start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=2
article-no=
start-page=bio062463
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260215
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Gap junction-mediated signaling coordinates Rhodopsin coupling for Drosophila color vision
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The Drosophila compound eye is composed of approximately 800 ommatidia, and every ommatidium contains eight photoreceptor cells, six outer cells (R1-R6) and two inner cells (R7 and R8), and accessory cells (cone and pigment cells). The expression of rhodopsin genes in R7 and R8 is highly coordinated through an instructive signal from R7 to R8. The activity of the homeodomain protein Defective proventriculus in R1 is also required to transmit this instructive signal, suggesting that cell–cell communication between R7, R1, and R8 is important to generate the pattern of Rh expression in R7/R8 (Rhodopsin coupling). As cell junctions play crucial roles in maintaining the structural and functional integrity of tissues, we tested whether cell junction proteins are involved in the interactions between photoreceptor cells. Here, we demonstrate that gap junction proteins innexin 2 and innexin 7 in accessory cells are necessary for transmitting signals from R7 to R8. In addition, Notch-mediated accessory cell development and Rhodopsin coupling in R7/R8 are highly correlated. Our results provide evidence that functional coupling of two different neurons, R7 and R8, is established through gap junction-mediated signaling from adjacent accessory cells.
en-copyright=
kn-copyright=

en-aut-name=ZhangXuanshuo
en-aut-sei=Zhang
en-aut-mei=Xuanshuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShinjoRyoki
en-aut-sei=Shinjo
en-aut-mei=Ryoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KitamataManabu
en-aut-sei=Kitamata
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OtsuneShinichi
en-aut-sei=Otsune
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakagoshiHideki
en-aut-sei=Nakagoshi
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

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

affil-num=3
en-affil=Division of Health Science, Advanced Comprehensive Research Organization, Teikyo University
kn-affil=

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

affil-num=5
en-affil=Division of Biological Sciences, Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Drosophila
kn-keyword=Drosophila
en-keyword=Eye
kn-keyword=Eye
en-keyword=Gap junction
kn-keyword=Gap junction
en-keyword=Innexin
kn-keyword=Innexin
en-keyword=Opsin
kn-keyword=Opsin
END

start-ver=1.4
cd-journal=joma
no-vol=49
cd-vols=
no-issue=2
article-no=
start-page=364
end-page=370
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260221
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Functional Transport Properties of Human Zinc Transporter 1: Kinetics and pH-Dependency
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Intracellular zinc (Zn2+) homeostasis is essential for physiological and pathological processes and is strictly regulated by Zn2+ transporters. Zinc transporter 1 (ZnT1) is a ubiquitously expressed plasma membrane-localized Zn transporter that exports Zn2+ from the cytoplasm to the extracellular space. However, the functional transport properties regarding kinetics and driving forces of ZnT1 remain debatable. In this study, we established a cell-free proteoliposome assay system and demonstrated that ZnT1 transports Zn2+ with high affinity in pH-dependent and pH-independent manners. The Km and Vmax of pH-dependent Zn2+ transport were 0.40 μM and 15.13 nmol/min/mg protein, and those of pH-independent Zn2+ transport were 0.52 μM and 8.88 nmol/min/mg protein (low concentrations of Zn2+), 3.02 μM and 17.59 nmol/min/mg protein (high concentrations of Zn2+), respectively, suggesting biphasic kinetic components of Zn2+ transport. Even without pH gradient formation, ZnT1 exhibits potent Zn2+ transport activity. In pH dependency, Zn2+ transport activity was higher at an inside pH of 6.0 than at 6.5–7.5 for proteoliposomes, despite the same ΔpH of 0.5–1.5. The Zn2+ transport activity decreased at an outside pH of 8.0, despite an increase in ΔpH. Although previous studies have proposed that ZnT1-mediated Zn2+ transport activity is driven by a calcium (Ca2+) gradient and not by a pH gradient, Ca2+ does not enhance Zn2+ transport activity in the presence or absence of a pH gradient. These results strongly suggest that ZnT1 protein transports Zn2+ optimally at a specific pH and exports excess intracellular Zn2+ even without ΔpH.
en-copyright=
kn-copyright=

en-aut-name=YoshiokaYuma
en-aut-sei=Yoshioka
en-aut-mei=Yuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

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

affil-num=2
en-affil=Department of Molecular Membrane Biology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=zinc transporter 1
kn-keyword=zinc transporter 1
en-keyword=SLC30A1
kn-keyword=SLC30A1
en-keyword=zinc
kn-keyword=zinc
en-keyword=pH
kn-keyword=pH
en-keyword=proteoliposome
kn-keyword=proteoliposome
END

start-ver=1.4
cd-journal=joma
no-vol=135
cd-vols=
no-issue=
article-no=
start-page=103134
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202605
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Regulation of brain-specific kinases 1 and 2 (BRSK1/2) by Ca2+/calmodulin
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We conducted a genome-wide calmodulin (CaM) interaction screening of 462 GST-fused human protein kinases to identify novel CaM-dependent protein kinases (CaMKs). In addition to known CaMKs, including myosin light chain kinases, CaMK2γ, and death-associated kinase 2, we identified the brain-specific protein kinase 2 (BRSK2, also known as SAD-A) as a novel CaM interactant. Proximity biotinylation and CaM–sepharose chromatography assays revealed that rat BRSK isoforms (BRSK1/2) interact with CaM in a Ca2+-dependent manner in vitro. We found that CaM suppresses the activation-loop phosphorylation of BRSK1 (at Thr189) and BRSK2 (at Thr175) by liver kinase B1 (LKB1), an activating kinase, in a Ca2+-dependent manner (IC50 of ∼7 µM), thereby inhibiting BRSK activation. LKB1-catalyzed phosphorylation of the catalytic domain mutant of BRSK1 (residues 1–294) at Thr189 was suppressed by the addition of Ca2+/CaM, consistent with direct CaM binding of the kinase domain, as well as wild-type BRSK1. We confirmed that the LKB1 activity was not directly suppressed by Ca2+/CaM, supporting the hypothesis that the direct interaction of Ca2+/CaM with the kinase domain blocks the phosphorylation/activation of BRSK1/2 by LKB1. The kinase activity and PP2Cα-catalyzed dephosphorylation of LKB1-phosphorylated BRSK1 were not altered by Ca2+/CaM, although it was demonstrated to bind to Ca2+/CaM like that of unphosphorylated BRSK1. This unrecognized mechanism of BRSK1/2 regulation, involving the direct role of Ca2+/CaM binding, which inhibits phosphorylation/activation by LKB1, may open a new Ca2+ signal transduction pathway in neurons.
en-copyright=
kn-copyright=

en-aut-name=WashidaNaoyuki
en-aut-sei=Washida
en-aut-mei=Naoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KataokaMoe
en-aut-sei=Kataoka
en-aut-mei=Moe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=BrunAnna R.
en-aut-sei=Brun
en-aut-mei=Anna R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakezakiUryu
en-aut-sei=Takezaki
en-aut-mei=Uryu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HijikawaKo
en-aut-sei=Hijikawa
en-aut-mei=Ko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamauchiHaruki
en-aut-sei=Yamauchi
en-aut-mei=Haruki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OhtsukaSatomi
en-aut-sei=Ohtsuka
en-aut-mei=Satomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

en-aut-name=MorishitaRyo
en-aut-sei=Morishita
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TokumitsuHiroshi
en-aut-sei=Tokumitsu
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

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

affil-num=2
en-affil=Department of Applied Chemistry and Biotechnology, Faculty of Engineering, Okayama University
kn-affil=

affil-num=3
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, 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=Department of Applied Chemistry and Biotechnology, Faculty of Engineering, Okayama University
kn-affil=

affil-num=6
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=7
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=8
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=9
en-affil=CellFree Sciences Co., Ltd.
kn-affil=

affil-num=10
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=BRSK1
kn-keyword=BRSK1
en-keyword=BRSK2
kn-keyword=BRSK2
en-keyword=calmodulin
kn-keyword=calmodulin
en-keyword=LKB1
kn-keyword=LKB1
en-keyword=phosphorylation
kn-keyword=phosphorylation
en-keyword=Ca2+
kn-keyword=Ca2+
en-keyword=CaM-dependent protein kinase
kn-keyword=CaM-dependent protein kinase
END

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=
article-no=
start-page=1
end-page=6
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260331
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The effects of cold compresses on itching in patients with atopic dermatitis: A cross-over controlled pilot trial
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This cross-over controlled trial aimed to evaluate the effectiveness and safety of two types of cold compresses (towels and ice packs) in alleviating itching among patients with atopic dermatitis. The study recruited 19 participants diagnosed with atopic dermatitis and suffering from chronic itching for over 6 months. Each participant received both types of cold compress interventions. Itching sensations were assessed repeatedly using a visual analogue scale before and after the application of the cold compress. The mean and standard deviation of itching scores for the towel intervention were 16.9 ± 19.1 (baseline) and 11.4 ± 16.1 (post-application). For the ice pack intervention, the scores were 13.6 ± 14.7 (baseline) and 6.2 ± 9.8 (post-application). Although there was a reduction in mean itching scores following the application of cold compresses, the differences were not statistically significant for either intervention. Despite the lack of statistical significance, this study suggests that cold compresses, which are user-friendly and inexpensive, may safely reduce subjective itching in patients with atopic dermatitis without causing pain or discomfort. However, further research with a larger sample size is needed to confirm these findings.
en-copyright=
kn-copyright=

en-aut-name=HIRAMIYuki
en-aut-sei=HIRAMI
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HARADANahoko
en-aut-sei=HARADA
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ONOMiho
en-aut-sei=ONO
en-aut-mei=Miho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KODAMasahide
en-aut-sei=KODA
en-aut-mei=Masahide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FUKAIKiyoko
en-aut-sei=FUKAI
en-aut-mei=Kiyoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

affil-num=2
en-affil=Department of Nursing Science, Faculty of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Nursing, Faculty of Health, Kagawa Prefectural University of Health Sciences
kn-affil=

affil-num=4
en-affil=Co-learning Community Healthcare Re-innovation Office, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Professor Emeritus, Okayama University, Graduate School of Nursing, The Jikei University School of Medicine
kn-affil=
en-keyword=Atopic Dermatitis
kn-keyword=Atopic Dermatitis
en-keyword=Pruritus
kn-keyword=Pruritus
en-keyword=Cryotherapy
kn-keyword=Cryotherapy
en-keyword=Quality of Life
kn-keyword=Quality of Life
en-keyword=Skin Temperature
kn-keyword=Skin Temperature
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=8840
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260317
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Tribolium castaneum with longer duration of tonic immobility have more variations corresponding to the human Parkinson’s disease genomic region
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Parkinson’s disease (PD) is a common neurodegenerative syndrome characterized by the loss of dopaminergic neurons and is also a progressive neurodegenerative disorder that is characterized by dopamine deficiency. We established strains artificially selected for longer and shorter durations of tonic immobility, an antipredator behavior that has received much attention recently, in the red flour beetle, Tribolium castaneum, a model insect species for molecular analyses different from Drosophila melanogaster. Previous studies have shown that the long strains (L-strain) have significantly lower levels of dopamine expression in the brain than the short strains (S-strain) and that they have an abnormal pattern of locomotor activity. Furthermore, previous studies have shown that administering dopamine to L-strain beetles reduces the duration of tonic immobility. Transcriptome analysis of brain and thorax of the L- and S-strains also showed differences in mRNA expression of genes involved in dopamine synthesis and tyrosine metabolism. These results indicate that the phenotype and molecular basis of the L-strain are similar to those of Parkinson’s syndrome symptoms. In order to establish a link between T. castaneum and PD, we compared the DNA sequences of the L- and S-strains to human genes affecting dopaminergic pathways. The DNA comparison revealed many mutated regions in these genes in the L-strain. We discuss the relationship between dopaminergic pathway genes and PD-like phenotypes across humans, Drosophila, and the red flour beetle.
en-copyright=
kn-copyright=

en-aut-name=TanakaKeisuke
en-aut-sei=Tanaka
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SasakiKen
en-aut-sei=Sasaki
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YajimaShunsuke
en-aut-sei=Yajima
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyatakeTakahisa
en-aut-sei=Miyatake
en-aut-mei=Takahisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=NODAI Genome Research Center, Tokyo University of Agriculture
kn-affil=

affil-num=2
en-affil=Graduate School of Agriculture, Tamagawa University
kn-affil=

affil-num=3
en-affil=NODAI Genome Research Center, Tokyo University of Agriculture
kn-affil=

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

start-ver=1.4
cd-journal=joma
no-vol=119
cd-vols=
no-issue=1
article-no=
start-page=9
end-page=17
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=Big data-driven target identification by machine learning: DRD2 as a therapeutic target for psoriasis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: The development of medical treatments has traditionally relied on researchers leveraging scientific knowledge to hypothesize disease mechanisms and identify therapeutic agents. However, the depletion of novel therapeutic targets has become a significant challenge, resulting in stagnation within pharmaceutical research.<br>
Objective: To address the scarcity of therapeutic targets, we developed a machine learning (ML)-based system capable of predicting therapeutic target molecules for diseases. To validate its utility, we applied this system to psoriasis, aiming to identify novel treatment strategies.<br>
Methods: Our approach utilized a large clinical database to calculate reporting odds ratios for all drugs associated with the prevention of diseases of interest. We identified target proteins by analyzing large chemical structure databases to discover proteins commonly associated with preventive drug candidates. Experimental validation was conducted by administering a predicted therapeutic candidate in an imiquimod-induced psoriasis mouse model.<br>
Results: The ML-based predictions identified drugs for Parkinson’s disease as potential preventive candidates for psoriasis. Further analysis highlighted dopamine receptor D2 (DRD2) as a therapeutic target. Administration of a DRD2 agonist alleviated psoriasis symptoms in mice, evidenced by the downregulation of mRNA expression in the IL-17 pathway and reduced serum tumor necrosis factor-α levels.<br>
Conclusion: This study demonstrates the utility of a novel ML-based system for identifying therapeutic targets, as shown by its successful application in uncovering the role of DRD2 in psoriasis. Beyond psoriasis, this system offers significant potential for exploring pathological mechanisms and discovering therapeutic targets across various diseases.
en-copyright=
kn-copyright=

en-aut-name=SakaiTakashi
en-aut-sei=Sakai
en-aut-mei=Takashi
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=IchinoseOtoha
en-aut-sei=Ichinose
en-aut-mei=Otoha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TerabayashiTakeshi
en-aut-sei=Terabayashi
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HatanoYutaka
en-aut-sei=Hatano
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamanishiYoshihiro
en-aut-sei=Yamanishi
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IshizakiToshimasa
en-aut-sei=Ishizaki
en-aut-mei=Toshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Dermatology, Faculty of Medicine, Oita University
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 Bioscience and Bioinformatics, Faculty of Computer Science and Systems Engineering, Kyushu Institute of Technology
kn-affil=

affil-num=4
en-affil=Department of Pharmacology, Faculty of Medicine, Oita University
kn-affil=

affil-num=5
en-affil=Department of Dermatology, Faculty of Medicine, Oita University
kn-affil=

affil-num=6
en-affil=Department of Complex Systems Science, Graduate School of Informatics, Nagoya University
kn-affil=

affil-num=7
en-affil=Department of Pharmacology, Faculty of Medicine, Oita University
kn-affil=
en-keyword=artificial intelligence
kn-keyword=artificial intelligence
en-keyword=big data
kn-keyword=big data
en-keyword=machine learning
kn-keyword=machine learning
en-keyword=dopamine receptor D2
kn-keyword=dopamine receptor D2
en-keyword=psoriasis
kn-keyword=psoriasis
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=1
article-no=
start-page=e70168
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202603
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mechanosensitive Ion Channel PIEZO1 Suppresses BMP2-Induced Ossification of the Annulus Fibrosus Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective: Major cause of low-back pain is intervertebral disc degeneration (IVDD), with mechanical stress playing a crucial role in its progression. A mechanosensitive ion channel, PIEZO1, is involved in various musculoskeletal tissues, but its role in the annulus fibrosus (AF) remains unclear. This study aimed to elucidate the function of PIEZO1 in AF cells under mechanical stimulation.<br>
Methods: Primary rat AF cells were subjected to cyclic tensile strain (CTS) at low (2%) and high (12%) strain levels to investigate strain-dependent effects on osteogenic gene expression. We evaluated the effects of Piezo1, Piezo2, and Trpv4 knockdown by RNA interference to identify the upstream mechanotransducer. Furthermore, PIEZO1 was activated using the agonist Yoda1, followed by RNA-sequencing analysis and evaluation of its effects on BMP2-induced osteogenesis in rat AF cells. We also examined the effects of Yoda1 in primary human AF cells.<br>
Results: Low-strain CTS significantly suppressed osteogenic marker expression, which was not observed with high strain. Piezo1 knockdown reversed this suppression, whereas Piezo2 and Trpv4 had no effect. Piezo1 activation by Yoda1 produced similar anti-osteogenic effects in both rat and human AF cells. RNA sequencing revealed the enrichment of ossification and calcineurin signaling pathways in rat cells. Furthermore, Piezo1 activation inhibited BMP2-induced osteogenesis and nuclear translocation of p-Smad1/5/9.<br>
Conclusions: Piezo1 maintains AF cell homeostasis under mechanical stress by suppressing osteogenic changes via calcineurin-mediated inhibition of BMP signaling, which may represent a novel therapeutic target for IVDD.
en-copyright=
kn-copyright=

en-aut-name=ShitozawaHisakazu
en-aut-sei=Shitozawa
en-aut-mei=Hisakazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamichiRyo
en-aut-sei=Nakamichi
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YoshidaAki
en-aut-sei=Yoshida
en-aut-mei=Aki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=UedaMasataka
en-aut-sei=Ueda
en-aut-mei=Masataka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SaitoTaichi
en-aut-sei=Saito
en-aut-mei=Taichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UotaniKoji
en-aut-sei=Uotani
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OdaYoshiaki
en-aut-sei=Oda
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakatoriRyo
en-aut-sei=Takatori
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YamashitaKazutaka
en-aut-sei=Yamashita
en-aut-mei=Kazutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OzakiToshifumi
en-aut-sei=Ozaki
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

affil-num=3
en-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

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

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

affil-num=8
en-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

affil-num=10
en-affil=Department of Orthopaedic Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=annulus fibrosus
kn-keyword=annulus fibrosus
en-keyword=calcification
kn-keyword=calcification
en-keyword=ossification
kn-keyword=ossification
en-keyword=PIEZO1
kn-keyword=PIEZO1
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=888
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251215
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=TRPV2 in muscle satellite cells is crucial for skeletal muscle remodelling
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Skeletal muscle remodelling relies on muscle stem cells (MuSCs) for regeneration after injury and hypertrophy in response to mechanical loading. However, the mechanisms that trigger MuSC activation and proliferation remain unclear. Transient receptor potential vanilloid 2 (TRPV2) ion channels respond to insulin-like growth factor-1 and mechanical stimuli to regulate the biological characteristics of various cells. Using a temporally inducible MuSC-specific conditional knockout (cKO) mouse, we show that TRPV2 regulates MuSC function and is essential for muscle remodelling. In cultured myofibre, MuSCs express TRPV2 and exhibit Ca2+ responses to the TRPV2 agonists 2-aminoethoxydiphenyl borate and probenecid, which are abolished upon TRPV2 deletion. TRPV2-deficient MuSCs exhibit reduced paired box 7 (Pax7) expression and impaired proliferation, suggesting TRPV2 is a factor that regulates the early stage of MuSC function. Myotube formation in MuSCs was enhanced by overexpression of TRPV2 and suppressed by TRPV2 deficiency, suggesting that TRPV2 is a factor that promotes myogenesis. Muscle-administered cardiotoxin promoted muscle regeneration and resulted in the appearance of numerous Pax7-positive MuSCs between myofibres. MuSC-specific TRPV2 cKO mice exhibit substantially impaired muscle regeneration after cardiotoxin-induced injury, drastically reducing Pax7-positive MuSCs between myofibres. In floxed mice, mechanical loading via synergist ablation induces hypertrophy and greatly increases the number of myonuclei per myofibre. In contrast, MuSC-specific TRPV2 cKO mice show no changes in myofibre thickness or nuclear number, either at baseline or after mechanical loading. Mechanical loading of floxed mice increased TRPV2+/Pax7+ double-positive MuSCs, but MuSC-specific TRPV2 cKO mice showed no change. Additionally, MuSCs exhibit Ca2+ responses to hypo-osmotic stimuli, which are suppressed by TRPV2 inhibitors and TRPV2 deletion, suggesting that MuSCs exhibit TRPV2-dependent mechanical responses. These results establish TRPV2 as a critical regulator of MuSC-mediated muscle remodelling, an important finding that may lead to therapeutic strategies for muscle repair and adaptation.
en-copyright=
kn-copyright=

en-aut-name=ChenYanzhu
en-aut-sei=Chen
en-aut-mei=Yanzhu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KatanosakaKimiaki
en-aut-sei=Katanosaka
en-aut-mei=Kimiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShibuyaMakoto
en-aut-sei=Shibuya
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=DongYubing
en-aut-sei=Dong
en-aut-mei=Yubing
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ZhangLidan
en-aut-sei=Zhang
en-aut-mei=Lidan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KanagawaMotoi
en-aut-sei=Kanagawa
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FukadaSo-ichiro
en-aut-sei=Fukada
en-aut-mei=So-ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

en-aut-name=KatanosakaYuki
en-aut-sei=Katanosaka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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 Biomedical Sciences, College of Life and Health Sciences, Chubu 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=Laboratory of Stem Cell Regeneration and Adaptation, Graduate School of Pharmaceutical Sciences, The University of Osaka
kn-affil=

affil-num=6
en-affil=Department of Cell Biology and Molecular Medicine, Ehime University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=Laboratory of Stem Cell Regeneration and Adaptation, Graduate School of Pharmaceutical Sciences, The University of Osaka
kn-affil=

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

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

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=
article-no=
start-page=RP99825
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250618
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Stimulatory and inhibitory G-protein signaling relays drive cAMP accumulation for timely metamorphosis in the chordate Ciona
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Larvae of the ascidian Ciona initiate metamorphosis tens of minutes after adhesion to a substratum via their adhesive organ. The gap between adhesion and metamorphosis initiation is suggested to ensure the rigidity of adhesion, allowing Ciona to maintain settlement after losing locomotive activity through metamorphosis. The mechanism producing the gap is unknown. Here, by combining gene functional analyses, pharmacological analyses, and live imaging, we propose that the gap represents the time required for sufficient cyclic adenosine monophosphate (cAMP) accumulation to trigger metamorphosis. Not only the Gs pathway but also the Gi and Gq pathways are involved in the initiation of metamorphosis in the downstream signaling cascade of the neurotransmitter GABA, the known initiator of Ciona metamorphosis. The mutual crosstalk of stimulatory and inhibitory G-proteins functions as the accelerator and brake for cAMP production, ensuring the faithful initiation of metamorphosis at an appropriate time and in the right situation.
en-copyright=
kn-copyright=

en-aut-name=HozumiAkiko
en-aut-sei=Hozumi
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TotsukaNozomu M
en-aut-sei=Totsuka
en-aut-mei=Nozomu M
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OnoderaArata
en-aut-sei=Onodera
en-aut-mei=Arata
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WangYanbin
en-aut-sei=Wang
en-aut-mei=Yanbin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HamadaMayuko
en-aut-sei=Hamada
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShiraishiAkira
en-aut-sei=Shiraishi
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SatakeHonoo
en-aut-sei=Satake
en-aut-mei=Honoo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HorieTakeo
en-aut-sei=Horie
en-aut-mei=Takeo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HottaKohji
en-aut-sei=Hotta
en-aut-mei=Kohji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SasakuraYasunori
en-aut-sei=Sasakura
en-aut-mei=Yasunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Shimoda Marine Research Center, University of Tsukuba
kn-affil=

affil-num=2
en-affil=Department of Biosciences and Informatics, Faculty of Science and Technology, Keio University
kn-affil=

affil-num=3
en-affil=Shimoda Marine Research Center, University of Tsukuba
kn-affil=

affil-num=4
en-affil=Shimoda Marine Research Center, University of Tsukuba
kn-affil=

affil-num=5
en-affil=Ushimado Marine Institute, Okayama University
kn-affil=

affil-num=6
en-affil=Bioorganic Research Institute, Suntory Foundation for Life Sciences
kn-affil=

affil-num=7
en-affil=Bioorganic Research Institute, Suntory Foundation for Life Sciences
kn-affil=

affil-num=8
en-affil=Laboratory for Single-cell Neurobiology, Graduate School of Frontier Biosciences, Osaka University
kn-affil=

affil-num=9
en-affil=Department of Biosciences and Informatics, Faculty of Science and Technology, Keio University
kn-affil=

affil-num=10
en-affil=Shimoda Marine Research Center, University of Tsukuba
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260225
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical and Genetic Landscape of Glioblastoma, IDH-Wildtype With FGFR Gene Family Alterations
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Glioblastoma, isocitrate dehydrogenase wildtype (GBM, IDH-wt), is a highly aggressive brain tumor with a poor prognosis. Alterations in the fibroblast growth factor receptor (FGFR) gene family—such as FGFR::TACC fusions and FGFR1 mutations—have emerged as potential therapeutic targets; however, their clinical and genetic features in GBM, IDH-wt remain unclear. We analyzed 1076 GBM, IDH-wt cases using comprehensive genomic profiling data from the Center for Cancer Genomics and Advanced Therapeutics (C-CAT) database in Japan. FGFR alterations were detected in 8.0% of patients, including FGFR::TACC fusions (3.3%) and FGFR1 mutations (2.9%). The FGFR::TACC fusion-positive group was older at diagnosis and showed higher frequencies of TERT promoter mutation and MDM2 amplification, and lower frequencies of EGFR amplification and TP53 mutation, compared with the fusion-negative group. The FGFR1 mutation-positive group was enriched for ATRX, NF1, and PIK3CA mutations and had significantly fewer TERT promoter and PTEN mutations, compared with the mutation-negative group. No significant differences in overall survival were observed, although both groups tended to have longer median overall survival compared with their respective negative groups. This study represents the largest genomic cohort to date of FGFR alterations in GBM, IDH-wt. FGFR::TACC fusion-positive and FGFR1 mutation-positive GBMs exhibited distinct genetic profiles, highlighting the clinical relevance of molecular subclassification and providing insight for future therapeutic strategies.
en-copyright=
kn-copyright=

en-aut-name=KegoyaYasuhito
en-aut-sei=Kegoya
en-aut-mei=Yasuhito
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=MizutaRyo
en-aut-sei=Mizuta
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=KamiuraMako
en-aut-sei=Kamiura
en-aut-mei=Mako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
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=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=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 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=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 Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=comprehensive genomic profiling
kn-keyword=comprehensive genomic profiling
en-keyword=copy number alteration
kn-keyword=copy number alteration
en-keyword=FGFR
kn-keyword=FGFR
en-keyword=glioblastoma
kn-keyword=glioblastoma
en-keyword=single-nucleotide variant
kn-keyword=single-nucleotide variant
END

