=immune checkpoint inhibitor
en-keyword=nivolumab
kn-keyword=nivolumab
en-keyword=ipilimumab
kn-keyword=ipilimumab
en-keyword=cytokine release syndrome
kn-keyword=cytokine release syndrome
en-keyword=immune effector cell-associated neurotoxicity syndrome
kn-keyword=immune effector cell-associated neurotoxicity syndrome
END

start-ver=1.4
cd-journal=joma
no-vol=391
cd-vols=
no-issue=2
article-no=
start-page=249
end-page=267
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20221122
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The medaka mutant deficient in eyes shut homolog exhibits opsin transport defects and enhanced autophagy in retinal photoreceptors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Eyes shut homolog (EYS) encodes a proteoglycan and the human mutation causes retinitis pigmentosa type 25 (RP25) with progressive retinal degeneration. RP25 most frequently affects autosomal recessive RP patients with many ethnic backgrounds. Although studies using RP models have facilitated the development of therapeutic medications, Eys has been lost in rodent model animals. Here we examined the roles for Eys in the maintenance of photoreceptor structure and function by generating eys-null medaka fish using the CRISPR-Cas9 system. Medaka EYS protein was present near the connecting cilium of wild-type photoreceptors, while it was absent from the eys?/? retina. The mutant larvae exhibited a reduced visual motor response compared with wild-type. In contrast to reported eys-deficient zebrafish at the similar stage, no retinal cell death was detected in the 8-month post-hatching (8-mph) medaka eys mutant. Immunohistochemistry showed a significant reduction in the length of cone outer segments (OSs), retention of OS proteins in the inner segments of photoreceptors, and abnormal filamentous actin network at the base of cone OSs in the mutant retina by 8 mph. Electron microscopy revealed aberrant structure of calyceal processes, numerous vesiculation and lamellar interruptions, and autophagosomes in the eys-mutant cone photoreceptors. In situ hybridization showed an autophagy component gene, gabarap, was ectopically expressed in the eys-null retina. These results suggest eys is required for regeneration of OS, especially of cone photoreceptors, and transport of OS proteins by regulating actin filaments. Enhanced autophagy may delay the progression of retinal degeneration when lacking EYS in the medaka retina.
en-copyright=
kn-copyright=

en-aut-name=SatoKeita
en-aut-sei=Sato
en-aut-mei=Keita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=LiuYang
en-aut-sei=Liu
en-aut-mei=Yang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamashitaTakahiro
en-aut-sei=Yamashita
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OhuchiHideyo
en-aut-sei=Ohuchi
en-aut-mei=Hideyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

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

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

affil-num=3
en-affil=Department of Biophysics, Graduate School of Science, Kyoto University
kn-affil=