start-ver=1.4
cd-journal=joma
no-vol=191
cd-vols=
no-issue=
article-no=
start-page=31
end-page=45
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The Creativity of Mind Wandering through Self-transformation: An Analysis of Four Types of Self-talk That Occur in Situations of Self-Loathing
kn-title=自己変容を通してみたマインドワンダリングの創造性について ― 自己嫌悪場面での４つの内言に着目した検討 ―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=　マインドワンダリング(以下MW)は心が自己内の複数の領域をさまようことで, 新たな気づきや発想
が生まれる土壌になるとされる。本稿では，この創造性を検討するため，水間(2003)を参考に，自己嫌悪
場面で生起する4 つの反応についての研究モデルを用いてこの創造性を検討した。その際，MW とその
他の類似の内省を区別するため，自己嫌悪場面で生起する内言として自己注目(省察・反芻), 自己への没
入(MW・空想)の4 つを想定した。またその内言が自己の成長にとって意味のある内言か否かを判断する
指標として本来感を用いた。分析の結果, 本来感高群において, MW による集中力の欠如が人の思考を
多領域にさまよわせ, 内的な個性の創造と内的な個人の成長を促すことが示された。また低群において
省察は自分らしさを求め変容を目指す意識が促進されることが示された。他方, 反芻と空想はいずれの
反応様式にも関わっていないことがわかった。
en-copyright=
kn-copyright=

en-aut-name=AOKITazuko
en-aut-sei=AOKI
en-aut-mei=Tazuko
kn-aut-name=青木多寿子
kn-aut-sei=青木
kn-aut-mei=多寿子
aut-affil-num=1
ORCID=

en-aut-name=HAGIWARAMakoto
en-aut-sei=HAGIWARA
en-aut-mei=Makoto
kn-aut-name=萩原麻琴
kn-aut-sei=萩原
kn-aut-mei=麻琴
aut-affil-num=2
ORCID=

en-aut-name=YASUNAGAKazuhiro
en-aut-sei=YASUNAGA
en-aut-mei=Kazuhiro
kn-aut-name=安永和央
kn-aut-sei=安永
kn-aut-mei=和央
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Faculty of Education, Okayama University
kn-affil=岡山大学学術研究院教育学域

affil-num=2
en-affil=a public employee
kn-affil=地方公共団体職員

affil-num=3
en-affil=Faculty of Education, Okayama University
kn-affil=岡山大学学術研究院教育学域
en-keyword=マインドワンダリング
kn-keyword=マインドワンダリング
en-keyword=自己変容
kn-keyword=自己変容
en-keyword=本来感
kn-keyword=本来感
en-keyword=創造性
kn-keyword=創造性
en-keyword=内言
kn-keyword=内言
END

start-ver=1.4
cd-journal=joma
no-vol=4
cd-vols=
no-issue=3
article-no=
start-page=179
end-page=187
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250901
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Synthesis and applications of porous carbonaceous materials with inherited molecular structural features from the precursor molecules
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The carbonization of organic crystalline materials, such as metal organic frameworks and covalent organic frameworks, has emerged as a promising approach for producing functional porous carbonaceous materials. However, both the chemically defined long-term ordered structures and the local chemical structures derived from these precursor materials are generally lost, resulting in amorphous carbons. As a result, controlling the molecular-level structure of nanoporous carbons remains a significant challenge. We report a new bottom-up synthesis approach for porous carbons with a molecular-level design, involving the carbonization of well-designed precursor molecules by thermal polymerization. Among the resulting carbons, ordered carbonaceous frameworks, which contain a high-density of regularly aligned single-atomic metal species, have been identified as promising platforms for single-atom catalysts. This approach also enables the synthesis of various three-dimensional porous carbons that reflect the structural features of their precursor molecules. Recent progress in the synthesis and applications of porous carbons derived from molecular precursors is summarized, highlighting their potential for the development of functional materials.
en-copyright=
kn-copyright=

en-aut-name=ChidaKoki
en-aut-sei=Chida
en-aut-mei=Koki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YoshiTakeharu
en-aut-sei=Yoshi
en-aut-mei=Takeharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NishinaYuta
en-aut-sei=Nishina
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KamiyaKazuhide
en-aut-sei=Kamiya
en-aut-mei=Kazuhide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakamotoRyota
en-aut-sei=Sakamoto
en-aut-mei=Ryota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TaniFumito
en-aut-sei=Tani
en-aut-mei=Fumito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OgoshiTomoki
en-aut-sei=Ogoshi
en-aut-mei=Tomoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NishiharaHirotomo
en-aut-sei=Nishihara
en-aut-mei=Hirotomo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Institute of Multidisciplinary Research for Advanced Materials, Tohoku University
kn-affil=

affil-num=2
en-affil=Institute of Multidisciplinary Research for Advanced Materials, Tohoku University
kn-affil=

affil-num=3
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=4
en-affil=Research Center for Solar Energy Chemistry, Graduate School of Engineering Science, The University of Osaka
kn-affil=

affil-num=5
en-affil=Department of Chemistry, Graduate School of Science, Tohoku University
kn-affil=

affil-num=6
en-affil=Institute for Materials Chemistry and Engineering, Kyushu University
kn-affil=

affil-num=7
en-affil=Department of Synthetic Chemistry and Biological Chemistry, Graduate School of Engineering, Kyoto University
kn-affil=

affil-num=8
en-affil=Institute of Multidisciplinary Research for Advanced Materials, Tohoku University
kn-affil=
en-keyword=Ordered carbonaceous frameworks (OCFs)
kn-keyword=Ordered carbonaceous frameworks (OCFs)
en-keyword=Porous carbon materials
kn-keyword=Porous carbon materials
en-keyword=Single-atom catalysts (SACs)
kn-keyword=Single-atom catalysts (SACs)
en-keyword=Catalyst supports
kn-keyword=Catalyst supports
END

start-ver=1.4
cd-journal=joma
no-vol=54
cd-vols=
no-issue=713
article-no=
start-page=13
end-page=21
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=2026
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=『光が見える』人工網膜の可能性 ― 有機色素分子を部材とする世界初の医療機器「光電変換色素薄膜型人工網膜OUReP」
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=　網膜色素変性や加齢黄斑変性では、光を細胞膜電位に変換する網膜視細胞が死んでいるが、視神経として脳に連絡する神経節細胞は生き残っている。人工網膜は視細胞を代替する人工物で、光を受け電流を出力する電極アレイ型が主流であるが、電流は拡散するため解像度向上が難しい。そこで人工網膜の解像度向上を目指して、光を電位差に変換する光電変換色素分子を絶縁体のポリエチレン薄膜表面に共有結合した光電変換色素薄膜型の人工網膜OURePを開発してきた。この人工網膜OURePは光受容と電位出力の一体型で外部起電力は不要、手術では薄膜を鋏で切って眼内に植込む大きさを自由に選べる。使い捨てインジェクタを使って薄膜を丸め眼球の網膜下に硝子体手術で植込み、網膜下に植込んだ人工網膜OURePは光を受けて電位差を出力し隣接する網膜組織の神経細胞の活動電位を誘発する。クリーンルームで製造品質管理を行い、安全性と有効性を証明して、医師主導治験を準備している。今後、日本の国民皆保険が維持できるよう比較安価な適正価格の人工網膜治療を提供したい。
en-copyright=
kn-copyright=

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

en-aut-name=UchidaTetsuya
en-aut-sei=Uchida
en-aut-mei=Tetsuya
kn-aut-name=内田哲也
kn-aut-sei=内田
kn-aut-mei=哲也
aut-affil-num=2
ORCID=

en-aut-name=IshikaneHiroshi
en-aut-sei=Ishikane
en-aut-mei=Hiroshi
kn-aut-name=石金浩史
kn-aut-sei=石金
kn-aut-mei=浩史
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学学術研究院ヘルスシステム統合科学学域

affil-num=2
en-affil=
kn-affil=岡山大学学術研究院環境生命自然科学学域

affil-num=3
en-affil=
kn-affil=専修大学人間科学部心理学科
en-keyword=人工網膜
kn-keyword=人工網膜
en-keyword=光電変換色素
kn-keyword=光電変換色素
en-keyword=医師主導治験
kn-keyword=医師主導治験
en-keyword=網膜活動電位
kn-keyword=網膜活動電位
en-keyword=製造品質管理
kn-keyword=製造品質管理
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=1
article-no=
start-page=123
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260119
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Streamlined Radiosynthesis of [18F]Fluproxadine (AF78): An Unprotected Guanidine Precursor Enables Efficient One-Step, Automation-Ready Labeling for Clinical Use
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/Objectives: [18F]Fluproxadine (formerly [18F]AF78) is a PET radiotracer targeting the norepinephrine transporter (NET) with potential applications in cardiac, neurological, and oncological imaging. Its guanidine moiety, while essential for NET binding, presents major radiosynthetic challenges due to high basicity and the harsh deprotection conditions required for protected precursors. Previous methods relied on multistep procedures, strong acids, and complex purification, limiting clinical translation. This study aimed to develop a practical one-step radiosynthesis suitable for routine and automated production. Methods: A direct SN2-type nucleophilic [18F]fluorination was performed using an unprotected guanidine precursor to eliminate deprotection steps. Reaction parameters, including the base system, solvent composition, precursor concentration, and temperature, were optimized under conventional and microwave heating. Radiochemical conversion (RCC) and operational robustness were evaluated, and purification strategies were assessed for automation compatibility. Results: Direct [18F]fluorination using the unprotected precursor reduced the total synthesis time to 60–70 min. Optimal conditions employed a tert-butanol/acetonitrile (4:1) solvent system with K2CO3/Kryptofix222, affording RCC up to 33% under conventional heating. Microwave irradiation further improved efficiency, achieving RCC of up to 64% within 1.5 min at 140 °C. The method showed broad tolerance to variations in the base molar ratio and precursor concentration and enabled isocratic HPLC purification. Conclusions: This one-step radiosynthesis overcomes longstanding challenges in [18F]fluproxadine production by eliminating harsh deprotection and enabling high-yield, automation-ready synthesis, thereby improving clinical feasibility.
en-copyright=
kn-copyright=

en-aut-name=ChenXinyu
en-aut-sei=Chen
en-aut-mei=Xinyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OhtaKaito
en-aut-sei=Ohta
en-aut-mei=Kaito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KimuraHiroyuki
en-aut-sei=Kimura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YagiYusuke
en-aut-sei=Yagi
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SasakiTakanori
en-aut-sei=Sasaki
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NoseNaoko
en-aut-sei=Nose
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AkehiMasaru
en-aut-sei=Akehi
en-aut-mei=Masaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamaneTomohiko
en-aut-sei=Yamane
en-aut-mei=Tomohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=WernerRudolf A.
en-aut-sei=Werner
en-aut-mei=Rudolf A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HiguchiTakahiro
en-aut-sei=Higuchi
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Nuclear Medicine, Faculty of Medicine, University of Augsburg
kn-affil=

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

affil-num=3
en-affil=Agency for Health, Safety and Environment, Kyoto University
kn-affil=

affil-num=4
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

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

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

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

affil-num=8
en-affil=Department of Molecular Imaging Research, Kobe City Medical Center General Hospital
kn-affil=

affil-num=9
en-affil=Department of Nuclear Medicine, LMU Hospital, and German Cancer Consortium (DKTK), Partner Site Munich, Ludwig-Maximilians-University of Munich
kn-affil=

affil-num=10
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=norepinephrine transporter
kn-keyword=norepinephrine transporter
en-keyword=positron emission tomography
kn-keyword=positron emission tomography
en-keyword=[18F]AF78
kn-keyword=[18F]AF78
en-keyword=[18F]fluproxadine
kn-keyword=[18F]fluproxadine
en-keyword=radiolabeling
kn-keyword=radiolabeling
END

start-ver=1.4
cd-journal=joma
no-vol=17
cd-vols=
no-issue=5
article-no=
start-page=e84161
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250515
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pseudoachalasia Due to Malignant Pleural Mesothelioma Involving the Esophagus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We report a rare case of pseudoachalasia secondary to malignant pleural mesothelioma involving the esophagus. A 66-year-old man presented with progressive dysphagia, weight loss, and postprandial hiccups. Endoscopic examination showed esophageal dilation with luminal narrowing at the esophagogastric junction, but no mucosal abnormalities. Computed tomography revealed an irregular-shaped mass extending from the peri-esophagogastric junction to the retroperitoneum, accompanied by pleural effusion, right-sided hydronephrosis, and multiple hepatic lesions. Endoscopic ultrasound-guided fine-needle aspiration from the mass lesion through the esophageal lumen revealed epithelioid malignant mesothelioma. This case highlights the importance of considering malignant mesothelioma in the differential diagnosis of pseudoachalasia, particularly when imaging reveals extrinsic esophageal compression without mucosal lesions.
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=MiyamotoKazuya
en-aut-sei=Miyamoto
en-aut-mei=Kazuya
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=OtsukaMotoyuki
en-aut-sei=Otsuka
en-aut-mei=Motoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

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

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

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

affil-num=5
en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=endoscopic ultrasound-guided fine-needle aspiration
kn-keyword=endoscopic ultrasound-guided fine-needle aspiration
en-keyword=esophageal diseases
kn-keyword=esophageal diseases
en-keyword=esophagogastroduodenoscopy (egd)
kn-keyword=esophagogastroduodenoscopy (egd)
en-keyword=malignant mesothelioma
kn-keyword=malignant mesothelioma
en-keyword=pseudoachalasia
kn-keyword=pseudoachalasia
END

start-ver=1.4
cd-journal=joma
no-vol=3
cd-vols=
no-issue=2
article-no=
start-page=100078
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Erythromelalgia presenting with posterior reversible encephalopathy syndrome: A pediatric case report
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Erythromelalgia is a rare disorder characterized by erythema, warmth, and burning pain in the extremities. We report a pediatric case of erythromelalgia in a patient who developed posterior reversible encephalopathy syndrome (PRES), without any cutaneous signs.<br>
Case presentation: A previously healthy 12-year-old girl presented to our pediatric clinic with burning extremity pain that had persisted for 6 weeks. The patient was treated with analgesics; however, the pain was refractory to these agents. Seven days after the first visit, she developed afebrile seizures and was transferred to our hospital. Her initial blood pressure was 139/105 mmHg (+2.0 SD), and brain magnetic resonance imaging revealed high intensity areas in the bilateral parietal and occipital lobes, leading to a diagnosis of PRES. Her blood pressure was difficult to control with anti-hypertensive agents. Burning pain in her extremities was relieved by cooling and worsened by warming. Although erythema was not observed in her hands or legs, erythromelalgia was suspected based on the characteristic nature of her pain. Intravenous lidocaine was administered for diagnosis, which was dramatically effective. After initiating mexiletine, the burning pain in her extremities disappeared, and hypertension improved. A final diagnosis of erythromelalgia with PRES was made.<br>
Conclusion: A history of temperature-dependent pain relief and deterioration are important indicators of disease diagnosis, even if patients indicate a lack of erythema or warmth. Physicians should be aware that persistent pain due to erythromelalgia can lead to refractory hypertension and development of PRES.
en-copyright=
kn-copyright=

en-aut-name=SuzukiKengo
en-aut-sei=Suzuki
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UdaKazuhiro
en-aut-sei=Uda
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=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=ArakawaKyosuke
en-aut-sei=Arakawa
en-aut-mei=Kyosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShigeharaKenji
en-aut-sei=Shigehara
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ObaraTakafumi
en-aut-sei=Obara
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=

en-aut-name=TsukaharaHirokazu
en-aut-sei=Tsukahara
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

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

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

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

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

affil-num=6
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

affil-num=8
en-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Erythromelalgia
kn-keyword=Erythromelalgia
en-keyword=Posterior reversible encephalopathy syndrome
kn-keyword=Posterior reversible encephalopathy syndrome
en-keyword=Hypertension
kn-keyword=Hypertension
en-keyword=Child
kn-keyword=Child
END

start-ver=1.4
cd-journal=joma
no-vol=115
cd-vols=
no-issue=
article-no=
start-page=13
end-page=26
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260301
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The List of Published by Members of the Faculty From January to December 2025.
kn-title=公表学術論文等リスト　2025
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=2
article-no=
start-page=110
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Slide Annotation System with Multimodal Analysis for Video Presentation Review
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=With the rapid growth of online presentations, there has been an increasing need for efficient review of recorded materials. In typical presentations, speakers verbally elaborate on each slide, providing details not captured in the slides themselves. Automatically extracting and embedding these verbal explanations at their corresponding slide locations can greatly enhance the review process for audiences. This paper presents a Slide Annotation System that employs a robust hybrid two-stage detector to identify slide boundaries, extracts slide text through Optical Character Recognition (OCR), transcribes narration, and employs a multimodal Large Language Model (LLM) to generate concise, context-aware annotations that are added to their corresponding slide locations. For evaluations, the technical performance was validated on five recorded presentations, while the user experience was assessed by 37 participants. The results showed that the system achieved a macro-average 𝐹1 score of 0.879 (𝑆𝐷=0.024, 95% 𝐶𝐼[0.849,0.909]) for slide segmentation and 90.0% accuracy (95% 𝐶𝐼[74.4%,96.5%]) for annotation alignment. Subjective evaluations revealed high annotation validity and usefulness as rated by presenters, and a high System Usability Scale (SUS) score of 80.5 (𝑆𝐷=6.7, 95% 𝐶𝐼[78.3,82.7]). Qualitative feedback further confirmed that the system effectively streamlined the review process, enabling users to locate key information more efficiently than standard video playback. These findings demonstrate the strong potential of the proposed system as an effective automated annotation system.
en-copyright=
kn-copyright=

en-aut-name=HazAmma Liesvarastranta
en-aut-sei=Haz
en-aut-mei=Amma Liesvarastranta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=BrataKomang Candra
en-aut-sei=Brata
en-aut-mei=Komang Candra
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FunabikiNobuo
en-aut-sei=Funabiki
en-aut-mei=Nobuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KyawHtoo Htoo Sandi
en-aut-sei=Kyaw
en-aut-mei=Htoo Htoo Sandi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FajriantiEvianita Dewi
en-aut-sei=Fajrianti
en-aut-mei=Evianita Dewi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SukaridhotoSritrusta
en-aut-sei=Sukaridhoto
en-aut-mei=Sritrusta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Information and Communication Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Information and Communication Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Information and Communication Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Information and Communication Systems, Okayama University
kn-affil=

affil-num=5
en-affil=Human Centric Multimedia Research Laboratory, Department of Informatic and Computer Engineering, Politeknik Elektronika Negeri Surabaya
kn-affil=

affil-num=6
en-affil=Human Centric Multimedia Research Laboratory, Department of Informatic and Computer Engineering, Politeknik Elektronika Negeri Surabaya
kn-affil=
en-keyword=slide annotation
kn-keyword=slide annotation
en-keyword=multimodal analysis
kn-keyword=multimodal analysis
en-keyword=speech-to-text
kn-keyword=speech-to-text
en-keyword=LLM
kn-keyword=LLM
en-keyword=SUS
kn-keyword=SUS
END

start-ver=1.4
cd-journal=joma
no-vol=80
cd-vols=
no-issue=1
article-no=
start-page=47
end-page=54
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202602
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Time Course of the Development and Loss of Delta-9-tetrahydrocannabinol Tolerance: Effects on Hypothermia and Spontaneous Locomotor Activity in Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Deregulation of cannabis use is gradually expanding in Europe and the United States. However, the biological processes driving tolerance to delta-9-tetrahydrocannabinol (Δ9-THC), the main psychoactive component of cannabis, remain unclear. Thus, this study aimed to investigate the mechanisms and time course of tolerance development and loss to Δ9-THC in mice. Male ICR mice (7 weeks old) were administered Δ9-THC once daily for 3 days and then divided into three groups according to the washout period (3-, 10-, and 17-day washout groups). After each washout, changes in body temperature and locomotor activity were measured following re-exposure to Δ9-THC. Furthermore, the mRNA expression levels of CB1 and CB2 receptors in the brain were evaluated using real-time PCR. On day 1, significant hypothermia and reduced spontaneous locomotor activity were observed in the Δ9-THC-treated mice compared with the vehicle-treated mice. Tolerance to the hypothermic and locomotor-suppressing effects of Δ9-THC developed on days 2 and 3, respectively, and dissipated after 3 and 11 days of washout, respectively. These differences in the rates of tolerance development and recovery may reflect distinct underlying mechanisms. No significant changes in receptor mRNA expression were observed. These findings highlight the complexity of Δ9-THC tolerance and its potential implications for long-term cannabis use.
en-copyright=
kn-copyright=

en-aut-name=EguchiYukiomi
en-aut-sei=Eguchi
en-aut-mei=Yukiomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

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

en-aut-name=IrieKeiichi
en-aut-sei=Irie
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamashitaYuta
en-aut-sei=Yamashita
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=EguchiMiyu
en-aut-sei=Eguchi
en-aut-mei=Miyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakanoTakafumi
en-aut-sei=Nakano
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MishimaKenichi
en-aut-sei=Mishima
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
kn-affil=

affil-num=2
en-affil=Department of Emergency and Disaster Medical Pharmacy, Faculty of Pharmaceutical Sciences, Fukuoka University
kn-affil=

affil-num=3
en-affil=Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
kn-affil=

affil-num=4
en-affil=Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
kn-affil=

affil-num=5
en-affil=Department of Emergency and Disaster Medical Pharmacy, Faculty of Pharmaceutical Sciences, Fukuoka University
kn-affil=

affil-num=6
en-affil=Department of Oncology and Infectious Disease Pharmacy, Faculty of Pharmaceutical Sciences, Fukuoka University
kn-affil=

affil-num=7
en-affil=Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
kn-affil=
en-keyword=delta-9-tetrahydrocannabinol
kn-keyword=delta-9-tetrahydrocannabinol
en-keyword=cannabis
kn-keyword=cannabis
en-keyword=tolerance
kn-keyword=tolerance
en-keyword=locomotor
kn-keyword=locomotor
en-keyword=hypothermic
kn-keyword=hypothermic
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=02
article-no=
start-page=113
end-page=125
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=2026
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Clinical genetics in comitant strabismus and idiopathic superior oblique muscle palsy
kn-title=斜視の遺伝子研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=共同性斜視は遺伝要因と環境要因からなる多因子疾患で、内斜視と外斜視に大別される。遺伝要因は家族歴、一卵性双生児の表現型一致率から推定され、環境要因には妊娠・分娩時の低酸素状態がある。一方、遺伝要因がある非共同性（麻痺性）斜視として上斜筋腱低形成を呈する特発性上斜筋麻痺がある。遺伝統計学の連鎖解析を使って、内斜視と外斜視の小家系群で4番染色体MGST2を疾患感受性遺伝子候補と同定し、MGST2ノックアウトマウスを作成した。小動物用MRIで解析すると、そのホモ接合体では野生型と比べて眼球形状が有意に横長で体積が大きいことを見出した。次いで遺伝統計学別法の全ゲノム関連解析を内斜視、外斜視、特発性上斜筋麻痺を対象として行った。Infinium Asian Screening Array-24 v1.0でSNPを決めた内斜視253検体、外斜視356検体、上斜筋麻痺102検体を疾患群とした。対照集団としては、バイオバンクジャパン (BBJ) の疾患群とは違うアレイ(OmniExpress)でSNPを決めた182,476検体「BBJ (180K)」、疾患群と同じアレイでSNPを決めたBBJの53409検体「BBJ (ASA)」および長浜コホート3570検体を使った。３対照集団との比較で共通して検出された遺伝子は、上斜筋麻痺群で神経細胞移動に関与するDAB1であった。最も大きい対照集団「BBJ (180K)」との比較では内斜視、外斜視、上斜筋麻痺を含む疾患群全体で眼発生に関与するRARB (retinoic acid receptor β) が検出された。斜視関連遺伝子は眼球形態に関与する可能性がある。特発性上斜筋麻痺は共同性斜視とは独立した疾患と理解されるが、共通の遺伝基盤もあるかもしれない。
en-copyright=
kn-copyright=

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

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=岡山大学学術研究院ヘルスシステム統合科学学域
en-keyword=双生児調査
kn-keyword=双生児調査
en-keyword=斜視頻度
kn-keyword=斜視頻度
en-keyword=家族歴
kn-keyword=家族歴
en-keyword=全ゲノム関連解析
kn-keyword=全ゲノム関連解析
en-keyword=連鎖解析
kn-keyword=連鎖解析
END

start-ver=1.4
cd-journal=joma
no-vol=33
cd-vols=
no-issue=1
article-no=
start-page=10
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260121
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Bridging the Gap Between Static Histology and Dynamic Organ-on-a-Chip Models
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=For more than a century, pathology has served as a cornerstone of modern medicine, relying primarily on static microscopic assessment of tissue morphology—such as H&E staining—which remains the “gold standard” for disease diagnosis. However, this conventional paradigm provides only a snapshot of disease states and often fails to capture their dynamic evolution and complex functional mechanisms. Moreover, animal models are constrained by marked interspecies differences, creating a persistent gap in translational research. To overcome these limitations, we propose the concept of New Pathophysiology, a research framework that transcends purely morphological descriptions and aims to resolve functional dynamics in real time. This approach integrates Organ-on-a-Chip (OOC) technology, multi-omics analyses, and artificial intelligence to reconstruct the entire course of disease initiation and to enable personalized medicine. In this review, we first outline the foundations and limitations of traditional pathology and animal models. We then systematically summarize more than one hundred existing OOC disease models across multiple organs—including the kidney, liver, and brain. Finally, we elaborate on how OOC technologies are reshaping the study of key pathological processes such as inflammation, metabolic dysregulation, and fibrosis by converting them into dynamic, mechanistic disease models, and we propose future perspectives in the field. This review adopts a relatively uncommon classification strategy based on pathological mechanisms (mechanism-based), rather than organ-based categorization, allowing readers to recognize shared principles underlying different diseases. Moreover, the focus of this work is not on emphasizing iteration or replacement of existing approaches, but on preserving past achievements from a historical perspective, with an emphasis on overcoming current limitations and enabling new advances.
en-copyright=
kn-copyright=

en-aut-name=WangZheyi
en-aut-sei=Wang
en-aut-mei=Zheyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
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=3
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=
en-keyword=new pathophysiology
kn-keyword=new pathophysiology
en-keyword=organ-on-a-chip/OOC
kn-keyword=organ-on-a-chip/OOC
en-keyword=dynamic disease modeling
kn-keyword=dynamic disease modeling
en-keyword=histopathology
kn-keyword=histopathology
en-keyword=large-model analysis
kn-keyword=large-model analysis
en-keyword=personalized medicine
kn-keyword=personalized medicine
END

start-ver=1.4
cd-journal=joma
no-vol=193
cd-vols=
no-issue=
article-no=
start-page=118724
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202512
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Deciphering the structural impact of norepinephrine analog radiopharmaceuticals on organic cation transporter affinity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose: Previous studies have investigated the kinetics and affinities of norepinephrine transporter (NET)-targeting radiotracers, including [123I]MIBG, but the role of organic cation transporters (OCTs) remains unclear. This study aimed to evaluate how the structural design of selective NET-targeting tracers affects OCT-mediated non-specific uptake, identifying factors influencing both NET and OCT affinity.<br>
Methods: Cellular uptake assays were conducted using SK-N-SH cells expressing human NET, and human OCT1-, OCT2-, and OCT3-expressing cells with [3H]norepinephrine, [3H]MPP+, and [131I]MIBG. Competitive uptake assays used non-radioactive reference compounds for several NET-targeting radiopharmaceuticals (MIBG, HED, EPI, PHEN, LMI1195, and PHPG), along with a new PET radiotracer [18F]AF78, and its two analogs with meta-iodide [18F]AF78(I) or hydroxyl group [18F]AF78(OH). Dynamic PET imaging in non-human primates assessed the in vivo uptake of [18F]AF78 after NET inhibition with desipramine.<br>
Results: Monoamine-based tracers (EPI, PHEN, HED) exhibited high NET selectivity with minimal OCTs interaction, while guanidine-containing tracers (e.g., MIBG, LMI1195) displayed substantial OCTs affinity. Lower lipophilicity in guanidine-containing compounds, influenced by substitutions on the benzene ring (e.g., PHPG, AF78), correlated with weaker OCT interactions. PET imaging confirmed that cardiac uptake of [18F]AF78 is sensitive to desipramine pretreatment (***P < 0.0005), indicating its NET-specificity, while persistent hepatic retention suggests an OCT-mediated transport mechanism.<br>
Conclusion: This study highlights the critical influence of the compounds’ chemical structure on NET and OCT affinities. Structural modifications that reduce OCT-mediated uptake while maintaining high NET affinity could improve the specificity and theranostic potential of NET-targeting ligands. These findings provide insights for designing next-generation radiotracers with enhanced selectivity and clinical utility.
en-copyright=
kn-copyright=

en-aut-name=MühligSaskia
en-aut-sei=Mühlig
en-aut-mei=Saskia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ChenXinyu
en-aut-sei=Chen
en-aut-mei=Xinyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TutovAnna
en-aut-sei=Tutov
en-aut-mei=Anna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NoseNaoko
en-aut-sei=Nose
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=LapaConstantin
en-aut-sei=Lapa
en-aut-mei=Constantin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WernerRudolf A.
en-aut-sei=Werner
en-aut-mei=Rudolf A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=DeckerMichael
en-aut-sei=Decker
en-aut-mei=Michael
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HiguchiTakahiro
en-aut-sei=Higuchi
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Nuclear Medicine and Comprehensive Heart Failure Center, University Hospital Würzburg
kn-affil=

affil-num=2
en-affil=Nuclear Medicine, Faculty of Medicine, University of Augsburg
kn-affil=

affil-num=3
en-affil=Pharmaceutical and Medicinal Chemistry, Institute of Pharmacy and Food Chemistry, University of Würzburg
kn-affil=

affil-num=4
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Nuclear Medicine, Faculty of Medicine, University of Augsburg
kn-affil=

affil-num=6
en-affil=Department of Nuclear Medicine, LMU Hospital, Ludwig-Maximilians-University of Munich
kn-affil=

affil-num=7
en-affil=Pharmaceutical and Medicinal Chemistry, Institute of Pharmacy and Food Chemistry, University of Würzburg
kn-affil=

affil-num=8
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Norepinephrine transporter
kn-keyword=Norepinephrine transporter
en-keyword=Organic cation transporter
kn-keyword=Organic cation transporter
en-keyword=Neuroendocrine tumor
kn-keyword=Neuroendocrine tumor
en-keyword=Competitive cell uptake
kn-keyword=Competitive cell uptake
en-keyword=PET radiotracer
kn-keyword=PET radiotracer
END

start-ver=1.4
cd-journal=joma
no-vol=64
cd-vols=
no-issue=20
article-no=
start-page=4309
end-page=4317
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251009
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Characterization of Autonomous and Ca2+/Calmodulin-Dependent Activities of CaMKK Isoforms In Vitro and in Mouse Tissues
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ca2+/CaM-dependent protein kinase kinase (CaMKK) phosphorylates and activates downstream kinases, including CaMKI, CaMKIV, PKB, and AMPK, regulating various cellular functions such as neuronal morphogenesis, metabolic control, and pathophysiological pathways, such as cancer progression. CaMKKα/1 is tightly regulated by an autoinhibitory mechanism. CaMKKβ/2 activity is highly Ca2+/CaM-independent (autonomous activity) in vitro and Ca2+/CaM-dependent in cultured cells. Whether these two activity states of CaMKKβ/2 exist in vivo and the detailed regulatory mechanisms for the transition of both activity states remain unclear due to the difficulty in distinguishing the two activity states. In this study, we detected Ca2+-dependent and autonomous CaMKK activity in HeLa cells and successfully separated both activity states of CaMKKβ/2 in mouse brain and testis extracts using a recently developed CaMKK inhibitor (TIM-063)-coupled sepharose, which binds to the catalytic domain in the active state but not in the autoinhibited state. Furthermore, lambda protein phosphatase treatment converted the Ca2+/CaM-dependent form to the autonomous form of CaMKKβ/2, which was not affected by Ala mutation of Ser128, Ser132, and Ser136. The two activity forms of CaMKKβ/2 had equivalent Ca2+/CaM-binding ability. The findings demonstrate the presence of autonomous and Ca2+/CaM-dependent forms of CaMKKβ/2 independently in mouse tissues and cultured cells. The transition of these states of CaMKKβ/2 may be dynamically regulated by the phosphorylation/dephosphorylation of serine residues in the N-terminal regulatory domain.
en-copyright=
kn-copyright=

en-aut-name=OhtsukaSatomi
en-aut-sei=Ohtsuka
en-aut-mei=Satomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ChenYerun
en-aut-sei=Chen
en-aut-mei=Yerun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
ORCID=

en-aut-name=IshikawaTeruhiko
en-aut-sei=Ishikawa
en-aut-mei=Teruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakagamiHiroyuki
en-aut-sei=Sakagami
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SuizuFutoshi
en-aut-sei=Suizu
en-aut-mei=Futoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TokumitsuHiroshi
en-aut-sei=Tokumitsu
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

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

affil-num=2
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

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

affil-num=4
en-affil=Department of Science Education, Graduate School of Education, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Anatomy, Kitasato University School of Medicine
kn-affil=

affil-num=6
en-affil=Clinical Examination Department, Kagawa Prefectural University of Health Sciences
kn-affil=

affil-num=7
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=64
cd-vols=
no-issue=12
article-no=
start-page=1811
end-page=1825
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250926
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Evaluation of Fentanyl-Emerged Adverse Events and Pharmacokinetics in Neonates: A Physiologically Based Pharmacokinetic Modeling Approach
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Despite its common use for analgesia in neonatal intensive care units, the optimal dosing and safety profile of fentanyl, particularly regarding suspected fentanyl-emerged adverse events (FEAEs), such as hypotension, desaturation, and oliguria, are not well-defined.<br>
Objective This study aimed to develop an optimal therapeutic monitoring and dosing strategy for fentanyl for neonates. A physiologically based pharmacokinetic (PBPK) model for predicting fentanyl pharmacokinetics across various populations, including preterm and term neonates, was developed, and the relationship between predicted fentanyl exposure and FEAE incidence in neonates was assessed.<br>
Methods A PBPK model was developed and validated against the observed values in the literature. The model’s predictive accuracy for fentanyl pharmacokinetics and association with FEAE incidence in an external retrospective cohort of Japanese neonates was evaluated using the predicted concentrations and pharmacokinetic parameters estimated by PBPK simulation.<br>
Results The PBPK model exhibited reasonable predictive performance for serum fentanyl concentrations in actual neonatal patients (mean error: 9.27% [standard error: 5.06%], root mean squared error: 54.7%). The incidence of any FEAE, particularly oxygen desaturation, was associated with the fentanyl concentration-to-dose ratio, but not with some exposure parameters, such as the area under the curve and maximum concentration. The recommended reduced infusion rate allowed serum fentanyl concentrations to fall within the ranges established by the reported values and our data.<br>
Conclusions Our PBPK model and proposed dosing strategy may contribute to safer and more effective fentanyl use in neonates.
en-copyright=
kn-copyright=

en-aut-name=MahdyWalaa Yousef Bassyouni
en-aut-sei=Mahdy
en-aut-mei=Walaa Yousef Bassyouni
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamamotoKazuhiro
en-aut-sei=Yamamoto
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=JojiRisa
en-aut-sei=Joji
en-aut-mei=Risa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HashimotoMari
en-aut-sei=Hashimoto
en-aut-mei=Mari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakasoneRuka
en-aut-sei=Nakasone
en-aut-mei=Ruka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FujiokaKazumichi
en-aut-sei=Fujioka
en-aut-mei=Kazumichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ItoharaKotaro
en-aut-sei=Itohara
en-aut-mei=Kotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KitahiroYumi
en-aut-sei=Kitahiro
en-aut-mei=Yumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OmuraTomohiro
en-aut-sei=Omura
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YanoIkuko
en-aut-sei=Yano
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Pharmacy, Kobe University Hospital
kn-affil=

affil-num=2
en-affil=Department of Integrated Clinical and Basic Pharmaceutical Sciences, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

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

affil-num=4
en-affil=Department of Pharmacy, Kobe University Hospital
kn-affil=

affil-num=5
en-affil=Department of Pediatrics, Graduate School of Medicine, Kobe University
kn-affil=

affil-num=6
en-affil=Department of Pediatrics, Graduate School of Medicine, Kobe University
kn-affil=

affil-num=7
en-affil=Department of Pharmacy, Kobe University Hospital
kn-affil=

affil-num=8
en-affil=Department of Pharmacy, Kobe University Hospital
kn-affil=

affil-num=9
en-affil=Department of Pharmacy, Kobe University Hospital
kn-affil=

affil-num=10
en-affil=Department of Pharmacy, Kobe University Hospital
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=46
cd-vols=
no-issue=1
article-no=
start-page=25
end-page=38
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Near-infrared Photoimmunotherapy Targeting High-risk Human Neuroblastoma Cells Expressing GD2
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/Aim: Neuroblastoma (NB) is a primary malignant tumor of the peripheral sympathetic nervous system in infancy. Despite advances in treatment, the prognosis remains poor for high-risk NB patients. Although immunotherapy using anti-GD2 antibodies is available for high-risk NB, the therapeutic efficacy is insufficient. Near-infrared photoimmunotherapy (NIR-PIT) is an antitumor strategy that induces tumor-specific cytotoxicity by combining an antibody-photoabsorber conjugate (APC) with NIR light irradiation. In this study, we investigated the therapeutic efficacy of GD2-targeted NIR-PIT against human NB cells.<br>
Materials and Methods: GD2 expression was analyzed on the surface of high-risk human NB cells (CHP-134, LA-N-5, IMR-32) and non-high-risk human NB cells (SK-N-SH) by flow cytometry. The APC was synthesized by incubating anti-GD2 antibody and IR700. The cytotoxic effect of GD2-targeted NIR-PIT was evaluated using the XTT assay. The distribution of dead cells within tumor spheres was evaluated using a live/dead assay. The in vivo antitumor effect of GD2-targeted NIR-PIT was assessed using a subcutaneous human NB xenograft tumor model.<br>
Results: GD2 protein was expressed on the surface of CHP-134, LA-N-5, and IMR-32 cells but not SK-N-SH cells. GD2-targeted NIR-PIT significantly suppressed the viability of GD2-positive NB cells but not GD2-negative NB cells, compared to the control and monotherapy groups. GD2-targeted NIR-PIT significantly reduced the volume of GD2-positive CHP-134 tumor spheres by inducing the accumulation of dead cells. Subcutaneous CHP-134 xenograft tumor models demonstrated that GD2-targeted NIR-PIT significantly inhibited tumor growth compared with the control and monotherapy groups.<br>
Conclusion: GD2-targeted NIR-PIT is a promising antitumor strategy for treating high-risk NB tumors expressing GD2.
en-copyright=
kn-copyright=

en-aut-name=NOUSOHIROSHI
en-aut-sei=NOUSO
en-aut-mei=HIROSHI
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=TANIMOTOTERUTAKA
en-aut-sei=TANIMOTO
en-aut-mei=TERUTAKA
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TANIMORIMICHI
en-aut-sei=TANI
en-aut-mei=MORIMICHI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WATANABEHINAKO
en-aut-sei=WATANABE
en-aut-mei=HINAKO
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OYAMATAKANORI
en-aut-sei=OYAMA
en-aut-mei=TAKANORI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NOMAKAZUHIRO
en-aut-sei=NOMA
en-aut-mei=KAZUHIRO
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KAGAWASHUNSUKE
en-aut-sei=KAGAWA
en-aut-mei=SHUNSUKE
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KOBAYASHIHISATAKA
en-aut-sei=KOBAYASHI
en-aut-mei=HISATAKA
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NODATAKUO
en-aut-sei=NODA
en-aut-mei=TAKUO
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
ORCID=

en-aut-name=FUJIWARATOSHIYOSHI
en-aut-sei=FUJIWARA
en-aut-mei=TOSHIYOSHI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

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

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

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

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

affil-num=7
en-affil=Department of Pediatric 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=Molecular Imaging Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health
kn-affil=

affil-num=10
en-affil=Department of Pediatric 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=
en-keyword=Neuroblastoma 
kn-keyword=Neuroblastoma 
en-keyword=GD2
kn-keyword=GD2
en-keyword=near-infrared photoimmunotherapy
kn-keyword=near-infrared photoimmunotherapy
en-keyword=IR700
kn-keyword=IR700
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=
article-no=
start-page=RP99936
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250811
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Redistribution of fragmented mitochondria ensures symmetric organelle partitioning and faithful chromosome segregation in mitotic mouse zygotes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In cleavage-stage embryos, preexisting organelles partition evenly into daughter blastomeres without significant cell growth after symmetric cell division. The presence of mitochondrial DNA within mitochondria and its restricted replication during preimplantation development makes their inheritance particularly important. While chromosomes are precisely segregated by the mitotic spindle, the mechanisms controlling mitochondrial partitioning remain poorly understood. In this study, we investigate the mechanism by which Dynamin-related protein 1 (Drp1) controls the mitochondrial redistribution and partitioning during embryonic cleavage. Depletion of Drp1 in mouse zygotes causes marked mitochondrial aggregation, and the majority of embryos arrest at the 2 cell stage. Clumped mitochondria are located in the center of mitotic Drp1-depleted zygotes with less uniform distribution, thereby preventing their symmetric partitioning. Asymmetric mitochondrial inheritance is accompanied by functionally inequivalent blastomeres with biased ATP and endoplasmic reticulum Ca2+ levels. We also find that marked mitochondrial centration in Drp1-depleted zygotes prevents the assembly of parental chromosomes, resulting in chromosome segregation defects and binucleation. Thus, mitochondrial fragmentation mediated by Drp1 ensures proper organelle positioning and partitioning into functional daughters during the first embryonic cleavage.
en-copyright=
kn-copyright=

en-aut-name=GekkoHaruna
en-aut-sei=Gekko
en-aut-mei=Haruna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NomuraRuri
en-aut-sei=Nomura
en-aut-mei=Ruri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KuzuharaDaiki
en-aut-sei=Kuzuhara
en-aut-mei=Daiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KaneyasuMasato
en-aut-sei=Kaneyasu
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KosekiGenpei
en-aut-sei=Koseki
en-aut-mei=Genpei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AdhikariDeepak
en-aut-sei=Adhikari
en-aut-mei=Deepak
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MioYasuyuki
en-aut-sei=Mio
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=CarrollJohn
en-aut-sei=Carroll
en-aut-mei=John
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KonoTomohiro
en-aut-sei=Kono
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
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=11
ORCID=

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

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

affil-num=3
en-affil=Reproductive Centre, Mio Fertility Clinic
kn-affil=

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

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

affil-num=6
en-affil=Development and Stem Cell Program and Department of Anatomy and Developmental Biology, Monash Biomedicine Discovery Institute, Monash University
kn-affil=

affil-num=7
en-affil=Reproductive Centre, Mio Fertility Clinic
kn-affil=

affil-num=8
en-affil=Development and Stem Cell Program and Department of Anatomy and Developmental Biology, Monash Biomedicine Discovery Institute, Monash University
kn-affil=

affil-num=9
en-affil=Department of Bioscience, Tokyo University of Agriculture
kn-affil=

affil-num=10
en-affil=Department of Animal Science, Graduate School of Environment and Life Science, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Animal Science, Graduate School of Environment and Life Science, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=1
article-no=
start-page=1720
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251205
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A genome-wide association study identifies the GPM6A locus associated with age at onset in ALS
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Amyotrophic lateral sclerosis (ALS) exhibits considerable clinical variability, such as differences in age at onset (AAO). Multiple factors, including genetic factors, may underlie this variability; however, the specific determinants remain unclear. To identify genes affecting AAO, we have conducted a genome-wide association study in Japanese patients with ALS (discovery cohort: n = 1808; replication cohort: n = 207). Here, we show that the minor A allele of rs113161727 at the ADAM29-GPM6A locus is associated with a younger AAO in the discovery cohort (effect, -4.27 years; p = 4.60 × 10-8); this finding has been confirmed in the replication cohort (p = 0.0068) and meta-analysis (p = 1.08 × 10−9). Among 65 ALS patients with a SOD1 mutation, the AAO has been found to be 10.2 years younger in those with the A allele than in those without it (p = 0.002). This variant correlates with GPM6A upregulation in iPSC-derived motor neurons, suggesting GPM6A as a candidate AAO modifier. Overall, our study highlights the impact of genetic modifiers on ALS heterogeneity and provides a potential target for delaying disease onset.
en-copyright=
kn-copyright=

en-aut-name=NakamuraRyoichi
en-aut-sei=Nakamura
en-aut-mei=Ryoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TohnaiGenki
en-aut-sei=Tohnai
en-aut-mei=Genki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AtsutaNaoki
en-aut-sei=Atsuta
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MatsudaYumi
en-aut-sei=Matsuda
en-aut-mei=Yumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MorimotoSatoru
en-aut-sei=Morimoto
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ItoDaisuke
en-aut-sei=Ito
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KatsunoMasahisa
en-aut-sei=Katsuno
en-aut-mei=Masahisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IzumiYuishin
en-aut-sei=Izumi
en-aut-mei=Yuishin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MoritaMitsuya
en-aut-sei=Morita
en-aut-mei=Mitsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=IwataIkuko
en-aut-sei=Iwata
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YabeIchiro
en-aut-sei=Yabe
en-aut-mei=Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NakazatoTomoko
en-aut-sei=Nakazato
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=HattoriNobutaka
en-aut-sei=Hattori
en-aut-mei=Nobutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=HirayamaTakehisa
en-aut-sei=Hirayama
en-aut-mei=Takehisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=KanoOsamu
en-aut-sei=Kano
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=TamuraAsako
en-aut-sei=Tamura
en-aut-mei=Asako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=SuzukiNaoki
en-aut-sei=Suzuki
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=AokiMasashi
en-aut-sei=Aoki
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=ShibuyaKazumoto
en-aut-sei=Shibuya
en-aut-mei=Kazumoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=KuwabaraSatoshi
en-aut-sei=Kuwabara
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=OdaMasaya
en-aut-sei=Oda
en-aut-mei=Masaya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=HashimotoRina
en-aut-sei=Hashimoto
en-aut-mei=Rina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=AibaIkuko
en-aut-sei=Aiba
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=IshiharaTomohiko
en-aut-sei=Ishihara
en-aut-mei=Tomohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=OnoderaOsamu
en-aut-sei=Onodera
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
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=26
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=27
ORCID=

en-aut-name=BokudaKota
en-aut-sei=Bokuda
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=ShimizuToshio
en-aut-sei=Shimizu
en-aut-mei=Toshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
ORCID=

en-aut-name=IkedaYoshio
en-aut-sei=Ikeda
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

en-aut-name=HasegawaKazuko
en-aut-sei=Hasegawa
en-aut-mei=Kazuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=31
ORCID=

en-aut-name=TanakaFumiaki
en-aut-sei=Tanaka
en-aut-mei=Fumiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=32
ORCID=

en-aut-name=YokotaTakanori
en-aut-sei=Yokota
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=33
ORCID=

en-aut-name=KanaiKazuaki
en-aut-sei=Kanai
en-aut-mei=Kazuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=34
ORCID=

en-aut-name=NotoYu-ichi
en-aut-sei=Noto
en-aut-mei=Yu-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=35
ORCID=

en-aut-name=KajiRyuji
en-aut-sei=Kaji
en-aut-mei=Ryuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=36
ORCID=

en-aut-name=WatanabeHirohisa
en-aut-sei=Watanabe
en-aut-mei=Hirohisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=37
ORCID=

en-aut-name=KonishiTomoko
en-aut-sei=Konishi
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=38
ORCID=

en-aut-name=HasegawaMikiko
en-aut-sei=Hasegawa
en-aut-mei=Mikiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=39
ORCID=

en-aut-name=FukayaHozuki
en-aut-sei=Fukaya
en-aut-mei=Hozuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=40
ORCID=

en-aut-name=NiwaJun-ichi
en-aut-sei=Niwa
en-aut-mei=Jun-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=41
ORCID=

en-aut-name=DoyuManabu
en-aut-sei=Doyu
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=42
ORCID=

en-aut-name=OkadaYohei
en-aut-sei=Okada
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=43
ORCID=

en-aut-name=NakamuraShiho
en-aut-sei=Nakamura
en-aut-mei=Shiho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=44
ORCID=

en-aut-name=OzawaFumiko
en-aut-sei=Ozawa
en-aut-mei=Fumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=45
ORCID=

en-aut-name=OkanoHideyuki
en-aut-sei=Okano
en-aut-mei=Hideyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=46
ORCID=

en-aut-name=NakatochiMasahiro
en-aut-sei=Nakatochi
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=47
ORCID=

en-aut-name=SobueGen
en-aut-sei=Sobue
en-aut-mei=Gen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=48
ORCID=

affil-num=1
en-affil=Department of Neurology, Aichi Medical University School of Medicine
kn-affil=

affil-num=2
en-affil=Division of ALS Research, Aichi Medical University School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Neurology, Aichi Medical University School of Medicine
kn-affil=

affil-num=4
en-affil=Public Health Informatics Unit, Department of Integrated Health Sciences, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=5
en-affil=Keio University Regenerative Medicine Research Center, Kawasaki
kn-affil=

affil-num=6
en-affil=Department of Neurology, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=Department of Neurology, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Neurology, Tokushima University Graduate School of Biomedical Sciences
kn-affil=

affil-num=9
en-affil=Division of Neurology, Department of Internal Medicine, Jichi Medical University
kn-affil=

affil-num=10
en-affil=Department of Neurology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University
kn-affil=

affil-num=11
en-affil=Department of Neurology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University
kn-affil=

affil-num=12
en-affil=Department of Neurology, Juntendo University School of Medicine
kn-affil=

affil-num=13
en-affil=Department of Neurology, Juntendo University School of Medicine
kn-affil=

affil-num=14
en-affil=Department of Neurology, Toho University Faculty of Medicine
kn-affil=

affil-num=15
en-affil=Department of Neurology, Toho University Faculty of Medicine
kn-affil=

affil-num=16
en-affil=Department of Neurology, Mie University Graduate School of Medicine
kn-affil=

affil-num=17
en-affil=Department of Neurology, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=18
en-affil=Department of Neurology, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=19
en-affil=Department of Neurology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=20
en-affil=Department of Neurology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=21
en-affil=Department of Neurology, Vihara Hananosato Hospital
kn-affil=

affil-num=22
en-affil=Department of Neurology, NHO Higashinagoya National Hospital
kn-affil=

affil-num=23
en-affil=Department of Neurology, NHO Higashinagoya National Hospital
kn-affil=

affil-num=24
en-affil=Department of Neurology, Brain Research Institute, Niigata University
kn-affil=

affil-num=25
en-affil=Department of Neurology, Brain Research Institute, Niigata University
kn-affil=

affil-num=26
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=27
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=28
en-affil=Department of Neurology, Tokyo Metropolitan Neurological Hospital
kn-affil=

affil-num=29
en-affil=Department of Neurology, Tokyo Metropolitan Neurological Hospital
kn-affil=

affil-num=30
en-affil=Department of Neurology, Gunma University Graduate School of Medicine
kn-affil=

affil-num=31
en-affil=Division of Neurology, NHO Sagamihara National Hospital
kn-affil=

affil-num=32
en-affil=Department of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine
kn-affil=

affil-num=33
en-affil=Department of Neurology and Neurological Science, NucleoTIDE and PepTIDE Drug Discovery Center (TIDE), Institute of Science Tokyo
kn-affil=

affil-num=34
en-affil=Department of Neurology, Fukushima Medical University School of Medicine
kn-affil=

affil-num=35
en-affil=Department of Neurology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=36
en-affil=Department of Neurology, Tokushima University Graduate School of Biomedical Sciences
kn-affil=

affil-num=37
en-affil=Department of Neurology, Fujita Health University
kn-affil=

affil-num=38
en-affil=Division of ALS Research, Aichi Medical University School of Medicine
kn-affil=

affil-num=39
en-affil=Division of ALS Research, Aichi Medical University School of Medicine
kn-affil=

affil-num=40
en-affil=Division of ALS Research, Aichi Medical University School of Medicine
kn-affil=

affil-num=41
en-affil=Department of Neurology, Aichi Medical University School of Medicine
kn-affil=

affil-num=42
en-affil=Department of Neurology, Aichi Medical University School of Medicine
kn-affil=

affil-num=43
en-affil=Department of Neurology, Aichi Medical University School of Medicine
kn-affil=

affil-num=44
en-affil=Keio University Regenerative Medicine Research Center, Kawasaki
kn-affil=

affil-num=45
en-affil=Keio University Regenerative Medicine Research Center, Kawasaki
kn-affil=

affil-num=46
en-affil=Keio University Regenerative Medicine Research Center, Kawasaki
kn-affil=

affil-num=47
en-affil=Public Health Informatics Unit, Department of Integrated Health Sciences, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=48
en-affil=Division of ALS Research, Aichi Medical University School of Medicine
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=
article-no=
start-page=489
end-page=492
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=Favorable outcomes of epilepsy with gait-induced seizures after resection of the unilateral supplementary motor area
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Gait-induced seizures are a rare manifestation of reflex epilepsy. Pathophysiology of this phenomenon has not been fully understood.<br>
Case presentation: A 28-year-old woman presented with a long history of “falls” following paroxysmal bilateral leg stiffness triggered by walking. Scalp electroencephalogram (EEG) revealed low-amplitude rhythmic beta activity, maximal at the Cz electrode, during these events. Magnetoencephalography demonstrated repetitive sharp waves source-localized to the right primary motor cortex. Multiple anti-seizure medications failed to improve her symptoms; however, the clinical manifestation was consistent with epilepsy with gait-induced seizures. Intracranial subdural EEG recording was performed and confirmed ictal activity originating from the right supplementary motor area. Resection of this area resulted in complete resolution of her symptoms.<br>
Discussion: This is the first reported case of successful resective surgery for epilepsy with gait-induced seizure. Brain networks involving cortical regions responsible for the initiation or execution of walking presumably played a key role in the generation of gait-induced seizures. Careful assessment using non-invasive neurophysiological studies facilitated accurate diagnosis, successful intracranial recordings, and effective resective surgery.
en-copyright=
kn-copyright=

en-aut-name=KodamaSatoshi
en-aut-sei=Kodama
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KuniiNaoto
en-aut-sei=Kunii
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShirotaYuichiro
en-aut-sei=Shirota
en-aut-mei=Yuichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ChouTakusei
en-aut-sei=Chou
en-aut-mei=Takusei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KawaiMizuho
en-aut-sei=Kawai
en-aut-mei=Mizuho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShimadaSeijiro
en-aut-sei=Shimada
en-aut-mei=Seijiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MaedaMeiko
en-aut-sei=Maeda
en-aut-mei=Meiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

en-aut-name=HamadaMasashi
en-aut-sei=Hamada
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=IkemuraMasako
en-aut-sei=Ikemura
en-aut-mei=Masako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SaitoYuko
en-aut-sei=Saito
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=AkamatsuNaoki
en-aut-sei=Akamatsu
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=UeharaTaira
en-aut-sei=Uehara
en-aut-mei=Taira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=SaitoNobuhito
en-aut-sei=Saito
en-aut-mei=Nobuhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurosurgery, Jichi Medical University
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=5
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=6
en-affil=Department of Neurosurgery, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