affil-num=4
en-affil=Department of Cytology and Histology, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Eyes shut homolog
kn-keyword=Eyes shut homolog
en-keyword=Eys
kn-keyword=Eys
en-keyword=Retinitis pigmentosa
kn-keyword=Retinitis pigmentosa
en-keyword=RP25
kn-keyword=RP25
en-keyword=Cone photoreceptor
kn-keyword=Cone photoreceptor
en-keyword=Autophagy
kn-keyword=Autophagy
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=単心室循環モデル動物における心臓幹細胞経静脈注射
kn-title=Intravenous infusion of cardiac progenitor cells in animal models of single ventricular physiology
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=GOTOTakuya
en-aut-sei=GOTO
en-aut-mei=Takuya
kn-aut-name=後藤拓弥
kn-aut-sei=後藤
kn-aut-mei=拓弥
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=鉄添加した底質微生物燃料電池を用いた農業排水路におけるリン内部負荷の削減
kn-title=Reduction of internal phosphorus loading in agricultural drainages using iron-incorporated sediment microbial fuel cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=GAMAMADA LIYANAGE ERANDI PRIYANGIKA PERERA
en-aut-sei=GAMAMADA LIYANAGE ERANDI PRIYANGIKA PERERA
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=岡山大学大学院環境生命科学研究科
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Streptococcus mutans の Cnm は細胞表面構造と膜透過性に重要である
kn-title=Cnm of Streptococcus mutans is important for cell surface structure and membrane permeability
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MATSUOKADaiki
en-aut-sei=MATSUOKA
en-aut-mei=Daiki
kn-aut-name=松岡大貴
kn-aut-sei=松岡
kn-aut-mei=大貴
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=軟骨細胞におけるCCN2に由来する環状RNAの発現とその機能
kn-title=Expression and function of CCN2-derived circRNAs in chondrocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KATOSoma
en-aut-sei=KATO
en-aut-mei=Soma
kn-aut-name=加藤壮真
kn-aut-sei=加藤
kn-aut-mei=壮真
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=抜歯窩骨再生における間葉系幹細胞の機能は、炎症巣に存在するTNF-αによって調節される
kn-title=Inflammatory macrophages modulate mesenchymal stem cell function via TNF-α in regeneration process of the tooth extraction socket
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=Aung Ye Mun
en-aut-sei=Aung Ye Mun
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=BMP2およびRANKLへの結合を介した口腔癌細胞の浸潤と骨への転移におけるCCN6の２つの役割
kn-title=Dual roles of cellular communication network factor6（CCN6）in the invasion and metastasis of oral cancer cells to bone via binding to BMP2 and RANKL
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=HOCHIHiroaki
en-aut-sei=HOCHI
en-aut-mei=Hiroaki
kn-aut-name=芳地浩彰
kn-aut-sei=芳地
kn-aut-mei=浩彰
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=口腔扁平上皮癌における頸部リンパ節転移と再発の多角的予測
kn-title=Multimodal Prediction of Cervical Lymph Node Metastasis and Recurrence in Oral Squamous Cell Carcinoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KANEMOTOHideka
en-aut-sei=KANEMOTO
en-aut-mei=Hideka
kn-aut-name=金本栄華
kn-aut-sei=金本
kn-aut-mei=栄華
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=EpCAMの可溶性細胞外ドメインであるEpEXは、EGFR高発現頭頸部扁平上皮癌のセツキシマブ治療抵抗性に関与する
kn-title=EpEX, the soluble extracellular domain of EpCAM, resists cetuximab treatment of EGFR-high head and neck squamous cell carcinoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=UMEMORIKoki
en-aut-sei=UMEMORI
en-aut-mei=Koki
kn-aut-name=梅森洸樹
kn-aut-sei=梅森
kn-aut-mei=洸樹
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

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cd-journal=joma
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dt-accepted=
dt-pub-year=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=ヒト副腎皮質細胞ステロイド合成におけるオレキシンとBMPの相互作用
kn-title=Interaction of Orexin and Bone Morphogenetic Proteins in Steroidogenesis by Human Adrenocortical Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SOEJIMAYoshiaki
en-aut-sei=SOEJIMA
en-aut-mei=Yoshiaki
kn-aut-name=副島佳晃
kn-aut-sei=副島
kn-aut-mei=佳晃
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=
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article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=卵胞ステロイド合成におけるNR5Aの役割と、時計遺伝子・BMPによる調節機序の検討
kn-title=Roles of NR5A1 and NR5A2 in the regulation of steroidogenesis by Clock gene and bone morphogenetic proteins by human granulosa cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SUYAMAAtsuhito
en-aut-sei=SUYAMA
en-aut-mei=Atsuhito
kn-aut-name=須山敦仁
kn-aut-sei=須山
kn-aut-mei=敦仁
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=
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article-no=
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end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=ALK融合遺伝子陽性非小細胞肺癌に対するgilteritinibの有効性についての検討
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=
en-copyright=
kn-copyright=