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

affil-num=9
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=10
en-affil=Department of Pathology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=11
en-affil=Department of Neuropahtology (Brain Bank for Aging Research), Tokyo Metropoliran Institute for Geriatrics and Gerontology
kn-affil=

affil-num=12
en-affil=Department of Neurology, International University of Health and Walfare Narita Hospital
kn-affil=

affil-num=13
en-affil=Department of Neurology, International University of Health and Walfare Narita Hospital
kn-affil=

affil-num=14
en-affil=Department of Neurosurgery, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=15
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
en-keyword=Reflex epilepsy
kn-keyword=Reflex epilepsy
en-keyword=Intracranial electroencephalogram (EEG)
kn-keyword=Intracranial electroencephalogram (EEG)
en-keyword=Electrocorticogram
kn-keyword=Electrocorticogram
en-keyword=magnetoencephalogram (MEG)
kn-keyword=magnetoencephalogram (MEG)
en-keyword=SMA
kn-keyword=SMA
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=20251203
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Novel in-frame duplication variant of SOD1 in a Japanese family with familial amyotrophic lateral sclerosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objectives: To analyze the cases of a family with a novel in-frame duplication variant (NM_000454.5:c.357_357 + 2dup, p.Val120dup) of SOD1 and a structural model of the mutated SOD1 protein. Methods: The clinical profiles of three patients in the family were analyzed, including the neuropathological findings of the proband’s mother. Genetic analyses were conducted for three patients. cDNA and in silico structural analyses were performed to evaluate the effects of duplication variants on the structure of SOD1. Results: The clinical features of the patients included predominant involvement of the lower motor neurons, asymmetric onset of motor symptoms in the lower limbs, and a relatively rapid progression of muscular weakness and respiratory insufficiency. Neuropathological findings revealed severe loss of spinal cord motor neurons, and immunohistochemistry using an anti-misfolded SOD1 antibody revealed aggregates in the spinal cord. Genetic analyses revealed a c.357_357 + 2dup at the exon 4–intron 4 boundary of SOD1 in three patients. cDNA analysis of the proband suggested the presence of a valine (p.Val120dup) duplication in the heterozygous state, and the SOD1 transcript level showed no significant differences from those of healthy controls. In silico structural analyses predicted that p.Val120dup could affect the structure of the β-barrels and copper ion binding site of SOD1, suggesting an abnormal conformation of SOD1 that is predicted to interfere with the binding of copper ions. Conclusion: We identified a novel in-frame duplication variant in the C-terminus of β7 of SOD1. This genotype–structure–phenotype study of SOD1 provides valuable insights into disease-causing mechanisms.
en-copyright=
kn-copyright=

en-aut-name=NakajimaMasanori
en-aut-sei=Nakajima
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NaruseHiroya
en-aut-sei=Naruse
en-aut-mei=Hiroya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=RikuYuichi
en-aut-sei=Riku
en-aut-mei=Yuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=UedaKunihiro
en-aut-sei=Ueda
en-aut-mei=Kunihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MatsukawaTakashi
en-aut-sei=Matsukawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MitsuiJun
en-aut-sei=Mitsui
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakamuraYoshitsugu
en-aut-sei=Nakamura
en-aut-mei=Yoshitsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IshidaShimon
en-aut-sei=Ishida
en-aut-mei=Shimon
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YamadaTakashi
en-aut-sei=Yamada
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MoroNaoki
en-aut-sei=Moro
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KotsukiNaoki
en-aut-sei=Kotsuki
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NagaiKentaro
en-aut-sei=Nagai
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TokushigeShin-ichi
en-aut-sei=Tokushige
en-aut-mei=Shin-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=UchiboriAyumi
en-aut-sei=Uchibori
en-aut-mei=Ayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=OishiChizuko
en-aut-sei=Oishi
en-aut-mei=Chizuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=YabataHiroyuki
en-aut-sei=Yabata
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=UrushitaniMakoto
en-aut-sei=Urushitani
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=IwasakiYasushi
en-aut-sei=Iwasaki
en-aut-mei=Yasushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
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=19
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=TsujiShoji
en-aut-sei=Tsuji
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=IchikawaYaeko
en-aut-sei=Ichikawa
en-aut-mei=Yaeko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

affil-num=1
en-affil=Department of Neurology, Kyorin University School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=5
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=6
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=7
en-affil=Division of Neurology, Department of Internal Medicine IV, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=8
en-affil=Division of Neurology, Department of Internal Medicine IV, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=9
en-affil=Department of Pathology, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=10
en-affil=Department of Neurology, Kyorin University School of Medicine
kn-affil=

affil-num=11
en-affil=Department of Neurology, Kyorin University School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Neurology, Kyorin University School of Medicine
kn-affil=

affil-num=13
en-affil=Department of Neurology, Kyorin University School of Medicine
kn-affil=

affil-num=14
en-affil=Department of Neurology, Kyorin University School of Medicine
kn-affil=

affil-num=15
en-affil=Department of Neurology, Kyorin University School of Medicine
kn-affil=

affil-num=16
en-affil=Department of Neurology, Shiga University of Medical Science
kn-affil=

affil-num=17
en-affil=Department of Neurology, Shiga University of Medical Science
kn-affil=

affil-num=18
en-affil=Department of Neuropathology, Institute for Medical Science of Aging, Aichi Medical University
kn-affil=

affil-num=19
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan;Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=20
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=21
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=22
en-affil=Department of Neurology, Kyorin University School of Medicine
kn-affil=
en-keyword=Familial amyotrophic lateral sclerosis
kn-keyword=Familial amyotrophic lateral sclerosis
en-keyword=SOD1
kn-keyword=SOD1
en-keyword=in-frame duplication
kn-keyword=in-frame duplication
en-keyword=protein structure
kn-keyword=protein structure
en-keyword=misfolded protein
kn-keyword=misfolded protein
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=20251114
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dorsolateral Cervical Cord T2 Hyperintensity in KIF1C-Related Disease (Spastic Paraplegia 58): Two Long-Duration Cases
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pathogenic variants in KIF1C cause Spastic Paraplegia 58 (SPG58), typically presenting with cerebellar ataxia and spastic paraparesis. We report two unrelated patients with spastic paraparesis, cerebellar ataxia, and tremor. Whole-exome sequence analysis identified novel homozygous variants in the motor domain of KIF1C (NM_006612.6): c.921G>A (p.Trp307Ter) and c.607C>T (p.Arg203Trp). In addition to the canonical brain MRI showing leukoencephalopathy with posterior dominance and hyperintensity along the corticospinal tracts, both patients showed symmetric T2 hyperintensity confined to the lateral and dorsal columns of the cervical cord. Given the long disease durations (22 and 51 years), these findings may represent late-emerging or previously overlooked spinal cord involvement and broaden the neuroradiological spectrum of SPG58.
en-copyright=
kn-copyright=

en-aut-name=MitsutakeAkihiko
en-aut-sei=Mitsutake
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OsakiMasao
en-aut-sei=Osaki
en-aut-mei=Masao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MatsukawaTakashi
en-aut-sei=Matsukawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OsakoMiho
en-aut-sei=Osako
en-aut-mei=Miho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakeuchiChisen
en-aut-sei=Takeuchi
en-aut-mei=Chisen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

en-aut-name=MitsuiJun
en-aut-sei=Mitsui
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KurokawaRyo
en-aut-sei=Kurokawa
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MoriHarushi
en-aut-sei=Mori
en-aut-mei=Harushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TakahashiYuji
en-aut-sei=Takahashi
en-aut-mei=Yuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=GotoJun
en-aut-sei=Goto
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TsujiShoji
en-aut-sei=Tsuji
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Department of Neurology, Tokyo Metropolitan Kita Medical and Rehabilitation Center for the Disabled
kn-affil=

affil-num=5
en-affil=Department of Neurology, Tokyo Metropolitan Kita Medical and Rehabilitation Center for the Disabled
kn-affil=

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

affil-num=7
en-affil=Department of Precision Medicine Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=8
en-affil=Department of Radiology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=9
en-affil=Department of Radiology, School of Medicine, Jichi Medical University
kn-affil=

affil-num=10
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=11
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=12
en-affil=Institute of Medical Genomics, International University of Health and Welfare
kn-affil=

affil-num=13
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
en-keyword=cerebellar ataxia
kn-keyword=cerebellar ataxia
en-keyword=hereditary spastic paraplegia
kn-keyword=hereditary spastic paraplegia
en-keyword=KIF1C
kn-keyword=KIF1C
en-keyword=leukoencephalopathy
kn-keyword=leukoencephalopathy
END

start-ver=1.4
cd-journal=joma
no-vol=194
cd-vols=
no-issue=
article-no=
start-page=50
end-page=62
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202601
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Increasing visual uncertainty modulates multisensory decision-making
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The brain integrates and transforms information from multiple senses to make optimal decisions, a process that is critical for navigating complex environments with perceptual uncertainty. Despite a growing consensus that individuals adapt flexibly to uncertain sensory input, whether increasing visual uncertainty influences the decision process itself or other, non-decision sensory processes during multisensory decision-making are unclear. Here, an audiovisual categorization task was used to examine the responses of human participants (N = 30) to visual and audiovisual stimuli under low-, medium-, and high-uncertainty conditions. Modeling the behavioral data using a drift‒diffusion model indicated that increased visual uncertainty in the audiovisual context decreased the evidence accumulation rate but had no effect on non-decision processes. Electrophysiological recordings confirmed and expanded upon these results: increased visual uncertainty in the audiovisual context reduced the amplitude during the late decision-making stage (300–380 msec) but had no effect on the amplitude during the early sensory encoding stage (140–220 msec). More importantly, electroencephalography analyses revealed that audiovisual integration in the early sensory encoding stage occurred robustly across all visual uncertainty conditions, whereas audiovisual integration in the late stage occurred only under medium and high visual uncertainty conditions. This study demonstrated that increased visual uncertainty modulates the decision process itself rather than early sensory encoding during multisensory decision-making. Moreover, multisensory integration strategies dynamically adapt to increasing visual uncertainty by engaging different mechanisms to maintain effective decision-making.
en-copyright=
kn-copyright=

en-aut-name=YangXiangfu
en-aut-sei=Yang
en-aut-mei=Xiangfu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YangWeiping
en-aut-sei=Yang
en-aut-mei=Weiping
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YuYinghua
en-aut-sei=Yu
en-aut-mei=Yinghua
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=EjimaYoshimichi
en-aut-sei=Ejima
en-aut-mei=Yoshimichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YangJiajia
en-aut-sei=Yang
en-aut-mei=Jiajia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

affil-num=2
en-affil=Department of Psychology, Faculty of Education, Hubei 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=
en-keyword=Multisensory decision-making
kn-keyword=Multisensory decision-making
en-keyword=Visual uncertainty
kn-keyword=Visual uncertainty
en-keyword=Audiovisual integration
kn-keyword=Audiovisual integration
en-keyword=Event-related potential
kn-keyword=Event-related potential
en-keyword=Drift‒diffusion model
kn-keyword=Drift‒diffusion model
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=4
article-no=
start-page=244
end-page=249
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250527
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Identification of New Repeat Expansion Diseases
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Through a genetic study of benign adult familial myoclonus epilepsy (BAFME) type 1, TTTCA and TTTTA repeat expansions have been identified in intron 4 of SAMD12. Lengths of expanded repeats inversely correlated with age at onset of epilepsy. Gain-of-toxic function mechanisms are suggested by the presence of UUUCA-repeat-containing RNA foci. From families with BAFME who did not have repeat expansions in SAMD12, we identified expanded TTTCA and TTTTA repeats in TNRC6A and RAPGEF2. These findings indicated a strong correlation between the repeat motif and the phenotype, leading to the identification of other types of BAFME. We then conducted genetic analysis of neuronal intranuclear inclusion disease (NIID), oculopharyngeal myopathy with leukoencephalopathy (OPML), and oculopharyngodistal myopathy (OPDM). From the observation that NIID, OPML, and OPDM, in addition to fragile X-associated tremor/ataxia syndrome, have shared clinical features, a direct search for CGG repeat expansions successfully led to the identification of the causative genes. Here, I review recent studies on repeat expansions.
en-copyright=
kn-copyright=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=9
article-no=
start-page=1068
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250830
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical Evaluation of Oxidative Stress Markers in Patients with Long COVID During the Omicron Phase in Japan
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To characterize changes in markers of oxidative stress for the clinical evaluation of patients with long COVID, we assessed oxidative stress and antioxidant activity based on serum samples from patients who visited our clinic between May and November 2024. Seventy-seven patients with long COVID (41 [53%] females and 36 [47%] males; median age, 44 years) were included. Median [interquartile range] serum levels of diacron-reactive oxygen metabolites (d-ROM; CARR Unit), biological antioxidant potential (BAP; μmol/L), and oxidative stress index (OSI) were 533.8 [454.9–627.6], 2385.8 [2169.2–2558.1] and 2.0 [1.7–2.5], respectively. Levels of d-ROMs (579.8 vs. 462.2) and OSI (2.3 vs. 1.8), but not BAP (2403.4 vs. 2352.6), were significantly higher in females than in males. OSI levels positively correlated with age and body mass index, whereas BAP levels negatively correlated with these parameters. d-ROM and OSI levels were significantly associated with inflammatory markers, including C-reactive protein (CRP) and fibrinogen, whereas BAP levels were inversely correlated with CRP and ferritin levels. Notably, serum free thyroxine levels were negatively correlated with d-ROMs and OSI, whereas cortisol levels were positively correlated with d-ROMs. Among long COVID symptoms, patients reporting brain fog exhibited significantly higher OSI levels (2.2 vs. 1.8), particularly among females (d-ROMs: 625.6 vs. 513.0; OSI: 2.4 vs. 2.0). The optimal OSI cut-off values were determined to be 1.32 for distinguishing long COVID from healthy controls and 1.92 for identifying brain fog among patients with long COVID. These findings suggest that oxidative stress markers may serve as indicators for the presence or prediction of psycho-neurological symptoms associated with long COVID in a gender-dependent manner.
en-copyright=
kn-copyright=

en-aut-name=MeseOsamu
en-aut-sei=Mese
en-aut-mei=Osamu
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=SakuradaYasue
en-aut-sei=Sakurada
en-aut-mei=Yasue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=SoejimaYoshiaki
en-aut-sei=Soejima
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MoritaSatoru
en-aut-sei=Morita
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=

en-aut-name=HondaHiroyuki
en-aut-sei=Honda
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=EguchiAkiko
en-aut-sei=Eguchi
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=FukudaSanae
en-aut-sei=Fukuda
en-aut-mei=Sanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NojimaJunzo
en-aut-sei=Nojima
en-aut-mei=Junzo
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=Biobank Center, Mie University Hospital
kn-affil=

affil-num=10
en-affil=Department of Health Welfare Sciences, Kansai University of Welfare Sciences
kn-affil=

affil-num=11
en-affil=Department of Laboratory Medicine, Yamaguchi University
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=biological antioxidant potential (BAP)
kn-keyword=biological antioxidant potential (BAP)
en-keyword=Coronavirus disease 2019 (COVID-19)
kn-keyword=Coronavirus disease 2019 (COVID-19)
en-keyword=diacron-reactive oxygen metabolites (d-ROM)
kn-keyword=diacron-reactive oxygen metabolites (d-ROM)
en-keyword=Long COVID
kn-keyword=Long COVID
en-keyword=oxidative stress index (OSI)
kn-keyword=oxidative stress index (OSI)
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=10
article-no=
start-page=1714
end-page=1722
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250829
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Osmotic pressure‐induced calcium response states
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Osmotic pressure is essential for maintaining cellular homeostasis; however, the mechanisms by which cells sense and respond to acute osmotic stress remain incompletely understood. Here, we applied rapid osmotic pressure stimulation to cultured HEK293T cells and observed dynamic intracellular calcium responses. Acute hypotonic stimulation evoked calcium response patterns, whereas hypertonic and isotonic stress did not elicit similar effects. Mechanistically, these calcium signals originated from the endoplasmic reticulum via ryanodine receptor 2 and propagated to neighboring cells through Connexin 43-mediated gap junctions. These findings reveal a previously unrecognized role for calcium signaling in the acute cellular response to osmotic stress, providing new insights into the mechanisms of intercellular communication during osmotic adaptation.
en-copyright=
kn-copyright=

en-aut-name=GaoZidan
en-aut-sei=Gao
en-aut-mei=Zidan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=MorimatsuMasatoshi
en-aut-sei=Morimatsu
en-aut-mei=Masatoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

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

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

affil-num=3
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University  Okayama Japan
kn-affil=
en-keyword=calcium wave
kn-keyword=calcium wave
en-keyword=Connexin 43
kn-keyword=Connexin 43
en-keyword=hypotonic pressure
kn-keyword=hypotonic pressure
en-keyword=osmotic pressure
kn-keyword=osmotic pressure
en-keyword=ryanodine receptor
kn-keyword=ryanodine receptor
END

start-ver=1.4
cd-journal=joma
no-vol=5
cd-vols=
no-issue=1
article-no=
start-page=2475735
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250408
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Linking structure and process in dendritic growth using persistent homology with energy analysis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We present a material analysis method that links structure and process in dendritic growth using explainable machine learning approaches. We employed persistent homology (PH) to quantitatively characterize the morphology of dendritic microstructures. By using interpretable machine learning with energy analysis, we established a robust relationship between structural features and Gibbs free energy. Through a detailed analysis of how Gibbs free energy evolves with morphological changes in dendrites, we uncovered specific conditions that influence the branching of dendritic structures. Moreover, energy gradient analysis based on morphological feature provides a deeper understanding of the branching mechanisms and offers a pathway to optimize thin-film growth processes. Integrating topology and free energy enables the optimization of a range of materials from fundamental research to practical applications.
en-copyright=
kn-copyright=

en-aut-name=ToneMisato
en-aut-sei=Tone
en-aut-mei=Misato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SatoShunsuke
en-aut-sei=Sato
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KuniiSotaro
en-aut-sei=Kunii
en-aut-mei=Sotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ObayashiIppei
en-aut-sei=Obayashi
en-aut-mei=Ippei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HiraokaYasuaki
en-aut-sei=Hiraoka
en-aut-mei=Yasuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OgawaYui
en-aut-sei=Ogawa
en-aut-mei=Yui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FukidomeHirokazu
en-aut-sei=Fukidome
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FoggiattoAlexandre Lira
en-aut-sei=Foggiatto
en-aut-mei=Alexandre Lira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MitsumataChiharu
en-aut-sei=Mitsumata
en-aut-mei=Chiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NagaokaRyunosuke
en-aut-sei=Nagaoka
en-aut-mei=Ryunosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=VaradwajArpita
en-aut-sei=Varadwaj
en-aut-mei=Arpita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MatsudaIwao
en-aut-sei=Matsuda
en-aut-mei=Iwao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KotsugiMasato
en-aut-sei=Kotsugi
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Department of Material Science and Technology, Tokyo University of Science
kn-affil=

affil-num=2
en-affil=Department of Material Science and Technology, Tokyo University of Science
kn-affil=

affil-num=3
en-affil=Department of Material Science and Technology, Tokyo University of Science
kn-affil=

affil-num=4
en-affil=Center for Artificial Intelligence and Mathematical Data Science, Okayama University
kn-affil=

affil-num=5
en-affil=Kyoto University Institute for Advanced Study, Kyoto University
kn-affil=

affil-num=6
en-affil=NTT Basic Research Laboratories, NTT Corporation
kn-affil=

affil-num=7
en-affil=Research Institute of Electrical Communication, Tohoku University
kn-affil=

affil-num=8
en-affil=Department of Material Science and Technology, Tokyo University of Science
kn-affil=

affil-num=9
en-affil=Department of Material Science and Technology, Tokyo University of Science
kn-affil=

affil-num=10
en-affil=Department of Material Science and Technology, Tokyo University of Science
kn-affil=

affil-num=11
en-affil=Department of Material Science and Technology, Tokyo University of Science
kn-affil=

affil-num=12
en-affil=Institute for Solid State Physics, The University of Tokyo
kn-affil=

affil-num=13
en-affil=Department of Material Science and Technology, Tokyo University of Science
kn-affil=
en-keyword=Persistent homology
kn-keyword=Persistent homology
en-keyword=free energy analysis
kn-keyword=free energy analysis
en-keyword=structure-toproperty linkage
kn-keyword=structure-toproperty linkage
en-keyword=dendrite growth
kn-keyword=dendrite growth
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=40522
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251118
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Long intervals between repetitive concussions reduce risk of cognitive impairment and limit microglial activation, astrogliosis, and tauopathy in adolescent rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Although previous studies have demonstrated the effects of concussions do not accumulate as the time interval between injuries increases, little is known about the relationship between this interval and the effects of repetitive concussions. The objective of this study is to explore the relationship between the time interval and changes in behavior and histology following repetitive concussions. Male adolescent rats received concussions by weight drop and were randomly assigned to one of five experimental groups, receiving concussions three times either daily, every other day, once per week, once every 2 weeks, or receiving sham procedures. Only rats that received daily concussions exhibited cognitive impairment, while the other groups did not. No groups showed motor or anxiety-like impairments. Histological analysis revealed accumulation of microglia, as well as astrogliosis, in the prefrontal cortex, corpus callosum, dentate gyrus, and cornu Ammonis 1 region of the hippocampus in rats subjected to daily concussions. Accumulation of phosphorylated tau was also observed in the prefrontal cortex and cornu Ammonis 1. Longer intervals between concussions may reduce the risk of cognitive impairment and limit microglial activation, astrogliosis, and phosphorylated tau accumulation. These findings may help guide decisions on the appropriate timing for return to play in humans.
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=KinKyohei
en-aut-sei=Kin
en-aut-mei=Kyohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
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=4
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=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=HirayamaTakahiro
en-aut-sei=Hirayama
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
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=9
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=10
ORCID=

en-aut-name=SaijoTomoya
en-aut-sei=Saijo
en-aut-mei=Tomoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NaitoHiromichi
en-aut-sei=Naito
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MasaiKaori
en-aut-sei=Masai
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
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=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=

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

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

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

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

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

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

affil-num=7
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University Hospital
kn-affil=

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

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

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

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

affil-num=12
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University Hospital
kn-affil=

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

affil-num=14
en-affil=Yasuhara Clinic
kn-affil=

affil-num=15
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital
kn-affil=
en-keyword=Concussion
kn-keyword=Concussion
en-keyword=Return to play
kn-keyword=Return to play
en-keyword=Sports-related head injury
kn-keyword=Sports-related head injury
en-keyword=Microglia
kn-keyword=Microglia
en-keyword=Astrocyte
kn-keyword=Astrocyte
en-keyword=Tauopathy
kn-keyword=Tauopathy
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=小胞型グルタミン酸輸送体3はポドサイトにおけるグルタミン酸を用いた細胞間シグナル伝達に関与する
kn-title=Vesicular Glutamate Transporter 3 Is Involved in Glutamatergic Signalling in Podocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NISHIINaoko
en-aut-sei=NISHII
en-aut-mei=Naoko
kn-aut-name=西井尚子
kn-aut-sei=西井
kn-aut-mei=尚子
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=1,3-オキサゾールをヘム鉄結合部位としたコレステロール24ヒドロキシラーゼ阻害剤の分子設計と合成
kn-title=Design and Synthesis of Cholesterol 24-Hydroxylase Inhibitors Using 1,3-Oxazole as a Heme-Iron Binding Group
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=ITOYoshiteru
en-aut-sei=ITO
en-aut-mei=Yoshiteru
kn-aut-name=伊藤吉輝
kn-aut-sei=伊藤
kn-aut-mei=吉輝
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama university
kn-affil=岡山大学大学院自然科学研究科
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=2025
dt-pub=20250925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Raspberry Pi に導入可能な軽量ディープラーニングベースの侵入検知システム
kn-title=Lightweight Deep Learning-Based Intrusion Detection System for Deployment on Raspberry Pi
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MUHAMMAD BISRI MUSTHAFA
en-aut-sei=MUHAMMAD BISRI MUSTHAFA
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 Natural Science and Technology, Okayama university
kn-affil=岡山大学大学院自然科学研究科
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=2025
dt-pub=20250925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=マカクザル神経内分泌系におけるバソプレシンの機能・形態連関
kn-title=Functional-morphological relationships of vasopressin in the macaque neuroendocrine system
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=OTSUBOAkito
en-aut-sei=OTSUBO
en-aut-mei=Akito
kn-aut-name=大坪秋人
kn-aut-sei=大坪
kn-aut-mei=秋人
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama university
kn-affil=岡山大学大学院自然科学研究科
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=2025
dt-pub=20250925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=機械学習を用いたバイパラメータ解析によるSimple Diffusion Kurtosis Imagingでの頭頸部腫瘍の良悪性診断能の向上
kn-title=Improving Diagnostic Performance for Head and Neck Tumors with Simple Diffusion Kurtosis Imaging and Machine Learning Bi-Parameter Analysis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=YOSHIDASuzuka
en-aut-sei=YOSHIDA
en-aut-mei=Suzuka
kn-aut-name=吉田鈴加
kn-aut-sei=吉田
kn-aut-mei=鈴加
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=COVID-19罹患後症状における血糖測定の予後への影響：日本での後方視的研究
kn-title=Importance of Blood Glucose Measurement for Predicting the Prognosis of Long COVID：A Retrospective Study in Japan
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=YOKOYAMASho
en-aut-sei=YOKOYAMA
en-aut-mei=Sho
kn-aut-name=横山将
kn-aut-sei=横山
kn-aut-mei=将
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=活動性食欲不振モデルマウスにおける前頭前野および海馬におけるペリニューロナルネットおよびパルブアルブミン介在ニューロンの変化、および血中コルチコステロンとの相関性
kn-title=Alteration of perineuronal nets and parvalbumin interneurons in prefrontal cortex and hippocampus, and correlation with blood corticosterone in activity-based anorexia model mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NGUYEN DUY HOANG
en-aut-sei=NGUYEN DUY HOANG
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=2025
dt-pub=20250925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=TRPV2はマウス心筋細胞のストレスレジリエンスを仲介する
kn-title=TRPV2 mediates stress resilience in mouse cardiomyocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=DONGYUBING
en-aut-sei=DONG
en-aut-mei=YUBING
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=2025
dt-pub=20250925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=虚血性脳卒中モデルラットにおけるヒト改変骨髄由来間質細胞（SB623）の脳内移植と随意運動および強制運動の治療効果
kn-title=Therapeutic effects of intracerebral transplantation of human modified bone marrow-derived stromal cells (SB623) with voluntary and forced exercise in a rat model of ischemic stroke
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NAGASETakayuki
en-aut-sei=NAGASE
en-aut-mei=Takayuki
kn-aut-name=永瀬喬之
kn-aut-sei=永瀬
kn-aut-mei=喬之
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=慢性外傷性脳症の再現性および定量的モデル：反復性の非出血性および非挫傷性の軽度外傷性脳損傷ラットは、ミクログリアの活性化、アストログリア症、およびタウオパチーを伴い行動障害を引き起こす
kn-title=Repeated non-hemorrhagic and non-contusional mild traumatic brain injury in rats elicits behavioral impairment with microglial activation, astrogliosis, and tauopathy: Reproducible and quantitative model of chronic traumatic encephalopathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SUGAHARAChiaki
en-aut-sei=SUGAHARA
en-aut-mei=Chiaki
kn-aut-name=菅原千明
kn-aut-sei=菅原
kn-aut-mei=千明
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=2025
dt-pub=20250925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=発達性読み書き障害の原因候補遺伝子（DYX1C1）のラット大脳皮質発達における時空間発現パターン
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=
en-copyright=
kn-copyright=

en-aut-name=ZENSHOKazumasa
en-aut-sei=ZENSHO
en-aut-mei=Kazumasa
kn-aut-name=禅正和真
kn-aut-sei=禅正
kn-aut-mei=和真
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=55
cd-vols=
no-issue=4
article-no=
start-page=313
end-page=326
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250203
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Current management of neurotrophic receptor tyrosine kinase fusion-positive sarcoma: an updated review
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In recent years, pembrolizumab has demonstrated significant efficacy in treating tumors characterized by a high tumor mutational burden and high microsatellite instability. Tropomyosin receptor kinase (TRK) inhibitors have shown considerable efficacy against tumors harboring neurotrophic receptor tyrosine kinase (NTRK) fusion genes, highlighting the growing importance of personalized medicine in cancer treatment. Advanced sequencing technologies enable the rapid analysis of numerous genetic abnormalities in tumors, facilitating the identification of patients with positive biomarkers. These advances have increased the likelihood of providing effective, tailored treatments. NTRK fusion genes are present in various cancer types, including sarcomas, and the TRK inhibitors larotrectinib and entrectinib have been effectively used for these malignancies. Consequently, the treatment outcomes for NTRK fusion-positive tumors have improved significantly, reflecting a shift toward more personalized therapeutic approaches. This review focuses on NTRK fusion-positive sarcomas and comprehensively evaluates their epidemiology, clinical features, and radiological and histological characteristics. We also investigated the treatment landscape, including the latest methodologies involving TRK inhibitors, and discussed the long-term efficacy of these inhibitors, and their optimal order of use. Notably, larotrectinib has demonstrated a high response rate in infantile fibrosarcoma, and its efficacy has been confirmed even in advanced cases. However, further research is warranted to optimize treatment duration and subsequent management strategies. The accumulation of clinical cases worldwide will play a pivotal role in refining the treatment approaches for tumors associated with NTRK fusion genes.
en-copyright=
kn-copyright=

en-aut-name=KubotaYuta
en-aut-sei=Kubota
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawanoMasanori
en-aut-sei=Kawano
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IwasakiTatsuya
en-aut-sei=Iwasaki
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ItonagaIchiro
en-aut-sei=Itonaga
en-aut-mei=Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KakuNobuhiro
en-aut-sei=Kaku
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

en-aut-name=TanakaKazuhiro
en-aut-sei=Tanaka
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Orthopaedic Surgery, Faculty of Medicine, Oita University
kn-affil=

affil-num=2
en-affil=Department of Orthopaedic Surgery, Faculty of Medicine, Oita University
kn-affil=

affil-num=3
en-affil=Department of Orthopaedic Surgery, Faculty of Medicine, Oita University
kn-affil=

affil-num=4
en-affil=Department of Orthopaedic Surgery, Faculty of Medicine, Oita University
kn-affil=

affil-num=5
en-affil=Department of Orthopaedic Surgery, Faculty of Medicine, Oita University
kn-affil=

affil-num=6
en-affil=Department of Orthopaedic Surgery , Science of Functional Recovery and Reconstruction, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Orthopaedic Surgery, Faculty of Medicine, Oita University
kn-affil=
en-keyword=NTRK fusion-positive sarcoma
kn-keyword=NTRK fusion-positive sarcoma
en-keyword=larotrectinib
kn-keyword=larotrectinib
en-keyword=entrectinib
kn-keyword=entrectinib
en-keyword=infantile fibrosarcoma
kn-keyword=infantile fibrosarcoma
en-keyword=NTRK-rearranged spindle cell neoplasms
kn-keyword=NTRK-rearranged spindle cell neoplasms
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=
article-no=
start-page=1568338
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250807
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A pilot transcriptomic study of a novel multitargeted BRT regimen for anti–MDA5 antibody-positive dermatomyositis: improving survival over conventional therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Anti-melanoma differentiation-associated gene 5 antibody-positive dermatomyositis (MDA5-DM) is associated with severe outcomes, primarily due to rapidly progressive interstitial lung disease (RP-ILD), which is often refractory to standard therapies such as calcineurin inhibitors (e.g., tacrolimus) combined with cyclophosphamide (TC-Tx). This study evaluated the efficacy of a novel multitargeted regimen combining baricitinib, rituximab, and tacrolimus (BRT-Tx) in improving survival outcomes for MDA5-DM patients with poor prognostic factors.<br>
Methods: Fourteen MDA5-DM patients with multiple adverse prognostic factors were studied. Seven received the BRT-Tx regimen, and the remaining seven, previously treated with TC-Tx, served as historical controls. Twelve-month survival was assessed. Transcriptome analysis was performed for six patients (BRT=3, TC=3), beginning with cluster analysis to evaluate whether changes in peripheral blood gene expression varied according to treatment or prognosis. Gene ontology analysis characterized expression profiles in survivors and distinguished treatment effects. Alterations in the type I, II, and III interferon signatures were also assessed.<br>
Results: In the TC-Tx group, four of seven patients succumbed to RP-ILD, whereas all seven BRT-Tx patients survived the 12-month observation period. Only one BRT-Tx patient required combined rescue therapies, including plasma exchange, and one case of unexplained limbic encephalitis (LE) occurred. Cytomegalovirus reactivation was observed in both groups (BRT: 5/7; TC: 6/7). Transcriptomic analysis revealed no treatment-specific clustering of differentially expressed genes (DEGs) before and after therapy. However, survivors and nonsurvivors formed distinct clusters, with survivors showing significant posttreatment suppression of B-cell-related gene expression. Moreover, interferon signature scores were significantly lower after treatment in survivors than in nonsurvivors. BRT-Tx effectively suppressed B-cell-mediated immune responses and maintained a low interferon signature, while TC-Tx resulted in nonspecific gene suppression, and in nonsurvivors, an elevated interferon signature was observed.<br>
Conclusion: BRT-Tx has the potential to improve survival in MDA5-DM patients by effectively targeting hyperactive immune pathways. The combination of rituximab and tacrolimus is expected to disrupt B-cell–T-cell interactions and reduce autoantibody production, whereas baricitinib may suppress both IFN and GM-CSF signaling, regulating excessive autoimmunity mediated by cells such as macrophages. Unlike TC-Tx, BRT-Tx avoids cyclophosphamide-associated risks such as infertility and secondary malignancies. Future randomized controlled trials are warranted to validate its efficacy and safety.
en-copyright=
kn-copyright=

en-aut-name=TokunagaMoe
en-aut-sei=Tokunaga
en-aut-mei=Moe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakaiYu
en-aut-sei=Nakai
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SatoYoshiharu
en-aut-sei=Sato
en-aut-mei=Yoshiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HiratsukaMitori
en-aut-sei=Hiratsuka
en-aut-mei=Mitori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=

en-aut-name=NakatsueTakeshi
en-aut-sei=Nakatsue
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SaekiTakako
en-aut-sei=Saeki
en-aut-mei=Takako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UmayaharaTakatsune
en-aut-sei=Umayahara
en-aut-mei=Takatsune
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

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

en-aut-name=KoyamaYoshinobu
en-aut-sei=Koyama
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

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

affil-num=2
en-affil=Division of Rheumatology, Center for Autoimmune Diseases, Japanese Red Cross Okayama Hospital
kn-affil=

affil-num=3
en-affil=DNA Chip Research Inc., Medical Laboratory
kn-affil=

affil-num=4
en-affil=DNA Chip Research Inc., Medical Laboratory
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=Division of Rheumatology and Nephrology, Department of Internal Medicine, Nagaoka Red Cross Hospital
kn-affil=

affil-num=7
en-affil=Division of Rheumatology and Nephrology, Department of Internal Medicine, Nagaoka Red Cross Hospital
kn-affil=

affil-num=8
en-affil=Division of Dermatology, Center for Autoimmune Diseases, Japanese Red Cross Okayama Hospital
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, Center for Autoimmune Diseases, Japanese Red Cross Okayama Hospital
kn-affil=
en-keyword=anti-MDA5 antibody-positive dermatomyositis (MDA5-DM)
kn-keyword=anti-MDA5 antibody-positive dermatomyositis (MDA5-DM)
en-keyword=JAK inhibitor
kn-keyword=JAK inhibitor
en-keyword=baricitinib
kn-keyword=baricitinib
en-keyword=rituximab
kn-keyword=rituximab
en-keyword=multitargeted treatment
kn-keyword=multitargeted treatment
en-keyword=IFN signature
kn-keyword=IFN signature
en-keyword=transcriptome analysis
kn-keyword=transcriptome analysis
END

start-ver=1.4
cd-journal=joma
no-vol=17
cd-vols=
no-issue=10
article-no=
start-page=e94951
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251019
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Bladder Trigone as a Sensory Hub: A Narrative Review
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The bladder trigone is an anatomically and functionally distinct region within the lower urinary tract (LUT), characterized by a dense network of afferent sensory fibers, specialized urothelial interactions, and prominent mechanotransduction mechanisms. Its intricate neuroarchitecture enables precise detection of bladder filling and coordination of micturition, whereas dysregulation of these pathways contributes to lower urinary tract symptoms (LUTS), including urgency, frequency, and bladder pain. Despite its recognized clinical relevance, the structural and functional basis of trigonal sensory signaling - and its role - remain incompletely understood.<br>
This review synthesizes current evidence on trigonal afferent organization, integrating data from anatomical mapping, receptor profiling, electrophysiological characterization, and translational research. Seminal anatomical observations are combined with recent advances in mechanotransduction and purinergic, peptidergic, and transient receptor potential (TRP) signaling to provide a comprehensive perspective. The trigone exhibits three principal afferent classes: (1) intraepithelial fibers penetrating umbrella cells, marked by P2X purinoceptor 3 (P2X3), transient receptor potential vanilloid 1 (TRPV1), calcitonin gene-related peptide (CGRP), and substance P (SP); (2) subepithelial plexuses surrounding microvasculature, enriched in vasoactive neuropeptides and exhibiting plastic hypertrophy in overactive bladder (OAB) and interstitial cystitis/bladder pain syndrome (IC/BPS); and (3) encapsulated corpuscular endings at the lamina propria-detrusor junction, expressing PIEZO1/2 and acid-sensing ion channels (ASICs) for rapid adaptation. In trigeminal dorsal root ganglion (DRG) neurons, high expression of PIEZO2, P2RX3, and voltage-gated sodium channel, type 1.8 (Nav1.8) was observed, revealing their role as the foundation for multisensory information processing. Functional assays highlight distinct mechanotransductive and chemosensory pathways, with aging, inflammation, and neurotrophic factors driving afferent plasticity underlying abnormal bladder sensation, such as urgency, frequency, and pain. Early clinical trials of P2X3 antagonists and intravesical TRPV1 inhibitors demonstrate promising symptomatic benefits. Collectively, evidence positions the bladder trigone as a critical sensory hub where neuronal, urothelial, and immune signals converge to regulate bladder sensation. Understanding its molecular and structural specialization may inform the development of region-specific neuromodulatory therapies targeting sensory urgency and afferent-driven bladder dysfunction.
en-copyright=
kn-copyright=

en-aut-name=SadahiraTakuya
en-aut-sei=Sadahira
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MaruyamaYuki
en-aut-sei=Maruyama
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MitsuiYosuke
en-aut-sei=Mitsui
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SekitoTakanori
en-aut-sei=Sekito
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WatanabeTomofumi
en-aut-sei=Watanabe
en-aut-mei=Tomofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
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=
en-keyword=bladder trigone
kn-keyword=bladder trigone
en-keyword=botulinum toxin
kn-keyword=botulinum toxin
en-keyword=lower urinary tract symptoms
kn-keyword=lower urinary tract symptoms
en-keyword=sensory afferents
kn-keyword=sensory afferents
en-keyword=varicosities
kn-keyword=varicosities
END

start-ver=1.4
cd-journal=joma
no-vol=786
cd-vols=
no-issue=
article-no=
start-page=152753
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202510
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Hydrogen-rich gas enhances mitochondrial membrane potential and respiratory function recovery in Caco-2 cells post-ischemia-reperfusion injury
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Ischemia-reperfusion (I/R) injury induces oxidative stress, leading to damage in highly susceptible intestinal tissues. Molecular hydrogen (H2) has shown therapeutic potential in I/R injuries, with our prior research showing its efficacy in improving outcomes in rat intestinal transplantation models. However, its impact on mitochondrial function remain insufficiently understood. This study aims to elucidate how H2 modulates mitochondrial function impaired by I/R injury.<br>
Methods: To assess the effects of H2 on I/R injury, cells were divided into three groups: a control group, a hypoxic group (99 % N2, 1 % O2, without H2 for 3, 6, or 24 h), and a hypoxic-H2 group (99 % H2, 1 % O2, for the same durations). After treatment, cells were reoxygenated under normoxic conditions (21 % O2) for 1, 2, 4, or 6 h. Mitochondrial membrane potential, oxygen consumption, and ATP production were measured. Reactive oxygen species production and apoptotic and metabolic regulators were also assessed.<br>
Results: H2 markedly promoting mitochondrial recovery following I/R injury, by enhancing ATP production, restoring mitochondrial membrane potential, and improving oxygen consumption. It also reduced ROS levels and suppressed pro-apoptotic signaling. Notably, H2 suppressed the expression of HIF1α and PDK1, suggesting that H2 may act upstream of hypoxia-driven signaling pathways. These changes promoted oxidative phosphorylation and overall cellular function during reperfusion.<br>
Conclusions: Our findings reveal that H2 therapy supports mitochondrial function, suppresses ROS, and modulates hypoxia-driven pathways in I/R injury. These insights advance the understanding of H2's potential in addressing I/R injury and provide a foundation for its application in other hypoxia-related conditions.
en-copyright=
kn-copyright=

en-aut-name=SeyaMizuki
en-aut-sei=Seya
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AokageToshiyuki
en-aut-sei=Aokage
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MengYing
en-aut-sei=Meng
en-aut-mei=Ying
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HirayamaTakahiro
en-aut-sei=Hirayama
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ObaraTakafumi
en-aut-sei=Obara
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NojimaTsuyoshi
en-aut-sei=Nojima
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshinoriKosaki
en-aut-sei=Yoshinori
en-aut-mei=Kosaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YumotoTetsuya
en-aut-sei=Yumoto
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=WatanabeAkihiro
en-aut-sei=Watanabe
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YamadaTaihei
en-aut-sei=Yamada
en-aut-mei=Taihei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NaitoHiromichi
en-aut-sei=Naito
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NakaoAtsunori
en-aut-sei=Nakao
en-aut-mei=Atsunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Biological Process of Aging, Tokyo Metropolitan Institute for Geriatrics and Gerontology
kn-affil=

affil-num=3
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Emergency, Disaster and Critical Care Medicine, Hyogo Medical University
kn-affil=

affil-num=10
en-affil=Department of Emergency, Disaster and Critical Care Medicine, Hyogo Medical University
kn-affil=

affil-num=11
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Intestinal ischemia-reperfusion injury
kn-keyword=Intestinal ischemia-reperfusion injury
en-keyword=Molecular hydrogen
kn-keyword=Molecular hydrogen
en-keyword=Hydrogen gas therapy
kn-keyword=Hydrogen gas therapy
en-keyword=Caco-2 cells
kn-keyword=Caco-2 cells
en-keyword=Mitochondrial function
kn-keyword=Mitochondrial function
en-keyword=Hypoxia-inducible factor-1α (HIF1α)
kn-keyword=Hypoxia-inducible factor-1α (HIF1α)
END

start-ver=1.4
cd-journal=joma
no-vol=17
cd-vols=
no-issue=17
article-no=
start-page=2770
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250825
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Refining the Role of Tumor-Associated Macrophages in Oral Squamous Cell Carcinoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In the tumor microenvironment, various immune and stromal cells, such as fibroblasts and vascular endothelial cells, contribute to tumor growth and progression by interacting with cancer cells. Tumor-associated macrophages (TAMs) have attracted attention as major players in the tumor microenvironment. The origin of TAMs is believed to be the infiltration of monocytes derived from bone marrow progenitor cells into tumor tissues and their differentiation into macrophages, whereas tissue-resident macrophages derived from yolk sacs have recently been reported. TAMs infiltrating tumor tissues act in a tumor-promoting manner through immunosuppression, angiogenesis, and the promotion of cancer cell invasion. Reflecting the nature of TAMs, increased TAM invasion and TAM-specific gene expression in tumor tissues may be the new biomarkers for cancer. Moreover, new therapeutic strategies targeting TAMs, such as transformation into immunostimulatory macrophages, suppression of TAM infiltration, and promotion of phagocytosis, are being investigated, and many clinical trials are underway. As the origin and function of TAMs are further elucidated, TAM-targeted therapy is expected to become a new option for the immunotherapy of various cancers, including oral cancers.
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=TianyanPiao
en-aut-sei=Tianyan
en-aut-mei=Piao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=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=KawaiHotaka
en-aut-sei=Kawai
en-aut-mei=Hotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
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=7
ORCID=

en-aut-name=MinZin Zin
en-aut-sei=Min
en-aut-mei=Zin Zin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=FujiiMasae
en-aut-sei=Fujii
en-aut-mei=Masae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=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 Oral Pathology and Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

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

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

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

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

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

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

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=tumor-associated macrophage (TAM)
kn-keyword=tumor-associated macrophage (TAM)
en-keyword=oral squamous cell carcinoma (OSCC)
kn-keyword=oral squamous cell carcinoma (OSCC)
en-keyword=macrophage polarity
kn-keyword=macrophage polarity
en-keyword=invasion
kn-keyword=invasion
en-keyword=carcinogenesis
kn-keyword=carcinogenesis
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=3
article-no=
start-page=965
end-page=970
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250404
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Decreased homovanillic acid and 5‐hydroxyindoleacetic acid levels in the cerebrospinal fluid of patients with Dravet syndrome with parkinsonism
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Dravet syndrome (DS) is an early onset, developmental, and epileptic encephalopathy characterized by drug-resistant seizures and multiple comorbidities. It has been reported that in adulthood, it may be accompanied by parkinsonism, but the pathogenesis of this condition remains unclear. We performed dopamine transporter single-photon emission computed tomography (DAT SPECT) and measured monoamine metabolite levels in the cerebrospinal fluid (CSF) in two adult patients with DS who developed parkinsonism around the age of 30 years. DAT SPECT showed no abnormalities in either patient, whereas CSF tests revealed significant decreases in the levels of homovanillic and 5-hydroxyindoleacetic acids. One patient with severe symptoms was treated with levodopa–carbidopa, which improved parkinsonism manifestations. The other patient initiated treatment with a low dose and has been continuing the treatment without any reported side effects. In conclusion, CSF testing can detect a decrease in dopamine synthesis and may be useful in monitoring the efficacy of levodopa treatment in patients with DS and parkinsonism.<br>
Plain Language Summary: Dravet syndrome (DS) is an early onset, developmental, and epileptic encephalopathy. DS can lead to the development of parkinsonism in adulthood, a clinical syndrome characterized by tremor, slowed movements, and rigidity. Although parkinsonism is a significant issue for patients, its underlying pathology has not yet been elucidated. In this study, we confirmed that the levels of monoamine metabolites in the CSF were low in two patients, potentially shedding light on the pathology involved.
en-copyright=
kn-copyright=

en-aut-name=SugiyamaRyo
en-aut-sei=Sugiyama
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SaitoTakashi
en-aut-sei=Saito
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KatsumotoAtsuko
en-aut-sei=Katsumoto
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YonenoShota
en-aut-sei=Yoneno
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AkiyamaTomoyuki
en-aut-sei=Akiyama
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KomakiHirofumi
en-aut-sei=Komaki
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Child Neurology, National Center Hospital, National Center of Neurology and Psychiatry
kn-affil=

affil-num=2
en-affil=Department of Child Neurology, National Center Hospital, National Center of Neurology and Psychiatry
kn-affil=

affil-num=3
en-affil=Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry
kn-affil=

affil-num=4
en-affil=Department of Child Neurology, National Center Hospital, National Center of Neurology and Psychiatry
kn-affil=

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

affil-num=6
en-affil=Department of Child Neurology, National Center Hospital, National Center of Neurology and Psychiatry
kn-affil=
en-keyword=dopamine transporter
kn-keyword=dopamine transporter
en-keyword=levodopa
kn-keyword=levodopa
en-keyword=monoamine metabolites
kn-keyword=monoamine metabolites
en-keyword=single-photon emission computed tomography
kn-keyword=single-photon emission computed tomography
END

start-ver=1.4
cd-journal=joma
no-vol=152
cd-vols=
no-issue=22
article-no=
start-page=dev204763
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251115
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=ROS produced by Dual oxidase regulate cell proliferation and haemocyte migration during leg regeneration in the cricket
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Many animals regenerate lost body parts through several signalling pathways; however, the triggers that initiate regeneration remain unclear. In the present study, we focused on the role of reactive oxygen species (ROS) produced by the NADPH oxidase Dual oxidase (Duox) during cricket leg regeneration. The results showed that ROS levels were upregulated during leg regeneration and decreased by DuoxRNAi. In DuoxRNAi nymphs, wound closure and scab formation were incomplete 2 days after amputation, and hypertrophy occurred in the distal region of the regenerating legs at 5 days after amputation. In addition, the hypertrophic phenotype was induced by DuoxARNAi and NADPH oxidase inhibitor treatment. During hypertrophy, haemocytes, including plasmatocytes, oenocytoids and granulocytes, accumulated. Proliferation of haemocytes in regenerating legs was not increased by DuoxRNAi; however, haemocyte accumulation was regulated by the Spatzle (Spz) family molecules, which are Toll receptor ligands. As the exoskeleton of DuoxRNAi nymphs was thinner than that of the control, excessive haemocyte accumulation can cause hypertrophy in DuoxRNAi nymphs. Thus, Duox-derived ROS are involved in wound healing and haemocyte accumulation through the Spz/Toll signalling pathway during leg regeneration in crickets.
en-copyright=
kn-copyright=

en-aut-name=Okumura-HironoMisa
en-aut-sei=Okumura-Hirono
en-aut-mei=Misa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=BandoTetsuya
en-aut-sei=Bando
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HamadaYoshimasa
en-aut-sei=Hamada
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=5
ORCID=

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

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

affil-num=3
en-affil=Department of Cytology and Histology, 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 Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Regeneration
kn-keyword=Regeneration
en-keyword=Reactive oxygen species (ROS)
kn-keyword=Reactive oxygen species (ROS)
en-keyword=NADPH oxidase (Nox)
kn-keyword=NADPH oxidase (Nox)
en-keyword=Dual oxidase (Duox)
kn-keyword=Dual oxidase (Duox)
en-keyword=Inflammation
kn-keyword=Inflammation
en-keyword=Gryllus bimaculatus
kn-keyword=Gryllus bimaculatus
END

start-ver=1.4
cd-journal=joma
no-vol=386
cd-vols=
no-issue=
article-no=
start-page=115145
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=Therapeutic effects of intracerebral transplantation of human modified bone marrow-derived stromal cells (SB623) with voluntary and forced exercise in a rat model of ischemic stroke
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ischemic stroke results in significant long-term disability and mortality worldwide. Although existing therapies, such as recombinant tissue plasminogen activator and mechanical thrombectomy, have shown promise, their application is limited by stringent conditions. Mesenchymal stem cell (MSC) transplantation, especially using SB623 cells (modified human bone marrow-derived MSCs), has emerged as a promising alternative, promoting neurogenesis and recovery. This study evaluated the effects of voluntary and forced exercise, alone and in combination with SB623 cell transplantation, on neurological and psychological outcomes in a rat model of ischemic stroke. Male Wistar rats that had undergone middle cerebral artery occlusion (MCAO) were divided into six groups: control, voluntary exercise (V-Ex), forced exercise (F-Ex), SB623 transplantation, SB623 + V-Ex, and SB623 + F-Ex. Voluntary exercise was facilitated using running wheels, while forced exercise was conducted on treadmills. Neurological recovery was assessed using the modified neurological severity score (mNSS). Psychological symptoms were evaluated through the open field test (OFT) and forced swim test (FST), and neurogenesis was assessed via BrdU labeling. Both exercise groups exhibited significant changes in body weight post-MCAO. Both exercises enhanced the treatment effect of SB623 transplantation. The forced exercise showed a stronger treatment effect on ischemic stroke than voluntary exercise alone, and the sole voluntary exercise improved depression-like behavior. The SB623 + F-Ex group demonstrated the greatest improvements in motor function, infarct area reduction, and neurogenesis. The SB623 + V-Ex group was most effective in alleviating depression-like behavior. Future research should optimize these exercise protocols and elucidate the underlying mechanisms to develop tailored rehabilitation strategies for stroke patients.
en-copyright=
kn-copyright=

en-aut-name=NagaseTakayuki
en-aut-sei=Nagase
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
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=3
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=4
ORCID=

en-aut-name=KawauchiSatoshi
en-aut-sei=Kawauchi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=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=HirataYuichi
en-aut-sei=Hirata
en-aut-mei=Yuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
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=10
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=11
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=12
ORCID=

en-aut-name=SaijoTomoya
en-aut-sei=Saijo
en-aut-mei=Tomoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
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=14
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=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 Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Ischemic stroke
kn-keyword=Ischemic stroke
en-keyword=Post-stroke depression
kn-keyword=Post-stroke depression
en-keyword=Regenerative medicine
kn-keyword=Regenerative medicine
en-keyword=Rehabilitation
kn-keyword=Rehabilitation
en-keyword=SB623
kn-keyword=SB623
END

start-ver=1.4
cd-journal=joma
no-vol=17
cd-vols=
no-issue=11
article-no=
start-page=1446
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251109
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Development of Propofol-Encapsulated Liposomes and the Effect of Intranasal Administration on Bioavailability in Rabbits
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/Objectives: Propofol is frequently used as an intravenous anesthetic and is rapidly metabolized. Therefore, if it could be administered non-invasively (e.g., orally) as premedication, it might hasten emergence from anesthesia, thereby improving patient safety. However, it undergoes extensive first-pass metabolism in the liver and intestines, limiting the route for premedication. We evaluated whether intranasal delivery of a propofol-encapsulated liposome solution improves systemic exposure and bioavailability in rabbits. Methods: A propofol-encapsulated liposome solution was administered to rabbits via the intravenous, oral, and intranasal routes. Blood propofol concentrations were measured for up to 60 min after administration and the area under the concentration–time curve (AUC0–60) and bioavailability of the propofol-encapsulated liposome solution were compared with those of the non-encapsulated propofol formulation. The differences were tested by two-way analysis of variance (ANOVA) with Šidák’s post hoc multiple-comparisons test and the Mann–Whitney test (α = 0.05). Results: The AUC0–60 for blood propofol concentrations after intravenous administration was significantly higher with the propofol-encapsulated liposome solution than with the non-encapsulated propofol formulation (3038.8 ± 661.5 vs. 1929.8 ± 58.2 ng·min/mL; p = 0.0286). By contrast, no increase in blood propofol concentrations was observed after oral administration, whereas intranasal administration increased blood propofol concentrations and yielded significantly higher bioavailability compared with the non-encapsulated propofol formulation (16.4 ± 7.3% vs. 2.0 ± 1.2%; p = 0.0286). Conclusions: The findings of the present study suggest that intranasal liposomal propofol increased systemic availability compared with a non-encapsulated formulation, supporting further evaluation as a candidate premedication approach for propofol.
en-copyright=
kn-copyright=

en-aut-name=UjitaHitomi
en-aut-sei=Ujita
en-aut-mei=Hitomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HiguchiHitoshi
en-aut-sei=Higuchi
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NishiokaYukiko
en-aut-sei=Nishioka
en-aut-mei=Yukiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyakeSaki
en-aut-sei=Miyake
en-aut-mei=Saki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SatoRiko
en-aut-sei=Sato
en-aut-mei=Riko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