en-aut-name=ANDOChihiro
en-aut-sei=ANDO
en-aut-mei=Chihiro
kn-aut-name=安東千裕
kn-aut-sei=安東
kn-aut-mei=千裕
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=
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end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=非小細胞肺癌におけるがん関連線維芽細胞由来ペリオスチンの腫瘍促進効果および薬剤耐性誘導効果
kn-title=Periostin secreted by cancer-associated fibroblasts promotes cancer progression and drug resistance in non-small cell lung cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TAKATSUFumiaki
en-aut-sei=TAKATSU
en-aut-mei=Fumiaki
kn-aut-name=��津史明
kn-aut-sei=��津
kn-aut-mei=史明
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=結合組織型肥満細胞はNoradrenalineを貯蔵、放出する
kn-title=Connective tissue mast cells store and release noradrenaline
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=OTANIYusuke
en-aut-sei=OTANI
en-aut-mei=Yusuke
kn-aut-name=大谷悠介
kn-aut-sei=大谷
kn-aut-mei=悠介
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=CDK4/6シグナル伝達は、EGFR変異型非小細胞肺がんにおける上皮成長因子受容体チロシンキナーゼ阻害剤の効果を減弱させる
kn-title=CDK4/6 signaling attenuates the effect of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in EGFR-mutant non-small cell lung cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=HARANaofumi
en-aut-sei=HARA
en-aut-mei=Naofumi
kn-aut-name=原尚史
kn-aut-sei=原
kn-aut-mei=尚史
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=糖尿病における近位尿細管細胞リソソーム機能障害と、アミノ酸流入阻害による改善効果
kn-title=Inhibition of?amino acids influx into proximal tubular cells improves lysosome function in diabetes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KANOYuzuki
en-aut-sei=KANO
en-aut-mei=Yuzuki
kn-aut-name=加納弓月
kn-aut-sei=加納
kn-aut-mei=弓月
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=p53搭載テロメラーゼ特異的腫瘍融解アデノウイルスの腹腔内投与はびまん性胃癌細胞による腹膜播種を抑制する
kn-title=Intraperitoneal Administration of p53-armed Oncolytic Adenovirus Inhibits Peritoneal Metastasis of Diffuse-type Gastric Cancer Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=HORINaoto
en-aut-sei=HORI
en-aut-mei=Naoto
kn-aut-name=堀直人
kn-aut-sei=堀
kn-aut-mei=直人
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=p53搭載腫瘍融解アデノウイルスは、KRASおよびBRAF変異結腸直腸癌細胞において、オートファジーとアポトーシスを誘導する
kn-title=p53-armed oncolytic adenovirus induces autophagy and apoptosis in KRAS and BRAF-mutant colorectal cancer cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TAMURAShuta
en-aut-sei=TAMURA
en-aut-mei=Shuta
kn-aut-name=田村周太
kn-aut-sei=田村
kn-aut-mei=周太
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=微小環境の栄養状態がメトホルミンによるCD8+ T細胞代謝とIFNγ産生促進を決定する
kn-title=Nutrient Condition in the Microenvironment Determines Essential Metabolisms of CD8+ T Cells for Enhanced IFNγ Production by Metformin
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=CHAORUOYU
en-aut-sei=CHAO
en-aut-mei=RUOYU
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
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=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=マウス系統によって異なる耐寒性が系統別ES細胞においても存在する
kn-title=Mouse embryonic stem cells embody organismal-level cold resistance
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SUITAKoukyou
en-aut-sei=SUITA
en-aut-mei=Koukyou
kn-aut-name=吹田晃享
kn-aut-sei=吹田
kn-aut-mei=晃享
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=64
cd-vols=
no-issue=2
article-no=
start-page=86
end-page=96
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=2024
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Spontaneous regression and rare relapse after excisional biopsy in long-term observation of 31 patients with primary conjunctival lymphoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To elucidate long-term outcome in primary conjunctival lymphoma, a review was conducted of 31 consecutive patients: 21 men and 10 women with an age range of 28 to 85 (median, 61) years at presentation and follow-up periods ranging from 1 to 19 (median, 7) years. Conjunctival lymphoma was on the right side in 10 patients, on the left side in 12, and on both sides in 9. Upper, lower, or both fornix lesions in 28 patients were all diagnosed as extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), while thick nasal bulbar conjunctival lesions in 3 patients were differently diagnosed as MALT lymphoma, diffuse large B-cell lymphoma, and follicular lymphoma, respectively. Seven patients underwent local radiation (30 Gy): as initial treatment in 5 patients and treatment for relapse in 2 patients. The remaining 24 patients were observed without additional treatment after excisional biopsy: 5 of these 24 patients showed relapse 0.5 to 6 years later and underwent excisional biopsy again that revealed MALT lymphoma. Of the 5 patients with relapse, only one with second-time relapse underwent radiation. Fluorodeoxyglucose positron emission tomography was performed in 18 patients and showed no systemic lesions: high uptake was noted in the residual conjunctival lesions of 4 patients and in the relapsed conjunctival lesions of 3 patients. One patient died of rectal cancer while no patients died of lymphoma. Observation is an option in patients with primary conjunctival lymphoma after excisional biopsy. Radiation is a treatment option in the case of relapse.
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=