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

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

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

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

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

affil-num=6
en-affil=Department of Dental Anesthesiology and Special Care Dentistry, Okayama University Graduate of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=liposome
kn-keyword=liposome
en-keyword=propofol
kn-keyword=propofol
en-keyword=bioavailability
kn-keyword=bioavailability
en-keyword=intranasal administration
kn-keyword=intranasal administration
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=1
article-no=
start-page=234
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251114
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Rotenone targets midbrain astrocytes to produce glial dysfunction-mediated dopaminergic neurodegeneration
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Exposure to pesticides, such as rotenone or paraquat, is an environmental factor that plays an important role in the pathogenesis of Parkinson's disease (PD). Rotenone induces PD-like pathology and is therefore used to develop parkinsonian animal models. Dopaminergic neurotoxicity caused by rotenone has been attributed to the inhibition of mitochondrial complex I, oxidative stress and neuroinflammation; however, the mechanisms underlying selective dopaminergic neurodegeneration by rotenone remain unclear. To resolve this, we focused on glial diversity and examined whether the brain region-specific glial response to rotenone could determine the vulnerability of dopaminergic neurons using primary cultured neurons, astrocytes and microglia from the midbrain and striatum of rat embryos and rotenone-injected PD model mice. Direct neuronal treatment with low-dose rotenone failed to damage dopaminergic neurons. Conversely, rotenone exposure in the presence of midbrain astrocyte and microglia or conditioned media from rotenone-treated midbrain glial cultures containing astrocytes and microglia produced dopaminergic neurotoxicity, but striatal glia did not. Surprisingly, conditioned media from rotenone-treated midbrain astrocytes or microglia monocultures did not affect neuronal survival. We also demonstrated that rotenone targeted midbrain astrocytes prior to microglia to induce dopaminergic neurotoxicity. Rotenone-treated astrocytes produced secreted protein acidic and rich in cysteine (SPARC) extracellularly, which induced microglial proliferation, increase in IL-1β and TNF-α, and NF-κB (p65) nuclear translocation in microglia, resulting in dopaminergic neurodegeneration. In addition, rotenone exposure caused the secretion of NFAT-related inflammatory cytokines and a reduction in the level of an antioxidant metallothionein (MT)-1 from midbrain glia. Furthermore, we observed microglial proliferation and a decrease in the number of MT-positive astrocytes in the substantia nigra, but not the striatum, of low-dose rotenone-injected PD model mice. Our data highlight that rotenone targets midbrain astrocytes, leading to SPARC secretion, which promotes the neurotoxic conversion of microglia and leads to glial dysfunction-mediated dopaminergic neurodegeneration.
en-copyright=
kn-copyright=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IsookaNami
en-aut-sei=Isooka
en-aut-mei=Nami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KikuokaRyo
en-aut-sei=Kikuoka
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ImafukuFuminori
en-aut-sei=Imafuku
en-aut-mei=Fuminori
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=TomimotoKana
en-aut-sei=Tomimoto
en-aut-mei=Kana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SogawaChiharu
en-aut-sei=Sogawa
en-aut-mei=Chiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SogawaNorio
en-aut-sei=Sogawa
en-aut-mei=Norio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KitamuraYoshihisa
en-aut-sei=Kitamura
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
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 Medical Neurobiology, 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 Food and Health Sciences, Faculty of Environmental Studies, Hiroshima Institute of Technology
kn-affil=

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

affil-num=10
en-affil=Department of Pharmacotherapy, School of Pharmacy, Shujitsu University
kn-affil=

affil-num=11
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Rotenone
kn-keyword=Rotenone
en-keyword=Astrocyte
kn-keyword=Astrocyte
en-keyword=Microglia
kn-keyword=Microglia
en-keyword=SPARC
kn-keyword=SPARC
en-keyword=Parkinson's disease
kn-keyword=Parkinson's disease
END

start-ver=1.4
cd-journal=joma
no-vol=178
cd-vols=
no-issue=
article-no=
start-page=106920
end-page=
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=End-to-end time-dependent probabilistic assessment of landslide hazards using hybrid deep learning simulator
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Early warning detection of landslide hazards often requires real-time or near real-time predictions, which can be challenging due to the presence of multiple geo-uncertainties and time-variant external environmental loadings. The propagation of these uncertainties at the system level for understanding the spatiotemporal behavior of slopes often requires time-consuming numerical calculations, significantly hindering the establishment of an early warning system. This paper presents a hybrid deep learning simulator, which fuses parallel convolutional neural networks (CNNs) and long short-term memory (LSTM) networks through attention mechanisms, termed PCLA-Net, to facilitate time-dependent probabilistic assessment of landslide hazards. PCLA-Net features two novelties. First, it is capable of simultaneously handling both temporal and spatial information. CNNs specialize in interpreting spatial data, while LSTM excels in handling time-variant data. Coupled with two attention mechanisms, the two modules are combined to probabilistically predict the spatiotemporal behavior of slopes. Second, PCLA-Net realizes end-to-end predictions. In this paper, the Liangshuijing landslide in the Three Gorges Reservoir area of China is used to illustrate PCLA-Net. It is first validated followed by a comparison with existing techniques to demonstrate its improved predictive capabilities. The proposed PCLA-Net simulator can achieve the same level of accuracy with at least 50% reduction in computation resources.
en-copyright=
kn-copyright=

en-aut-name=HuangMenglu
en-aut-sei=Huang
en-aut-mei=Menglu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishimuraShin-ichi
en-aut-sei=Nishimura
en-aut-mei=Shin-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShibataToshifumi
en-aut-sei=Shibata
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WangZe Zhou
en-aut-sei=Wang
en-aut-mei=Ze Zhou
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Civil and Environmental Engineering, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Civil and Environmental Engineering, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Civil and Environmental Engineering, Okayama University
kn-affil=

affil-num=4
en-affil=Marie Skłodowska-Curie Fellow, Department of Engineering, University of Cambridge
kn-affil=
en-keyword=Spatial variability
kn-keyword=Spatial variability
en-keyword=Time-dependent reliability
kn-keyword=Time-dependent reliability
en-keyword=Convolutional neural networks
kn-keyword=Convolutional neural networks
en-keyword=Long short-term memory networks
kn-keyword=Long short-term memory networks
en-keyword=Attention mechanisms
kn-keyword=Attention mechanisms
en-keyword=Landslide hazards
kn-keyword=Landslide hazards
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=11
article-no=
start-page=1680
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251029
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Kidney Organoids: Current Advances and Applications
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Kidney organoids, derived from stem cells, including pluripotent stem cells and adult progenitor cells, have been reported as three-dimensional in vitro models that reflect key aspects of kidney development, structure, and function. Advances in differentiation protocols and tissue engineering have enabled the generation of organoids that exhibit nephron-like structures, including glomerular and tubular structures. Kidney organoids have been widely applied in several directions, including disease modeling and therapeutic screening, drug nephrotoxicity evaluation, and regenerative medicine. In particular, kidney organoids offer a promising platform for studying genetic kidney diseases, such as polycystic kidney disease and congenital anomalies of the kidney and urinary tract (CAKUT), by allowing patient-specific modeling for the analysis of pathophysiology and therapeutic screening. Despite several current limitations, such as incomplete maturation, lack of full nephron segmentation, and variability between protocols and cell conditions, further technological innovations such as microfluidics and bioengineering may refine kidney organoid systems. This review highlights recent advances in kidney organoid research, outlines major applications, and discusses future directions to enhance their physiological relevance, functional maturity, and translational integration into preclinical and clinical nephrology.
en-copyright=
kn-copyright=

en-aut-name=NakanohHiroyuki
en-aut-sei=Nakanoh
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

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

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

en-aut-name=UchidaNaruhiko
en-aut-sei=Uchida
en-aut-mei=Naruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HaraguchiSoichiro
en-aut-sei=Haraguchi
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KitamuraShinji
en-aut-sei=Kitamura
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=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, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

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

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

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

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

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

affil-num=7
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=kidney organoid
kn-keyword=kidney organoid
en-keyword=stem cell
kn-keyword=stem cell
en-keyword=disease modeling
kn-keyword=disease modeling
en-keyword=drug toxicity
kn-keyword=drug toxicity
en-keyword=drug screening
kn-keyword=drug screening
en-keyword=regenerative medicine
kn-keyword=regenerative medicine
END

start-ver=1.4
cd-journal=joma
no-vol=17
cd-vols=
no-issue=9
article-no=
start-page=e92587
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250917
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Intranasal Administration of Semaphorin 3A Inhibitor in a Mouse Model of Olfactory Disorder
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This study investigated the effects of intranasal administration of a semaphorin 3A inhibitor (Sema3A-I) in a mouse model of olfactory disorder, where olfactory sensory neuron (OSN) axons had been severely damaged. We performed axotomy (transection of OSN axons) of the OSNs in mice and administered Sema3A‑I intranasally to seven mice and saline to another seven mice. Following treatment, we assessed the thickness of the olfactory epithelium and the regeneration ratio of OSN axons. Intranasal administration of Sema3A-I did not significantly promote OSN regeneration, axonal outgrowth, or improve axonal projection compared to saline administration. Although Sema3A-I administration showed some promotion of axonal outgrowth, the difference was not statistically significant. Continuous subcutaneous administration of Sema3A-I in rats after axotomy promotes OSN regeneration and axonal outgrowth. Given that intranasal administration is minimally invasive, we believe that it may still be a feasible route when combined with additional treatment strategies. Further investigation into administration methods and therapeutic combinations is warranted.
en-copyright=
kn-copyright=

en-aut-name=MuraiAya
en-aut-sei=Murai
en-aut-mei=Aya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NodaMinori
en-aut-sei=Noda
en-aut-mei=Minori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
ORCID=

en-aut-name=TakaharaJunko
en-aut-sei=Takahara
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MakiharaSeiichiro
en-aut-sei=Makihara
en-aut-mei=Seiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

affil-num=1
en-affil=Otolaryngology - Head and Neck Surgery, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Otolaryngology - Head and Neck Surgery, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Otolaryngology - Head and Neck Surgery, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Division of Technical Support for Medical Science, Department of Comprehensive Technical Solutions, Okayama University
kn-affil=

affil-num=5
en-affil=Otolaryngology - Head and Neck Surgery, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Otolaryngology - Head and Neck Surgery, Okayama University
kn-affil=
en-keyword=axon growth
kn-keyword=axon growth
en-keyword=intranasal administration
kn-keyword=intranasal administration
en-keyword=olfactory disorder
kn-keyword=olfactory disorder
en-keyword=olfactory sensory neurons
kn-keyword=olfactory sensory neurons
en-keyword=semaphorin3a
kn-keyword=semaphorin3a
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=5
article-no=
start-page=e200293
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202510
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Vanishing White Matter Disease With EIF2B2 c.254T >A Variant
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objectives<br>
Typical MRI findings of vanishing white matter disease (VWM) include diffuse white matter lesions with cystic degeneration. However, mild cases may lack these typical features, posing diagnostic challenges.<br>
Methods<br>
We describe 2 of 3 individuals carrying the homozygous c.254T >A variant in EIF2B2 identified at our hospital, excluding 1 previously reported case.1 Genetic analyses were performed using whole-genome sequence or whole-exome sequence analysis, and detected variants were confirmed by direct nucleotide sequence analysis. Brain MRI findings and clinical features were reviewed for the 2 individuals along with other cases in the literature with the same variant.<br>
Results<br>
A 69-year-old woman presented with recurrent transient dizziness and secondary amenorrhea. MRI of the brain revealed small T2-hyperintense lesions confined to the subcortical white matter with hyperintensities on diffusion-weighted images and mildly elevated apparent diffusion coefficient values. A 28-year-old woman presented with transient dizziness and secondary amenorrhea. MRI of the brain showed mild T2-hyperintense lesions in the cerebral white matter with frontal predominance.<br>
Discussion<br>
This report highlights the clinically mild cases of VWM with subtle abnormalities on brain MRI who had the homozygous c.254T >A in EIF2B2, further expanding the clinical spectrum of VWM and underscoring the importance of genetic assessments in the diagnosis of individuals with mild clinical and MRI findings.
en-copyright=
kn-copyright=

en-aut-name=KakumotoToshiyuki
en-aut-sei=Kakumoto
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsukawaTakashi
en-aut-sei=Matsukawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TokimuraRyo
en-aut-sei=Tokimura
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TsuboyamaYoko
en-aut-sei=Tsuboyama
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HayashiYasufumi
en-aut-sei=Hayashi
en-aut-mei=Yasufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MitsutakeAkihiko
en-aut-sei=Mitsutake
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IwataAtsushi
en-aut-sei=Iwata
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MaedaMeiko Hashimoto
en-aut-sei=Maeda
en-aut-mei=Meiko Hashimoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShimizuJun
en-aut-sei=Shimizu
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=GonoiWataru
en-aut-sei=Gonoi
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
ORCID=

en-aut-name=MitsuiJun
en-aut-sei=Mitsui
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TsujiShoji
en-aut-sei=Tsuji
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
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, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=5
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=6
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=8
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=9
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=10
en-affil=Department of Radiology, Graduate School of Medicine, The University of Tokyo
kn-affil=

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

affil-num=12
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=13
en-affil=Department of Molecular Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=14
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=11
article-no=
start-page=2261
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250531
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=An Automatic Code Generation Tool Using Generative Artificial Intelligence for Element Fill-in-the-Blank Problems in a Java Programming Learning Assistant System
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Presently, Java is a fundamental object-oriented programming language that can be mastered by any student in information technology or computer science. To assist both teachers and students, we developed the Java Programming Learning Assistant System (JPLAS). It offers several types of practice problems with different levels and learning goals for step-by-step self-study, where any answer is automatically marked in the system. One challenge for teachers that is addressed with JPLAS is the generation of proper exercise problems that meet learning requirements. We implemented programs for generating new problems from given source codes, as collecting and evaluating suitable codes remains time-consuming. In this paper, we present an automatic code generation tool using generative AI to solve this challenge. Prompt engineering is used to help generate an appropriate source code, and the quality is controlled by optimizing the prompt based on the outputs. For applications in JPLAS, we implement a web application system to automatically generate an element fill-in-the-blank problem (EFP) in JPLAS. For evaluation, we select the element fill-in-the-blank problem (EFP) as the target type in JPLAS and generate several instances using this tool. The results confirm the validity and effectiveness of the proposed method.
en-copyright=
kn-copyright=

en-aut-name=ZhuZihao
en-aut-sei=Zhu
en-aut-mei=Zihao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FunabikiNobuo
en-aut-sei=Funabiki
en-aut-mei=Nobuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MentariMustika
en-aut-sei=Mentari
en-aut-mei=Mustika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AungSoe Thandar
en-aut-sei=Aung
en-aut-mei=Soe Thandar
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KaoWen-Chung
en-aut-sei=Kao
en-aut-mei=Wen-Chung
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=LeeYi-Fang
en-aut-sei=Lee
en-aut-mei=Yi-Fang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Information and Communication Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Information and Communication Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Information and Communication Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Information and Communication Systems, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Electrical Engineering, National Taiwan Normal University
kn-affil=

affil-num=6
en-affil=Department of Industrial Education, National Taiwan Normal University
kn-affil=
en-keyword=JPLAS
kn-keyword=JPLAS
en-keyword=Java programming learning
kn-keyword=Java programming learning
en-keyword=learning requirements
kn-keyword=learning requirements
en-keyword=generative AI
kn-keyword=generative AI
en-keyword=prompt engineering
kn-keyword=prompt engineering
en-keyword=quality control
kn-keyword=quality control
en-keyword=prompt optimization
kn-keyword=prompt optimization
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=21
article-no=
start-page=11479
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241025
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dennd2c Negatively Controls Multinucleation and Differentiation in Osteoclasts by Regulating Actin Polymerization and Protrusion Formation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Osteoclasts are bone-resorbing multinucleated giant cells formed by the fusion of monocyte/macrophage lineages. Various small GTPases are involved in the multinucleation and differentiation of osteoclasts. However, the roles of small GTPases regulatory molecules in osteoclast differentiation remain unclear. In the present study, we examined the role of Dennd2c, a putative guanine nucleotide exchange factor for Rab GTPases, in osteoclast differentiation. Knockdown of Dennd2c promoted osteoclast differentiation, resorption, and expression of osteoclast markers. Morphologically, Dennd2c knockdown induced the formation of larger osteoclasts with several protrusions. In contrast, overexpression of Dennd2c inhibited the multinucleation and differentiation of osteoclasts, bone resorption, and the expression of osteoclast markers. Dennd2c-overexpressing macrophages exhibited spindle-shaped mononuclear cells and long thin protrusions. Treatment of Dennd2c-overexpressing cells with the Cdc42 inhibitor ML-141 or the Rac1 inhibitor 6-thio-GTP prevented protrusion formation. Moreover, treatment of Dennd2c-overexpressing cells with the actin polymerization inhibitor latrunculin B restored multinucleated and TRAP-positive osteoclast formation. These results indicate that Dennd2c negatively regulates osteoclast differentiation and multinucleation by modulating protrusion formation in macrophages.
en-copyright=
kn-copyright=

en-aut-name=KoyanagiYu
en-aut-sei=Koyanagi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakaiEiko
en-aut-sei=Sakai
en-aut-mei=Eiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamaguchiYu
en-aut-sei=Yamaguchi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FarhanaFatima
en-aut-sei=Farhana
en-aut-mei=Fatima
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TairaYohsuke
en-aut-sei=Taira
en-aut-mei=Yohsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OkamotoKuniaki
en-aut-sei=Okamoto
en-aut-mei=Kuniaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MurataHiroshi
en-aut-sei=Murata
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TsukubaTakayuki
en-aut-sei=Tsukuba
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

affil-num=2
en-affil=Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

affil-num=3
en-affil=Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

affil-num=4
en-affil=Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

affil-num=5
en-affil=Division of Cariology and Restorative Dentistry, Department of Prosthetic Dentistry, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

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

affil-num=7
en-affil=Division of Cariology and Restorative Dentistry, Department of Prosthetic Dentistry, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

affil-num=8
en-affil=Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=
en-keyword=osteoclast
kn-keyword=osteoclast
en-keyword=actin polymerization
kn-keyword=actin polymerization
en-keyword=protrusion formation
kn-keyword=protrusion formation
en-keyword=Dennd2c
kn-keyword=Dennd2c
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=2
article-no=
start-page=22
end-page=32
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250805
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Data inventory, processing, and reporting on plant blindness among high school students in three schools in West Java
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Plant blindness is a problem related to a person's inability to realize, recognize, and know the benefits and roles of plants. After some research, there was a shift in the term, from Plant Blindness to Plant Awareness Disparity. This study aims to find out the prevalence of Plant Blindness in three high schools in West Java. The method used in this study is descriptive Cross sectional. The results of this study revealed that there were differences in the level of plant awareness in the three schools studied. One of the schools in the city of Bandung showed the highest plant awareness rate. In addition, it was also found that students who had a high level of plant awareness had a high perception of plant awareness. As a follow-up, further research can be carried out to collect more data so that it becomes a whole population. In addition, researchers can then use additional instruments so that more things can be revealed about plant blindness.
en-copyright=
kn-copyright=

en-aut-name=SorayaPuan Helwa Rezha
en-aut-sei=Soraya
en-aut-mei=Puan Helwa Rezha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SolihatRini
en-aut-sei=Solihat
en-aut-mei=Rini
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SanjayaYayan
en-aut-sei=Sanjaya
en-aut-mei=Yayan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HaradaTaro
en-aut-sei=Harada
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Biology Education, Faculty of Mathematics and Science Education, Universitas Pendidikan Indonesia
kn-affil=

affil-num=2
en-affil=Biology Education, Faculty of Mathematics and Science Education, Universitas Pendidikan Indonesia
kn-affil=

affil-num=3
en-affil=Biology Education, Faculty of Mathematics and Science Education, Universitas Pendidikan Indonesia
kn-affil=

affil-num=4
en-affil=Graduate School of Education, Okayama University
kn-affil=
en-keyword=Descriptive statistics
kn-keyword=Descriptive statistics
en-keyword=Inferential statistics
kn-keyword=Inferential statistics
en-keyword=Plant Blindness
kn-keyword=Plant Blindness
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=20250811
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=RNA Delivery Using a Graphene Oxide-Polyethylenimine Hybrid Inhibiting Myotube Differentiation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Graphene oxide (GO) conjugated with short polyethylenimine (PEI) chains (GO-PEI) has been designed as a candidate nanocarrier for small interfering RNA (siRNA) delivery to mammalian cells based on the efficient interaction between the positively charged GO-based platform and the negatively charged siRNA. The function and efficiency of siRNA delivery using GO-PEI were compared to those using the positive control Lipofectamine RNAiMax by analyzing the differentiation to myotubes, and myogenin gene and protein expression in C2C12 cells. RNAiMax transfection induced cellularization and reduction of both myogenin gene and protein expression, suggesting that the differentiation of C2C12 cells was triggered by gene silencing. While GO-PEI also promoted cellularization, the myogenin gene expression remained comparable to scrambled controls, whereas the protein levels were higher than those observed with RNAiMax. Mechanistically, we attributed the reduced gene silencing efficiency of GO-PEI to a poor endosomal escape, despite strong siRNA complexation. This limitation was likely due to a low buffering capacity of GO-PEI, as a significant fraction of nitrogen atoms were already protonated, reducing the availability of free amines necessary for endosomal disruption. An appropriate chemical modification to enhance siRNA release from the endosomes is therefore essential for advancing the development of GO-based platforms as versatile and efficient nanocarriers in gene therapy applications.
en-copyright=
kn-copyright=

en-aut-name=MatsuuraKoji
en-aut-sei=Matsuura
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ReinaGiacomo
en-aut-sei=Reina
en-aut-mei=Giacomo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=GaoZhengfeng
en-aut-sei=Gao
en-aut-mei=Zhengfeng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NishinaYuta
en-aut-sei=Nishina
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=BiancoAlberto
en-aut-sei=Bianco
en-aut-mei=Alberto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=CNRS, Immunology, Immunopathology and Therapeutic Chemistry, UPR3572, University of Strasbourg, ISIS
kn-affil=

affil-num=2
en-affil=CNRS, Immunology, Immunopathology and Therapeutic Chemistry, UPR3572, University of Strasbourg, ISIS
kn-affil=

affil-num=3
en-affil=CNRS, Immunology, Immunopathology and Therapeutic Chemistry, UPR3572, University of Strasbourg, ISIS
kn-affil=

affil-num=4
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=5
en-affil=CNRS, Immunology, Immunopathology and Therapeutic Chemistry, UPR3572, University of Strasbourg, ISIS
kn-affil=
en-keyword=graphene oxide
kn-keyword=graphene oxide
en-keyword=polyethylenimine
kn-keyword=polyethylenimine
en-keyword=myotubes
kn-keyword=myotubes
en-keyword=myogenin
kn-keyword=myogenin
en-keyword=small interfering RNA
kn-keyword=small interfering RNA
en-keyword=transfection
kn-keyword=transfection
END

start-ver=1.4
cd-journal=joma
no-vol=1869
cd-vols=
no-issue=12
article-no=
start-page=130860
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250913
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The F54L mutation of Thioredoxin shows protein instability and increased fluctuations of the catalytic center
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Thioredoxin is a ubiquitous redox protein that acts as an electron donor via its conserved dithiol motif (C32GPC35), catalyzing dithiol–disulfide exchange to regulate the redox state of target proteins. It supports antioxidant defense via peroxiredoxins, facilitates DNA synthesis by donating electrons to ribonucleotide reductase, and regulates redox-sensitive signaling pathways, including those controlling transcription and apoptosis. Neuronal degeneration and chronic kidney disease have been observed in Txn-F54L mutant rats; however, the details of why the Txn mutation causes these phenomena remain unknown. The present study aimed to elucidate the functional and structural changes caused by the F54L mutation. The Thioredoxin-F54L showed less insulin-reducing activity and more thermosensitivity to denaturation in the body temperature range compared to the wild type. The crystal structure revealed that F54 forms hydrophobic interactions with the surrounding hydrophobic amino acids. In addition, molecular dynamics simulation predicts increased fluctuations around the F54L mutation and a tendency for the distance between residues C32 and C35 at the catalytic center to be widened. The increased distance between residues C32 and C35 of the catalytic center may affect the reducing activity of the enzyme on the substrate. The finding that Thioredoxin-F54L is prone to denaturation at normal body temperature may reduce the normally functioning Thioredoxin. These molecular characteristics of Thioredoxin-F54L may be related to brain and kidney disease development in the Txn-F54L rats.
en-copyright=
kn-copyright=

en-aut-name=BabaTakumi
en-aut-sei=Baba
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UenoGo
en-aut-sei=Ueno
en-aut-mei=Go
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OheChika
en-aut-sei=Ohe
en-aut-mei=Chika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SajiShuku
en-aut-sei=Saji
en-aut-mei=Shuku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamamotoSachiko
en-aut-sei=Yamamoto
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamamotoMasaki
en-aut-sei=Yamamoto
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=

en-aut-name=OkazakiNobuo
en-aut-sei=Okazaki
en-aut-mei=Nobuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OuchidaMamoru
en-aut-sei=Ouchida
en-aut-mei=Mamoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=Kawasaki-OhmoriIori
en-aut-sei=Kawasaki-Ohmori
en-aut-mei=Iori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakeshitaKohei
en-aut-sei=Takeshita
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=

affil-num=2
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=

affil-num=3
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=

affil-num=4
en-affil=Structural Biology Division, Japan Synchrotron Radiation Research Institute
kn-affil=

affil-num=5
en-affil=Structural Biology Division, Japan Synchrotron Radiation Research Institute
kn-affil=

affil-num=6
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=

affil-num=7
en-affil=Materials Sciences Research Center, Japan Atomic Energy Agency
kn-affil=

affil-num=8
en-affil=Neutron Science and Technology Center, Comprehensive Research Organization for Science and Society (CROSS)
kn-affil=

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

affil-num=10
en-affil=Section of Developmental Physiology and Pathology, Faculty of Education, Okayama University
kn-affil=

affil-num=11
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=
en-keyword=Txn
kn-keyword=Txn
en-keyword=Thioredoxin
kn-keyword=Thioredoxin
en-keyword=Protein instability
kn-keyword=Protein instability
en-keyword=Thermosensitivity
kn-keyword=Thermosensitivity
en-keyword=Crystal structure
kn-keyword=Crystal structure
en-keyword=Molecular dynamics simulation
kn-keyword=Molecular dynamics simulation
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=1
end-page=3
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250919
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dual-action intranasal oxytocin enhances both male sexual performance and fertility in rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=EnomotoChica
en-aut-sei=Enomoto
en-aut-mei=Chica
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OtiTakumi
en-aut-sei=Oti
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamanakaTakahiro
en-aut-sei=Yamanaka
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShimadaMasayuki
en-aut-sei=Shimada
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=

affil-num=1
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Laboratory of Reproductive Endocrinology, Graduate School of Integrated Sciences for Life, Hiroshima University
kn-affil=

affil-num=4
en-affil=Laboratory of Reproductive Endocrinology, Graduate School of Integrated Sciences for Life, Hiroshima University
kn-affil=

affil-num=5
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=oxytocin
kn-keyword=oxytocin
en-keyword=intranasal administration
kn-keyword=intranasal administration
en-keyword=sexual behavior
kn-keyword=sexual behavior
en-keyword=sperm motility
kn-keyword=sperm motility
en-keyword=paraventricular nucleus
kn-keyword=paraventricular nucleus
en-keyword=male sexual function
kn-keyword=male sexual function
en-keyword=androgen signaling
kn-keyword=androgen signaling
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=17
article-no=
start-page=8643
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250905
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Anti-HMGB1 Antibody Therapy Ameliorates Spinal Cord Ischemia–Reperfusion Injury in Rabbits
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Spinal cord ischemia–reperfusion (SCI/R) injury remains a major clinical challenge with limited therapeutic options. High-mobility group box 1 (HMGB1), a proinflammatory mediator released during cellular stress, has been implicated in the pathogenesis of ischemia–reperfusion-induced neural damage. In this study, we investigated the neuroprotective potential of the anti-HMGB1 monoclonal antibody (mAb) in a rabbit model of SCI/R injury. Male New Zealand White rabbits were anesthetized and subjected to 11 min of abdominal aortic occlusion using a micro-bulldog clamp following heparinization. Anti-HMGB1 mAb or control IgG was administered intravenously immediately after reperfusion and again at 6 h post-reperfusion. Neurological function was assessed at 6, 24, and 48 h after reperfusion using the modified Tarlov scoring system. The rabbits were euthanized 48 h after reperfusion for spinal cord and blood sampling. Treatment with anti-HMGB1 mAb significantly improved neurological outcomes, reduced the extent of spinal cord infarction, preserved motor neuron viability, and decreased the presence of activated microglia and infiltrating neutrophils. Furthermore, it attenuated apoptosis, oxidative stress, and inflammatory responses in the spinal cord, and helped maintain the integrity of the blood–spinal cord barrier. These findings suggest that anti-HMGB1 mAb may serve as a promising therapeutic agent for SCI/R injury.
en-copyright=
kn-copyright=

en-aut-name=MuraokaGenya
en-aut-sei=Muraoka
en-aut-mei=Genya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujiiYasuhiro
en-aut-sei=Fujii
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

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

en-aut-name=QiaoHandong
en-aut-sei=Qiao
en-aut-mei=Handong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WangDengli
en-aut-sei=Wang
en-aut-mei=Dengli
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OusakaDaiki
en-aut-sei=Ousaka
en-aut-mei=Daiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OozawaSusumu
en-aut-sei=Oozawa
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

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

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

affil-num=2
en-affil=Department of Translational Research, Center for Innovative Clinical Medicine, Medical Development Field, Okayama University
kn-affil=

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

affil-num=4
en-affil=Department of Pharmacology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

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

affil-num=6
en-affil=Department of Medical Technology, Faculty of Science, Okayama University of Science
kn-affil=

affil-num=7
en-affil=Division of Medical Safety Management, Safety Management Facility, Okayama University Hospital
kn-affil=

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

affil-num=9
en-affil=Department of Translational Research and Drug Development, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=thoracoabdominal aortic aneurysm
kn-keyword=thoracoabdominal aortic aneurysm
en-keyword=spinal cord ischemia–reperfusion injury
kn-keyword=spinal cord ischemia–reperfusion injury
en-keyword=high mobility group box 1
kn-keyword=high mobility group box 1
en-keyword=neuroprotection
kn-keyword=neuroprotection
en-keyword=blood–spinal cord barrier
kn-keyword=blood–spinal cord barrier
en-keyword=aortic surgery
kn-keyword=aortic surgery
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=
article-no=
start-page=113544
end-page=113556
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Optimized Ensemble Deep Learning for Real-Time Intrusion Detection on Resource-Constrained Raspberry Pi Devices
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The rapid growth of Internet of Things (IoT) networks has increased security risks, making it essential to have effective Intrusion Detection Systems (IDS) for real-time threat detection. Deep learning techniques offer promising solutions for such detection due to their superior complex pattern recognition and anomaly detection capabilities in large datasets. This paper proposes an optimized ensemble-based IDS designed specifically for efficient deployment on edge hardware. However, deploying such computationally intensive models on resource-limited edge devices remains a significant challenge due to model size and computational overhead on devices with limited processing capabilities. Building upon our previously developed stacked Long Short-Term Memory (LSTM) model integrated with ANOVA feature selection, we optimize it by integrating dual-stage model compression: pruning and quantization to create a lightweight model suitable for real-time inference on Raspberry Pi devices. To evaluate the system under realistic conditions, we combined with a Kafka-based testbed to simulate dynamic IoT environments with variable traffic loads, delays, and multiple simultaneous attack sources. This enables the assessment of detection performance under varying traffic volumes, latency, and overlapping attack scenarios. The proposed system maintains high detection performance with accuracy of 97.3% across all test scenarios, while efficiently leveraging multi-core processing with peak CPU usage reaching 111.8%. These results demonstrate the system’s practical viability for real-time IoT security at the edge.
en-copyright=
kn-copyright=

en-aut-name=MusthafaMuhammad Bisri
en-aut-sei=Musthafa
en-aut-mei=Muhammad Bisri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HudaSamsul
en-aut-sei=Huda
en-aut-mei=Samsul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NguyenTuy Tan
en-aut-sei=Nguyen
en-aut-mei=Tuy Tan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KoderaYuta
en-aut-sei=Kodera
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NogamiYasuyuki
en-aut-sei=Nogami
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

affil-num=2
en-affil=Interdisciplinary Education and Research Field, Okayama University
kn-affil=

affil-num=3
en-affil=School of Informatics, Computing, and Cyber Systems, Northern Arizona 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=
en-keyword=Internet of things
kn-keyword=Internet of things
en-keyword=intrusion detection system
kn-keyword=intrusion detection system
en-keyword=stacked lstm
kn-keyword=stacked lstm
en-keyword=pruning model
kn-keyword=pruning model
en-keyword=optimizing model
kn-keyword=optimizing model
en-keyword=quantization model
kn-keyword=quantization model
en-keyword=raspberry pi
kn-keyword=raspberry pi
en-keyword=real-time detection
kn-keyword=real-time detection
en-keyword=apache kafka
kn-keyword=apache kafka
END

start-ver=1.4
cd-journal=joma
no-vol=149
cd-vols=
no-issue=1
article-no=
start-page=36
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250426
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cerebral Braak stage and amygdala granular fuzzy astrocyte status have independent effects on neuronal 3R-tau and 4R-tau accumulations in the olfactory bulb, respectively, in cases with low to intermediate AD neuropathologic change
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=YokotaOsamu
en-aut-sei=Yokota
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MikiTomoko
en-aut-sei=Miki
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Nakashima-YasudaHanae
en-aut-sei=Nakashima-Yasuda
en-aut-mei=Hanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshizuHideki
en-aut-sei=Ishizu
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HaraguchiTakashi
en-aut-sei=Haraguchi
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyashitaAkinori
en-aut-sei=Miyashita
en-aut-mei=Akinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IkeuchiTakeshi
en-aut-sei=Ikeuchi
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HasegawaMasato
en-aut-sei=Hasegawa
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NishikawaNaoto
en-aut-sei=Nishikawa
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TakenoshitaShintaro
en-aut-sei=Takenoshita
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TeradaSeishi
en-aut-sei=Terada
en-aut-mei=Seishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
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=12
ORCID=

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

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

affil-num=3
en-affil=Okayama University Medical School
kn-affil=

affil-num=4
en-affil=Okayama University Medical School
kn-affil=

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

affil-num=6
en-affil=Department of Molecular Genetics, Brain Research Institute, Niigata University
kn-affil=

affil-num=7
en-affil=Department of Molecular Genetics, Brain Research Institute, Niigata University
kn-affil=

affil-num=8
en-affil=Dementia Research Project, Tokyo Metropolitan Institute of Medical Science
kn-affil=

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

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

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

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

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250612
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Asymptomatic intracranial vascular lesions and cognitive function in a general population of Japanese men: Shiga Epidemiological Study of Subclinical Atherosclerosis (SESSA)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction: Intracranial subclinical vessel diseases are considered important indicators of cognitive impairment. However, a comprehensive assessment of various types of vessel disease, particularly in Asian populations, is lacking. We aimed to compare multiple types of intracranial vessel disease in association with cognitive function among a community-based Japanese male population. Methods: The Shiga Epidemiological Study of Subclinical Atherosclerosis (SESSA) randomly recruited and examined a community-based cohort of Japanese men from Shiga, Japan. We analyzed those who underwent the Cognitive Abilities Screening Instrument (CASI) assessment and cranial magnetic resonance imaging/angiogram (MRI/MRA) in 2010–2015. Using MRI/MRA, we assessed lacunar infarction, microbleeds, periventricular hyperintensity (PVH), deep subcortical white matter hyperintensity (DSWMH), and intracranial artery stenosis (ICAS). We divided these subclinical cerebrovascular diseases (SCDs) into three categories according to severity. Using linear regression, we calculated the CASI score according to the grade of each vessel disease, adjusted for age and years of education. Results: In the adjusted models, CASI scores were significantly associated with both PVH and DSWMH. Specifically, multivariable-adjusted CASI scores declined across increasing severity categories of DSWMH (91.7, 91.2, and 90.4; p for trend = 0.011) and PVH (91.5, 90.4, and 89.7; p for trend = 0.006). Other SCDs did not show significant associations. In stratified analyses based on the presence or absence of each SCD, both DSWMH and PVH demonstrated significant inverse trends with CASI scores in the absence of lacunar infarcts and microbleeds and in the presence of ICAS. Additionally, among participants with PVH (+), ≥moderate ICAS was significantly associated with lower CASI scores. Conclusion: PVH and DSWMH showed significant dose-response relationships with cognitive function among community-based Japanese men. These findings suggest that white matter lesions may be an important indicator of early cognitive impairment, and severe ICAS may also play a role in those with PVH.
en-copyright=
kn-copyright=

en-aut-name=ItoTakahiro
en-aut-sei=Ito
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujiyoshiAkira
en-aut-sei=Fujiyoshi
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OhkuboTakayoshi
en-aut-sei=Ohkubo
en-aut-mei=Takayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShiinoAkihiko
en-aut-sei=Shiino
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShitaraSatoshi
en-aut-sei=Shitara
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyagawaNaoko
en-aut-sei=Miyagawa
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ToriiSayuki
en-aut-sei=Torii
en-aut-mei=Sayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HisamatsuTakashi
en-aut-sei=Hisamatsu
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SegawaHiroyoshi
en-aut-sei=Segawa
en-aut-mei=Hiroyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KondoKeiko
en-aut-sei=Kondo
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KadotaAya
en-aut-sei=Kadota
en-aut-mei=Aya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TooyamaIkuo
en-aut-sei=Tooyama
en-aut-mei=Ikuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=WatanabeYoshiyuki
en-aut-sei=Watanabe
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=YoshidaKazumichi
en-aut-sei=Yoshida
en-aut-mei=Kazumichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NozakiKazuhiko
en-aut-sei=Nozaki
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=MiuraKatsuyuki
en-aut-sei=Miura
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=The SESSA Research Group
en-aut-sei=The SESSA Research Group
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

affil-num=1
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=2
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=3
en-affil=Department of Hygiene and Public Health, Teikyo University School of Medicine
kn-affil=

affil-num=4
en-affil=Molecular Neuroscience Research Center, Shiga University of Medical Science
kn-affil=

affil-num=5
en-affil=Department of Neurosurgery, Shiga University of Medical Science
kn-affil=

affil-num=6
en-affil=Department of Preventive Medicine and Public Health, Keio University School of Medicine
kn-affil=

affil-num=7
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

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

affil-num=9
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=10
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=11
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=12
en-affil=Molecular Neuroscience Research Center, Shiga University of Medical Science
kn-affil=

affil-num=13
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=14
en-affil=Department of Neurosurgery, Shiga University of Medical Science
kn-affil=

affil-num=15
en-affil=Department of Neurosurgery, Shiga University of Medical Science
kn-affil=

affil-num=16
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=17
en-affil=
kn-affil=
en-keyword=Cognitive impairment
kn-keyword=Cognitive impairment
en-keyword=Cerebrovascular disease
kn-keyword=Cerebrovascular disease
en-keyword=Brain magnetic resonance imaging
kn-keyword=Brain magnetic resonance imaging
en-keyword=White matter lesion
kn-keyword=White matter lesion
en-keyword=Community-based population study
kn-keyword=Community-based population study
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=
article-no=
start-page=244
end-page=256
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Postnatal expression of Cat-315-positive perineuronal nets in the SAMP10 mouse primary somatosensory cortex
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Perineuronal nets (PNNs) form at the end of the critical period of plasticity in the mouse primary somatosensory cortex. PNNs are said to have functions that control neuroplasticity and provide neuroprotection. However, it is not clear which molecules in PNNs have these functions. We have previously reported that Cat-315-positive molecules were not expressed in the PNNs of the senescence-accelerated model (SAM)P10 strain model mice at 12 months of age. To confirm whether the loss of Cat-315-positive molecules occurred early in life in SAMP10 mice, we examined Cat-315-positive PNNs in the primary somatosensory cortex during postnatal development. This research helps to elucidate the function of PNNs and the mechanism of cognitive decline associated with ageing. To confirm whether Cat-315-positive PNNs changed in an age-dependent manner in SAMP10 mice, we examined the primary somatosensory cortex at 21, 28, and 56 days after birth. We compared these results with those of senescence-accelerated mouse-resistant (SAMR) mice. In SAMP10 mice, Cat-315-positive PNNs were expressed in the primary somatosensory cortex early after birth, but their expression was significantly lower than that in SAMR1 mice. Many other molecules that calibrated the PNN were unchanged between SAMP10 and SAMR1 mice. This study revealed that the expression of the Cat-315 epitope was decreased in the primary somatosensory cortex of SAMP10 mice during postnatal development. SAMP10 mice have had histological abnormalities in their brains since early life. Furthermore, using SAMP10 will be useful in elucidating the mechanism of age-related abnormalities in brain function as well as in elucidating the function and structure of PNNs.
en-copyright=
kn-copyright=

en-aut-name=UenoHiroshi
en-aut-sei=Ueno
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakahashiYu
en-aut-sei=Takahashi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoriSachiko
en-aut-sei=Mori
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KitanoEriko
en-aut-sei=Kitano
en-aut-mei=Eriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MurakamiShinji
en-aut-sei=Murakami
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WaniKenta
en-aut-sei=Wani
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsumotoYosuke
en-aut-sei=Matsumoto
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OkamotoMotoi
en-aut-sei=Okamoto
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IshiharaTakeshi
en-aut-sei=Ishihara
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Medical Technology, Kawasaki University of Medical Welfare
kn-affil=

affil-num=2
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

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

affil-num=4
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=5
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=6
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

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

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

affil-num=9
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=
en-keyword=Ageing
kn-keyword=Ageing
en-keyword=Brain function
kn-keyword=Brain function
en-keyword=Neuroplasticity
kn-keyword=Neuroplasticity
en-keyword=Neuroprotection
kn-keyword=Neuroprotection
en-keyword=Cognitive decline
kn-keyword=Cognitive decline
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250225
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Age-related behavioural abnormalities in C57BL/6.KOR–Apoe shl mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Spontaneously hyperlipidaemic (Apoeshl) mice were discovered in 1999 as mice lacking apolipoprotein E (ApoE) owing to a mutation in the Apoe gene. However, age-related behavioural changes in commercially available Apoeshl mice have not yet been clarified. The behavioural abnormalities of ApoE-deficient mice, which are genetically modified mice artificially deficient in ApoE, have been investigated in detail, and it has been reported that they can serve as a model of Alzheimer’s disease (AD). To understand whether Apoeshl mice can also serve as a murine model of AD, it is necessary to investigate age-related behavioural abnormalities in Apoeshl mice. In this study, we conducted a series of behavioural experiments on 7- and 11-month-old Apoeshl mice to investigate the behavioural abnormalities associated with ageing in Apoeshl mice. In this study, 7-month-old Apoeshl mice showed decreased body weight and grip strength compared to age-matched wild-type mice. In the open field test, 7-month-old Apoeshl mice showed increased anxiety-like behaviour compared to wild-type mice, whereas 11-month-old Apoeshl mice showed decreased anxiety-like behaviour. Moreover, Apoeshl mice aged 7 and 11 months had increased serum cholesterol levels. These results indicate that the behaviour of Apoeshl mice changes with age. However, 11-month-old Apoeshl mice did not show a decline in cognitive function or memory ability similar to murine models of AD. Our findings indicate that Apoeshl mice can be used to investigate the function of ApoE in the central nervous system.
en-copyright=
kn-copyright=

en-aut-name=UenoHiroshi
en-aut-sei=Ueno
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakahashiYu
en-aut-sei=Takahashi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoriSachiko
en-aut-sei=Mori
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KitanoEriko
en-aut-sei=Kitano
en-aut-mei=Eriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MurakamiShinji
en-aut-sei=Murakami
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WaniKenta
en-aut-sei=Wani
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MiyazakiTetsuji
en-aut-sei=Miyazaki
en-aut-mei=Tetsuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MatsumotoYosuke
en-aut-sei=Matsumoto
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OkamotoMotoi
en-aut-sei=Okamoto
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=IshiharaTakeshi
en-aut-sei=Ishihara
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Medical Technology, Kawasaki University of Medical Welfare
kn-affil=

affil-num=2
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

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

affil-num=4
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=5
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=6
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

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

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

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

affil-num=10
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=
en-keyword=age
kn-keyword=age
en-keyword=apolipoprotein
kn-keyword=apolipoprotein
en-keyword=behavioural test
kn-keyword=behavioural test
en-keyword=central nervous system
kn-keyword=central nervous system
en-keyword=mouse
kn-keyword=mouse
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250222
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Rearing in an envy-like environment increases anxiety-like behaviour in mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Interest in the societal and psychological harm caused by widespread envy and social comparison is increasing. Envy is associated with anxiety and depression, though the mechanism by which envy affects neuropsychiatric disorders, such as depression, remains unclear. Clarifying the neurobiological basis of envy’s effects on behaviour and emotion regulation in experimental mice is essential for developing disease-prevention and treatment strategies. As mice recognize other mice in neighbouring cages, this study investigated whether they recognize neighbouring cages housed in environmentally enriched cages and suffer psychological stress due to envy. After being raised in an envy-like environment for 3 weeks, we revealed changes in the behaviour of the mice through a series of behavioural experiments. Mice raised in an envious environment showed increased body weight and anxiety-like behaviour but decreased social behaviour and serum corticosterone levels compared to control mice. Thus, mice recognize their neighbouring cages and experience psychological stress due to envy. This study revealed a part of the scientific basis for why envy increased anxiety. Using this novel experimental breeding environment, it may be possible to create an experimental animal model of anxiety disorders.
en-copyright=
kn-copyright=

en-aut-name=UenoHiroshi
en-aut-sei=Ueno
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KitanoEriko
en-aut-sei=Kitano
en-aut-mei=Eriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakahashiYu
en-aut-sei=Takahashi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MoriSachiko
en-aut-sei=Mori
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MurakamiShinji
en-aut-sei=Murakami
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WaniKenta
en-aut-sei=Wani
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsumotoYosuke
en-aut-sei=Matsumoto
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OkamotoMotoi
en-aut-sei=Okamoto
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IshiharaTakeshi
en-aut-sei=Ishihara
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Medical Technology, Kawasaki University of Medical Welfare
kn-affil=

affil-num=2
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

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

affil-num=4
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=5
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=6
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

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

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

affil-num=9
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=
en-keyword=behaviour
kn-keyword=behaviour
en-keyword=anxiety
kn-keyword=anxiety
en-keyword=mouse
kn-keyword=mouse
en-keyword=envy
kn-keyword=envy
en-keyword=rodent
kn-keyword=rodent
END

start-ver=1.4
cd-journal=joma
no-vol=2024
cd-vols=
no-issue=
article-no=
start-page=9215607
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mice Recognise Mice in Neighbouring Rearing Cages and Change Their Social Behaviour
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Mice are social animals that change their behaviour primarily in response to visual, olfactory, and auditory information from conspecifics. Rearing conditions such as cage size and colour are important factors influencing mouse behaviour. In recent years, transparent plastic cages have become standard breeding cages. The advantage of using a transparent cage is that the experimenter can observe the mouse from outside the cage without touching the cage. However, mice may recognise the environment outside the cage and change their behaviour. We speculated that mice housed in transparent cages might recognise mice in neighbouring cages. We used only male mice in this experiment. C57BL/6 mice were kept in transparent rearing cages with open lids, and the cage positions were maintained for 3 weeks. Subsequently, we examined how mice behaved toward cagemate mice, mice from neighbouring cages, and mice from distant cages. We compared the level of interest in mice using a social preference test. Similar to previous reports, subject mice showed a high degree of interest in unfamiliar mice from distant cages. By contrast, subject mice reacted to mice from neighbouring cages as familiar mice, similar to cagemate mice. This suggests that mice housed in transparent cages with open lids perceive the external environment and identify mice in neighbouring cages. Researchers should pay attention to the environment outside the mouse cage, especially for the social preference test.
en-copyright=
kn-copyright=

en-aut-name=UenoHiroshi
en-aut-sei=Ueno
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakahashiYu
en-aut-sei=Takahashi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoriSachiko
en-aut-sei=Mori
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MurakamiShinji
en-aut-sei=Murakami
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WaniKenta
en-aut-sei=Wani
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsumotoYosuke
en-aut-sei=Matsumoto
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OkamotoMotoi
en-aut-sei=Okamoto
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IshiharaTakeshi
en-aut-sei=Ishihara
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Medical Technology, Kawasaki University of Medical Welfare
kn-affil=

affil-num=2
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

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

affil-num=4
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=5
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=6
en-affil=Department of Neuropsychiatry, Graduate School of Medicine, Dentistry and Pharmaceutical 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 Psychiatry, Kawasaki Medical School
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=12
article-no=
start-page=1399
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250611
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Association Between Chewing Status and Steatotic Liver Disease in Japanese People Aged ≥50 Years: A Cohort Study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/Objectives: In this longitudinal study, the relationship between chewing status and steatotic liver disease (SLD) was examined in 3775 people aged ≥50 years who underwent medical checkups at Junpukai Health Maintenance Center in Okayama, Japan. Methods: Participants without SLD at the time of a baseline survey in 2018 were followed until 2022. Chewing status was assessed by a self-administered questionnaire. The presence or absence of SLD was ascertained from the medical records of Junpukai Health Maintenance Center. Results: A total of 541 participants (14%) were diagnosed as having a poor chewing status at baseline. Furthermore, 318 (8%) participants were newly diagnosed with SLD at follow-up. In multivariate logistic regression analyses, the presence or absence of SLD was found to be associated with the following characteristics at baseline: sex (male: odds ratio [ORs] = 1.806; 95% confidence interval [CIs]: 1.399–2.351), age (ORs = 0.969; 95% CIs: 0.948–0.991), body mass index (≥25.0 kg/m2; ORs = 1.934; 95% CIs: 1.467–2.549), diastolic blood pressure (ORs = 1.017; 95% CIs: 1.002–1.032), and chewing status (poor: ORs = 1.472; 95% CIs: 1.087–1.994). Conclusions: The results indicate that a poor chewing status was associated with SLD development after 4 years. Aggressively recommending dental visits to participants with poor chewing status may not only improve their ability to chew well but may also reduce the incidence of SLD.
en-copyright=
kn-copyright=

en-aut-name=IwaiKomei
en-aut-sei=Iwai
en-aut-mei=Komei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=EkuniDaisuke
en-aut-sei=Ekuni
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AzumaTetsuji
en-aut-sei=Azuma
en-aut-mei=Tetsuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YonenagaTakatoshi
en-aut-sei=Yonenaga
en-aut-mei=Takatoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TabataKoichiro
en-aut-sei=Tabata
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ToyamaNaoki
en-aut-sei=Toyama
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KataokaKota
en-aut-sei=Kataoka
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MaruyamaTakayuki
en-aut-sei=Maruyama
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TomofujiTakaaki
en-aut-sei=Tomofuji
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Community Oral Health, School of Dentistry, Asahi University
kn-affil=

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

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

affil-num=4
en-affil=Department of Community Oral Health, School of Dentistry, Asahi University
kn-affil=

affil-num=5
en-affil=Department of Community Oral Health, School of Dentistry, Asahi University
kn-affil=

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

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

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

affil-num=9
en-affil=Department of Community Oral Health, School of Dentistry, Asahi University
kn-affil=
en-keyword=oral health
kn-keyword=oral health
en-keyword=liver diseases
kn-keyword=liver diseases
en-keyword=longitudinal studies
kn-keyword=longitudinal studies
en-keyword=mastication
kn-keyword=mastication
en-keyword=physical examination
kn-keyword=physical examination
en-keyword=surveys and questionnaires
kn-keyword=surveys and questionnaires
END

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=S1
article-no=
start-page=7
end-page=12
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=Basic biology is not just “for the birds”: how avian studies have informed us about vertebrate reproduction
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Avian reproductive physiology has been studied for centuries, largely because of the importance of birds as food animals. It is likely that the ubiquity and ease of access to domesticated chickens led to them being used in some of the first experiments on transplantation of endocrine structures—in this case, the testes. Since then, study of seasonal changes in reproductive physiology (photoperiodism) in different orders of bird species has led to advances in the understanding of endocrine regulation of reproductive physiology and behavior. These include mechanisms of adult neuroplasticity, sexual selection, sperm competition, stress physiology, and circadian physiology. Here, we focus mainly on the discovery in birds of a neuropeptide named gonadotropin-inhibitory hormone that mostly has inhibitory effects on reproduction. This hormone has since been shown to exist in all mammals studied to date, including humans (it is known as RFamide-related peptide in mammals). We discuss the history and implications of avian studies on gonadotropin-inhibitory hormone/RFamide-related peptide for human reproductive biology.
en-copyright=
kn-copyright=

en-aut-name=BentleyGeorge E.
en-aut-sei=Bentley
en-aut-mei=George E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

affil-num=1
en-affil=Department of Integrative Biology and Helen Wills Neuroscience Institute, University of California at Berkeley
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=GnRH
kn-keyword=GnRH
en-keyword=GnIH
kn-keyword=GnIH
en-keyword=RFamide
kn-keyword=RFamide
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=7661
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=Neurotransmitter recognition by human vesicular monoamine transporter 2
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Human vesicular monoamine transporter 2 (VMAT2), a member of the SLC18 family, plays a crucial role in regulating neurotransmitters in the brain by facilitating their uptake and storage within vesicles, preparing them for exocytotic release. Because of its central role in neurotransmitter signalling and neuroprotection, VMAT2 is a target for neurodegenerative diseases and movement disorders, with its inhibitor being used as therapeutics. Despite the importance of VMAT2 in pharmacophysiology, the molecular basis of VMAT2-mediated neurotransmitter transport and its inhibition remains unclear. Here we show the cryo-electron microscopy structure of VMAT2 in the substrate-free state, in complex with the neurotransmitter dopamine, and in complex with the inhibitor tetrabenazine. In addition to these structural determinations, monoamine uptake assays, mutational studies, and pKa value predictions were performed to characterize the dynamic changes in VMAT2 structure. These results provide a structural basis for understanding VMAT2-mediated vesicular transport of neurotransmitters and a platform for modulation of current inhibitor design.
en-copyright=
kn-copyright=

en-aut-name=ImDohyun
en-aut-sei=Im
en-aut-mei=Dohyun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=JormakkaMika
en-aut-sei=Jormakka
en-aut-mei=Mika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=JugeNarinobu
en-aut-sei=Juge
en-aut-mei=Narinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KishikawaJun-ichi
en-aut-sei=Kishikawa
en-aut-mei=Jun-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KatoTakayuki
en-aut-sei=Kato
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SugitaYukihiko
en-aut-sei=Sugita
en-aut-mei=Yukihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NodaTakeshi
en-aut-sei=Noda
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UemuraTomoko
en-aut-sei=Uemura
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShiimuraYuki
en-aut-sei=Shiimura
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
ORCID=

en-aut-name=AsadaHidetsugu
en-aut-sei=Asada
en-aut-mei=Hidetsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=IwataSo
en-aut-sei=Iwata
en-aut-mei=So
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=2
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=3
en-affil=Department of Genomics and Proteomics, Advanced Science Research Center, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Applied Biology, Kyoto Institute of Technology
kn-affil=

affil-num=5
en-affil=Institute for Protein Research, Osaka University
kn-affil=

affil-num=6
en-affil=Laboratory of Ultrastructural Virology, Institute for Life and Medical Sciences, Kyoto University
kn-affil=

affil-num=7
en-affil=Laboratory of Ultrastructural Virology, Institute for Life and Medical Sciences, Kyoto University
kn-affil=

affil-num=8
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=9
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=10
en-affil=Department of Genomics and Proteomics, Advanced Science Research Center, Okayama University
kn-affil=