affil-num=1
en-affil=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=
en-keyword= conjunctival lymphoma
kn-keyword= conjunctival lymphoma
en-keyword=extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma)
kn-keyword=extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma)
en-keyword=follicular lymphoma
kn-keyword=follicular lymphoma
en-keyword=diffuse large B-cell lymphoma
kn-keyword=diffuse large B-cell lymphoma
en-keyword=fluorodeoxyglucose positron emission tomography (FDG-PET)
kn-keyword=fluorodeoxyglucose positron emission tomography (FDG-PET)
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=2
article-no=
start-page=323
end-page=331
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=Topical application of activator protein-1 inhibitor T-5224 suppresses inflammation and improves skin barrier function in a murine atopic dermatitis-like dermatitis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Selective activator protein (AP)-1 inhibitors are potentially promising therapeutic agents for atopic dermatitis (AD) because AP-1 is an important regulator of skin inflammation. However, few studies have investigated the effect of topical application of AP-1 inhibitors in treating inflammatory skin disorders. <br>
Methods: Immunohistochemistry was conducted to detect phosphorylated AP-1/c-Jun expression of skin lesions in AD patients. In the in vivo study, 1 % T-5224 ointment was topically applied for 8 days to the ears of 2,4 dinitrofluorobenzene challenged AD-like dermatitis model mice. Baricitinib, a conventional therapeutic agent Janus kinase (JAK) inhibitor, was also topically applied. In the in vitro study, human epidermal keratinocytes were treated with T-5224 and stimulated with AD-related cytokines. <br>
Results: AP-1/c-Jun was phosphorylated at skin lesions in AD patients. In vivo, topical T-5224 application inhibited ear swelling (P < 0.001), restored filaggrin (Flg) expression (P < 0.01), and generally suppressed immune-related pathways. T-5224 significantly suppressed Il17a and l17f expression, whereas baricitinib did not.Baricitinib suppressed Il4, Il19, Il33 and Ifnb expression, whereas T-5224 did not. Il1a, Il1b, Il23a, Ifna, S100a8, and S100a9 expression was cooperatively downregulated following the combined use of T5224 and baricitinib. In vitro, T-5224 restored the expression of FLG and loricrin (LOR) (P < 0.05) and suppressed IL33 expression (P < 0.05) without affecting cell viability and cytotoxicity. <br>
Conclusions: Topical T-5224 ameliorates clinical manifestations of AD-like dermatitis in mice. The effect of this inhibitor is amplified via combined use with JAK inhibitors.
en-copyright=
kn-copyright=

en-aut-name=SasakuraMinori
en-aut-sei=Sasakura
en-aut-mei=Minori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=TachibanaKota
en-aut-sei=Tachibana
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IkedaKenta
en-aut-sei=Ikeda
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
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=6
ORCID=

en-aut-name=SunagawaKo
en-aut-sei=Sunagawa
en-aut-mei=Ko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

en-aut-name=TomidaShuta
en-aut-sei=Tomida
en-aut-mei=Shuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
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=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

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

affil-num=8
en-affil=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=AP-1 inhibitor
kn-keyword=AP-1 inhibitor
en-keyword=Atopic dermatitis
kn-keyword=Atopic dermatitis
en-keyword=Baricitinib
kn-keyword=Baricitinib
en-keyword=T-5224
kn-keyword=T-5224
en-keyword=Topical application
kn-keyword=Topical application
END