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

affil-num=12
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=2
article-no=
start-page=53
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250606
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=An Endocrine-Disrupting Chemical, Bisphenol A Diglycidyl Ether (BADGE), Accelerates Neuritogenesis and Outgrowth of Cortical Neurons via the G-Protein-Coupled Estrogen Receptor
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Bisphenol A diglycidyl ether (BADGE) is the main component of epoxy resin and is used for the inner coating of canned foods and plastic food containers. BADGE can easily migrate from containers and result in food contamination; the compound is known as an endocrine-disrupting chemical. We previously reported that maternal exposure to bisphenol A bis (2,3-dihydroxypropyl) ether (BADGE·2H2O), which is the most detected BADGE derivative not only in canned foods but also in human specimens, during gestation and lactation, could accelerate neuronal differentiation in the cortex of fetuses and induce anxiety-like behavior in juvenile mice. In this study, we investigated the effects of low-dose BADGE·2H2O (1–100 pM) treatment on neurites and the mechanism of neurite outgrowth in cortical neurons. BADGE·2H2O exposure significantly increased the number of dendrites and neurite length in cortical neurons; these accelerating effects were inhibited by estrogen receptor (ER) antagonist ICI 182,780 and G-protein-coupled estrogen receptor (GPER) antagonist G15. BADGE·2H2O down-regulated Hes1 expression, which is a transcriptional repressor, and increased levels of neuritogenic factor neurogenin-3 (Ngn3) in the cortical neurons; the changes were significantly blocked by G15. These data suggest that direct BADGE·2H2O exposure can accelerate neuritogenesis and outgrowth in cortical neurons through down-regulation of Hes1 and by increasing Ngn3 levels through ERs, particularly GPER.
en-copyright=
kn-copyright=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishiyamaChiharu
en-aut-sei=Nishiyama
en-aut-mei=Chiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NagoshiTakeru
en-aut-sei=Nagoshi
en-aut-mei=Takeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyakoAkane
en-aut-sei=Miyako
en-aut-mei=Akane
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OnoSuzuka
en-aut-sei=Ono
en-aut-mei=Suzuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
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=7
ORCID=

en-aut-name=TomimotoKana
en-aut-sei=Tomimoto
en-aut-mei=Kana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
ORCID=

en-aut-name=ZenshoKazumasa
en-aut-sei=Zensho
en-aut-mei=Kazumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
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 Medical School
kn-affil=

affil-num=4
en-affil=Department of Medical Neurobiology, Okayama University Medical School
kn-affil=

affil-num=5
en-affil=Department of Medical Neurobiology, Okayama University Medical School
kn-affil=

affil-num=6
en-affil=Department of Medical Neurobiology, Okayama University Medical School
kn-affil=

affil-num=7
en-affil=Department of Medical Neurobiology, Okayama University Medical School
kn-affil=

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

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

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

affil-num=11
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=BADGE
kn-keyword=BADGE
en-keyword=neurite outgrowth
kn-keyword=neurite outgrowth
en-keyword=estrogen receptor
kn-keyword=estrogen receptor
en-keyword=GPER
kn-keyword=GPER
en-keyword=Hes1
kn-keyword=Hes1
en-keyword=neurogenin-3
kn-keyword=neurogenin-3
END

start-ver=1.4
cd-journal=joma
no-vol=472
cd-vols=
no-issue=
article-no=
start-page=123486
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202505
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical, neuroimaging and genetic findings in the Japanese case series of CLCN2-related leukoencephalopathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Biallelic loss-of-function variants in CLCN2 lead to CLCN2-related leukoencephalopathy (CC2L), also called leukoencephalopathy with ataxia (LKPAT). CC2L is characterized clinically by a spectrum of clinical presentations including childhood- to adult-onset mild ataxia, spasticity, cognitive decline, and vision loss as well as typical MRI findings of symmetrical high signal intensities on the DWIs/T2WIs of the middle cerebellar peduncles (MCPs). We searched for pathogenic variants of CLCN2 in a case series of undiagnosed leukoencephalopathy accompanied by MCP signs, which led to the identification of four Japanese patients with CC2L. All the patients carried at least one allele of c.61dupC (p.Leu21Profs*27) in CLCN2, including compound heterozygosity with either the novel pathogenic variant c.983 + 2 T > A or the previously reported pathogenic variant c.1828C > T (p.Arg610*). Of note, all the four previously reported cases from Japan also harbored c.61dupC, and no reports of this variant have been documented from outside Japan. The allele frequency of c.61dupC in the Japanese population is 0.002152, raising the possibility of a relatively high prevalence of CC2L in Japan. Patients in this study developed symptoms after the age of 30, and demonstrated neurological signs including cerebellar ataxia, pyramidal signs, and mild cognitive impairment, consistent with previous reports. One male patient had two children, supporting preserved fertility, and another patient had calcifications in the cerebral and cerebellar surfaces. These findings provide valuable insights into the broader clinical and genetic spectra of CC2L in the Japanese population, and emphasize the importance of considering this disease in the differential diagnoses of leukoencephalopathy with MCP signs.
en-copyright=
kn-copyright=

en-aut-name=OrimoKenta
en-aut-sei=Orimo
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsukawaTakashi
en-aut-sei=Matsukawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MitsutakeAkihiko
en-aut-sei=Mitsutake
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ChoTakusei
en-aut-sei=Cho
en-aut-mei=Takusei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NaruseHiroya
en-aut-sei=Naruse
en-aut-mei=Hiroya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SakiyamaYoshio
en-aut-sei=Sakiyama
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SumiKensho
en-aut-sei=Sumi
en-aut-mei=Kensho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UchioNaohiro
en-aut-sei=Uchio
en-aut-mei=Naohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SatakeAkane
en-aut-sei=Satake
en-aut-mei=Akane
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TakiyamaYoshihisa
en-aut-sei=Takiyama
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MatsushitaTakuya
en-aut-sei=Matsushita
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OmaeYosuke
en-aut-sei=Omae
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KawaiYosuke
en-aut-sei=Kawai
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=TokunagaKatsushi
en-aut-sei=Tokunaga
en-aut-mei=Katsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=MitsuiJun
en-aut-sei=Mitsui
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
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=16
ORCID=

en-aut-name=TsujiShoji
en-aut-sei=Tsuji
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=5
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=6
en-affil=Division of Neurology, First Department of Integrated Medicine, Saitama Medical Center, Jichi Medical University
kn-affil=

affil-num=7
en-affil=Department of Neurology, Mitsui Memorial Hospital
kn-affil=

affil-num=8
en-affil=Department of Neurology, Mitsui Memorial Hospital
kn-affil=

affil-num=9
en-affil=Department of Neurology, Fuefuki Central Hospital
kn-affil=

affil-num=10
en-affil=Department of Neurology, Fuefuki Central Hospital
kn-affil=

affil-num=11
en-affil=Department of Neurology, Kochi Medical School, Kochi University
kn-affil=

affil-num=12
en-affil=Genome Medical Science Project, National Center for Global Health and Medicine
kn-affil=

affil-num=13
en-affil=Genome Medical Science Project, National Center for Global Health and Medicine
kn-affil=

affil-num=14
en-affil=Genome Medical Science Project, National Center for Global Health and Medicine
kn-affil=

affil-num=15
en-affil=Department of Precision Medicine Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=16
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=17
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=18
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
en-keyword=Leukodystrophy
kn-keyword=Leukodystrophy
en-keyword=CC2L
kn-keyword=CC2L
en-keyword=CLCN2
kn-keyword=CLCN2
en-keyword=MCP sign
kn-keyword=MCP sign
END

start-ver=1.4
cd-journal=joma
no-vol=219
cd-vols=
no-issue=
article-no=
start-page=104944
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202510
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Establishment of a transgenic strain for the whole brain calcium imaging in larval medaka fish (Oryzias latipes)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=GCaMP-based calcium imaging is a powerful tool for investigating neural function in specific neurons. We generated transgenic (Tg) medaka strains expressing jGCaMP7s across extensive brain regions under the control of the gap43 promoter. Using these Tg larvae, calcium imaging successfully detected a tricaine-induced suppression of spontaneous neural activity and topographical visual responses in the optic tectum elicited by moving paramecia or optical fiber stimulation. These results indicate that our Tg medaka strains provide a versatile platform for investigating neural dynamics and their responses to various stimuli.
en-copyright=
kn-copyright=

en-aut-name=SekiTakahide
en-aut-sei=Seki
en-aut-mei=Takahide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyanariKazuhiro
en-aut-sei=Miyanari
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShiraishiAsuka
en-aut-sei=Shiraishi
en-aut-mei=Asuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TsudaSachiko
en-aut-sei=Tsuda
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AnsaiSatoshi
en-aut-sei=Ansai
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakeuchiHideaki
en-aut-sei=Takeuchi
en-aut-mei=Hideaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=

affil-num=2
en-affil=Graduate School of Science and Engineering, Saitama University
kn-affil=

affil-num=3
en-affil=Graduate School of Science and Engineering, Saitama University
kn-affil=

affil-num=4
en-affil=Graduate School of Science and Engineering, Saitama University
kn-affil=

affil-num=5
en-affil=Ushimado Marine Institute, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=
en-keyword=gap43
kn-keyword=gap43
en-keyword=JGCaMP7s
kn-keyword=JGCaMP7s
en-keyword=Ac/Ds
kn-keyword=Ac/Ds
en-keyword=Visuotopy
kn-keyword=Visuotopy
en-keyword=slc2a15b
kn-keyword=slc2a15b
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=77
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Impact of amyloid and tau positivity on longitudinal brain atrophy in cognitively normal individuals
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Individuals on the preclinical Alzheimer's continuum, particularly those with both amyloid and tau positivity (A + T +), display a rapid cognitive decline and elevated disease progression risk. However, limited studies exist on brain atrophy trajectories within this continuum over extended periods.<br>
Methods This study involved 367 ADNI participants grouped based on combinations of amyloid and tau statuses determined through cerebrospinal fluid tests. Using longitudinal MRI scans, brain atrophy was determined according to the whole brain, lateral ventricle, and hippocampal volumes and cortical thickness in AD-signature regions. Cognitive performance was evaluated with the Preclinical Alzheimer's Cognitive Composite (PACC). A generalized linear mixed-effects model was used to examine group × time interactions for these measures. In addition, progression risks to mild cognitive impairment (MCI) or dementia were compared among the groups using Cox proportional hazards models.<br>
Results A total of 367 participants (48 A + T + , 86 A + T − , 63 A − T + , and 170 A − T − ; mean age 73.8 years, mean follow-up 5.1 years, and 47.4% men) were included. For the lateral ventricle and PACC score, the A + T − and A + T + groups demonstrated statistically significantly greater volume expansion and cognitive decline over time than the A − T − group (lateral ventricle: β = 0.757 cm3/year [95% confidence interval 0.463 to 1.050], P < .001 for A + T − , and β = 0.889 cm3/year [0.523 to 1.255], P < .001 for A + T + ; PACC: β =  − 0.19 /year [− 0.36 to − 0.02], P = .029 for A + T − , and β =  − 0.59 /year [− 0.80 to − 0.37], P < .001 for A + T +). Notably, the A + T + group exhibited additional brain atrophy including the whole brain (β =  − 2.782 cm3/year [− 4.060 to − 1.504], P < .001), hippocampus (β =  − 0.057 cm3/year [− 0.085 to − 0.029], P < .001), and AD-signature regions (β =  − 0.02 mm/year [− 0.03 to − 0.01], P < .001). Cox proportional hazards models suggested an increased risk of progressing to MCI or dementia in the A + T + group versus the A − T − group (adjusted hazard ratio = 3.35 [1.76 to 6.39]).<br>
Conclusions In cognitively normal individuals, A + T + compounds brain atrophy and cognitive deterioration, amplifying the likelihood of disease progression. Therapeutic interventions targeting A + T + individuals could be pivotal in curbing brain atrophy, cognitive decline, and disease progression.
en-copyright=
kn-copyright=

en-aut-name=FujishimaMotonobu
en-aut-sei=Fujishima
en-aut-mei=Motonobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawasakiYohei
en-aut-sei=Kawasaki
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
ORCID=

en-aut-name=MatsudaHiroshi
en-aut-sei=Matsuda
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Radiology, Kumagaya General Hospital
kn-affil=

affil-num=2
en-affil=Department of Biostatistics, Graduate School of Medicine, Saitama Medical University
kn-affil=

affil-num=3
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Biofunctional Imaging, Fukushima Medical University
kn-affil=
en-keyword=Preclinical
kn-keyword=Preclinical
en-keyword=Alzheimer’s disease
kn-keyword=Alzheimer’s disease
en-keyword=Longitudinal MRI
kn-keyword=Longitudinal MRI
en-keyword=Tau
kn-keyword=Tau
en-keyword=Amyloid-β
kn-keyword=Amyloid-β
END

start-ver=1.4
cd-journal=joma
no-vol=79
cd-vols=
no-issue=4
article-no=
start-page=253
end-page=259
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202508
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Study of Periprosthetic Femoral Stem Fractures in Hip Arthroplasty for Femoral Neck Fracture
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This study investigated the risk factors for bone fragility and perioperative periprosthetic femoral stem fractures in patients undergoing hip arthroplasty for femoral neck fractures. The records of 215 patients (42 male, 173 female; mean age, 84.4 years) were analyzed to assess correlations among periprosthetic fracture rates and sex, age, body mass index (BMI), Dorr classification, femoral stem fixation type (cemented/cementless), and bone mineral density (BMD) of the contralateral proximal femur. The overall prevalence of perioperative periprosthetic fractures was 4.7%. All patients with periprosthetic fractures were female, and all but one were ≥ 80 years of age. Fracture rates were higher in patients with lower BMI, although this difference was not significant. The fracture rates were 0%, 4.7%, and 7.9% for Dorr types A, B, and C, respectively, and 0% and 5.3% for patients who received cemented and cementless stems, respectively. The findings indicated that female patients, those of advanced age, those with lower BMI, and those with Dorr type C had lower BMDs. Although BMD was significantly lower in patients who received cemented stems compared to those who received cementless stems, no fractures were observed in the former group, suggesting that the use of cemented stems is safe for this high-risk population.
en-copyright=
kn-copyright=

en-aut-name=MiyakeYoshiaki
en-aut-sei=Miyake
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakagiToru
en-aut-sei=Takagi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KonishiikeTaizo
en-aut-sei=Konishiike
en-aut-mei=Taizo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Orthopaedic Surgery, Japanese Red Cross Okayama Hospital
kn-affil=

affil-num=2
en-affil=Department of Orthopaedic Surgery, Japanese Red Cross Okayama Hospital
kn-affil=

affil-num=3
en-affil=Department of Orthopaedic Surgery, Japanese Red Cross Okayama Hospital
kn-affil=
en-keyword=bone mineral density
kn-keyword=bone mineral density
en-keyword=cemented stem
kn-keyword=cemented stem
en-keyword=Dorr classification
kn-keyword=Dorr classification
en-keyword=femoral neck fracture
kn-keyword=femoral neck fracture
en-keyword=periprosthetic femoral stem fracture
kn-keyword=periprosthetic femoral stem fracture
END

start-ver=1.4
cd-journal=joma
no-vol=31
cd-vols=
no-issue=
article-no=
start-page=100776
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202509
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Investigation of the relationship between 0.5–1200 Hz signal characteristics of cortical high-frequency oscillations and epileptogenicity through multivariate analysis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Fast ripples (FRs) (250–500 Hz) on the electroencephalogram (EEG) are closely related to epileptogenicity and are important to determine cortical regions resected in epilepsy surgery. However, FR-related epileptogenicity may be variable, and may depend on information associated with FRs. We enrolled nine epilepsy patients who had undergone intracranial 5 kHz-sampling-rate EEG for surgical treatment and had final Engel class I outcomes. Three electrodes were selected from each epileptogenic area (EA) and the unlikely EA (the region outside the EA) in each patient. Up to 100 candidate FRs were automatically detected from interictal nocturnal EEG at each of the selected electrodes and were visually reviewed independently by two researchers. Multivariate logistic regression analysis was performed using the frequency and log-power value of the corresponding FRs, presence of concurrent spike, ripple, very-high-frequency oscillations (vHFO)1 (500–600 Hz), and vHFO2 (600–1200 Hz), and whether the timing of the spectral peak of corresponding FRs was in the peak–trough or trough–peak transition of each slow activity (0.5–1, 1–2, 2–3, 3–4, and 4–8 Hz) as independent variables. Factors significantly related to epileptogenicity were FR power, the concurrent presence of spike and vHFO2, coupling with 0.5–1 and 1–2 Hz slow waves in the peak–trough transition, and coupling with 3–4 and 4–8 Hz slow waves in the trough–peak transition. Multifactorial analysis of FRs may increase their usefulness, potentially leading to improved treatment outcomes in epilepsy surgery.
en-copyright=
kn-copyright=

en-aut-name=ShibataTakashi
en-aut-sei=Shibata
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TsuchiyaHiroki
en-aut-sei=Tsuchiya
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AkiyamaMari
en-aut-sei=Akiyama
en-aut-mei=Mari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AkiyamaTomoyuki
en-aut-sei=Akiyama
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MatsuhashiMasao
en-aut-sei=Matsuhashi
en-aut-mei=Masao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KobayashiKatsuhiro
en-aut-sei=Kobayashi
en-aut-mei=Katsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

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

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

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

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

affil-num=5
en-affil=Department of Epilepsy, Movement Disorders and Physiology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=6
en-affil=Department of Pediatric Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital
kn-affil=
en-keyword=Epilepsy surgery
kn-keyword=Epilepsy surgery
en-keyword=Multivariate logistic regression analysis
kn-keyword=Multivariate logistic regression analysis
en-keyword=Phase-amplitude coupling
kn-keyword=Phase-amplitude coupling
en-keyword=Ripple
kn-keyword=Ripple
en-keyword=Very high-frequency oscillations
kn-keyword=Very high-frequency oscillations
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=1
article-no=
start-page=104318
end-page=
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=Hypotheses of pathophysiological mechanisms in epileptic encephalopathies: A review
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction: Epileptic encephalopathy (EE) is a serious clinical issue that manifests as part of developmental and epileptic encephalopathy (DEE), particularly in childhood epilepsy. In EE, neurocognitive functions and behavior are impaired by intense epileptiform electroencephalogram (EEG) activity. Hypotheses of pathophysiological mechanisms behind EE are reviewed to contribute to an effective solution for EE.<br>
Review: Current hypotheses are as follows: 1) neuronal dysfunction based on genetic abnormalities that may affect neurocognitive functions and epilepsy separately; 2) impairment of synaptic homeostasis during sleep that may be responsible for DEE/EE with spike-and-wave activation in sleep; 3) abnormal subcortical regulation of the cerebral cortex; 4) abnormal cortical metabolism and hemodynamics with impairment of the neural network including default mode network; 5) neurotransmitter imbalance and disordered neural excitability; 6) the effects of neuroinflammation that may be caused by epileptic seizures and in turn aggravate epileptogenesis; 7) the interaction between physiological and pathological high-frequency EEG activity; etc. The causal relationship between epileptiform EEG activity and neurocognitive dysfunctions is small in DEE based on genetic abnormalities and it is largely unestablished in the other hypothetical mechanisms.<br>
Conclusion: We have not yet found answers to the question of whether the single-central or multiple derangements are present and what seizures and intense epileptiform EEG abnormalities mean in EE. We need to continue our best efforts in both aspects to elucidate the pathophysiological mechanisms of DEE/EE and further develop epilepsy treatment and precision medicine.
en-copyright=
kn-copyright=

en-aut-name=KobayashiKatsuhiro
en-aut-sei=Kobayashi
en-aut-mei=Katsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShibataTakashi
en-aut-sei=Shibata
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TsuchiyaHiroki
en-aut-sei=Tsuchiya
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AkiyamaMari
en-aut-sei=Akiyama
en-aut-mei=Mari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AkiyamaTomoyuki
en-aut-sei=Akiyama
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Pediatrics, Asahigawaso Rehabilitation and Medical Center
kn-affil=

affil-num=2
en-affil=Department of Pediatric Neurology, Okayama University Hospital and Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Pediatric Neurology, Okayama University Hospital and Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Pediatric Neurology, Okayama University Hospital and Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Pediatric Neurology, Okayama University Hospital and Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Behavior
kn-keyword=Behavior
en-keyword=Childhood epilepsy
kn-keyword=Childhood epilepsy
en-keyword=Cognitive function
kn-keyword=Cognitive function
en-keyword=Developmental and epileptic encephalopathy
kn-keyword=Developmental and epileptic encephalopathy
en-keyword=Regression
kn-keyword=Regression
END

start-ver=1.4
cd-journal=joma
no-vol=272
cd-vols=
no-issue=1
article-no=
start-page=36
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Genetic and functional analyses of SPTLC1 in juvenile amyotrophic lateral sclerosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder of the motor system. Pathogenic variants in SPTLC1, encoding a subunit of serine palmitoyltransferase, cause hereditary sensory and autonomic neuropathy type 1 (HSAN1), and have recently been associated with juvenile ALS. SPTLC1 variants associated with ALS cause elevated levels of sphinganines and ceramides. Reports on ALS associated with SPTLC1 remain limited. This study aimed to investigate the frequency of SPTLC1 variants in ALS and relevant clinical characteristics.<br>
Methods We analyzed whole-exome and whole-genome sequence data from 40 probands with familial ALS and 413 patients with sporadic ALS without previously identified causative variants. Reverse transcription polymerase chain reaction (RT-PCR) analysis and droplet digital PCR (ddPCR) were used to assess splicing and mosaicism, respectively. Plasma sphingolipid levels were quantified to analyze biochemical consequences.<br>
Results The heterozygous c.58G>A, p.Ala20Thr variant was identified in a 21-year-old Japanese female patient presenting with symmetric weakness which slowly progressed over 15 years. RT-PCR analysis showed no splice defects. Plasma sphingolipid levels in the patient were significantly increased compared to her asymptomatic parents. ddPCR revealed that the asymptomatic father harbored a mosaic variant with 17% relative mutant allele abundance in peripheral blood leukocytes.<br>
Conclusions We identified a pathogenic c.58G>A, p.Ala20Thr SPTLC1 variant in a patient with juvenile ALS, likely inherited from an asymptomatic parent with mosaicism. Lipid analysis results are consistent with previous findings on SPTLC1-associated ALS. Further studies are necessary to determine the clinical effect of mosaic variants of SPTLC1.
en-copyright=
kn-copyright=

en-aut-name=OkuboSo
en-aut-sei=Okubo
en-aut-mei=So
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NaruseHiroya
en-aut-sei=Naruse
en-aut-mei=Hiroya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
ORCID=

en-aut-name=SudoAtsushi
en-aut-sei=Sudo
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=EsakiKayoko
en-aut-sei=Esaki
en-aut-mei=Kayoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MitsuiJun
en-aut-sei=Mitsui
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsukawaTakashi
en-aut-sei=Matsukawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SatakeWataru
en-aut-sei=Satake
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=GreimelPeter
en-aut-sei=Greimel
en-aut-mei=Peter
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ShingaiNanoka
en-aut-sei=Shingai
en-aut-mei=Nanoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OyaYasushi
en-aut-sei=Oya
en-aut-mei=Yasushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=YoshikawaTakeo
en-aut-sei=Yoshikawa
en-aut-mei=Takeo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TsujiShoji
en-aut-sei=Tsuji
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
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, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

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

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=5
en-affil=Department of Biotechnology and Life Sciences, Faculty of Biotechnology and Life Sciences, Sojo University
kn-affil=

affil-num=6
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=8
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=9
en-affil=Laboratory for Cell Function Dynamics, RIKEN Centre for Brain Sciences
kn-affil=

affil-num=10
en-affil=Division of Applied Life Science, Graduate School of Engineering, Sojo University
kn-affil=

affil-num=11
en-affil=Department of Neurology, National Center of Neurology and Psychiatry
kn-affil=

affil-num=12
en-affil=Laboratory of Molecular Psychiatry, RIKEN Center for Brain Science
kn-affil=

affil-num=13
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=14
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
en-keyword=Juvenile amyotrophic lateral sclerosis
kn-keyword=Juvenile amyotrophic lateral sclerosis
en-keyword=SPTLC1
kn-keyword=SPTLC1
en-keyword=Sphingolipids
kn-keyword=Sphingolipids
en-keyword=Mosaicism
kn-keyword=Mosaicism
END

start-ver=1.4
cd-journal=joma
no-vol=64
cd-vols=
no-issue=12
article-no=
start-page=1900
end-page=1905
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250615
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Subacute Upper Motor Neuron Dysfunction Possibly Associated with the Anti-GM1 Autoantibody
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Anti-GM1 antibodies are associated with Guillain-Barré syndrome (GBS), primarily peripheral neuropathy. However, there are cases of anti-GM1 IgG antibody-positive GBS with upper motor neuron (UMN) signs. We herein report a case of gastrointestinal infection followed by subacute gait disturbance with predominant signs of UMN on a neurological examination. The serum and cerebrospinal fluid tests were positive for anti-GM1 and anti-asialo-GM1 IgG antibodies. An electrophysiological evaluation revealed normal nerve conduction and prolonged central motor conduction times. No magnetic resonance imaging abnormalities were observed. The symptoms improved with treatment, which was accompanied by decreased antibody titers. This case highlights the fact that anti-GM1 IgG-associated disorders may present with predominant UMN involvement.
en-copyright=
kn-copyright=

en-aut-name=OkuboSo
en-aut-sei=Okubo
en-aut-mei=So
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MaedaMeiko
en-aut-sei=Maeda
en-aut-mei=Meiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KatsuseKazuto
en-aut-sei=Katsuse
en-aut-mei=Kazuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=ShirotaYuichiro
en-aut-sei=Shirota
en-aut-mei=Yuichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HamadaMasashi
en-aut-sei=Hamada
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SatakeWataru
en-aut-sei=Satake
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
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, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

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

affil-num=5
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=6
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=8
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
en-keyword=anti-GM1 antibody
kn-keyword=anti-GM1 antibody
en-keyword=anti-GA1 antibody
kn-keyword=anti-GA1 antibody
en-keyword=upper motor neuron
kn-keyword=upper motor neuron
en-keyword=motor-evoked potentials
kn-keyword=motor-evoked potentials
en-keyword=central motor conduction time
kn-keyword=central motor conduction time
en-keyword=Guillain-Barré syndrome
kn-keyword=Guillain-Barré syndrome
END

start-ver=1.4
cd-journal=joma
no-vol=638
cd-vols=
no-issue=8049
article-no=
start-page=225
end-page=236
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=Immune evasion through mitochondrial transfer in the tumour microenvironment
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cancer cells in the tumour microenvironment use various mechanisms to evade the immune system, particularly T cell attack1. For example, metabolic reprogramming in the tumour microenvironment and mitochondrial dysfunction in tumour-infiltrating lymphocytes (TILs) impair antitumour immune responses2,3,4. However, detailed mechanisms of such processes remain unclear. Here we analyse clinical specimens and identify mitochondrial DNA (mtDNA) mutations in TILs that are shared with cancer cells. Moreover, mitochondria with mtDNA mutations from cancer cells are able to transfer to TILs. Typically, mitochondria in TILs readily undergo mitophagy through reactive oxygen species. However, mitochondria transferred from cancer cells do not undergo mitophagy, which we find is due to mitophagy-inhibitory molecules. These molecules attach to mitochondria and together are transferred to TILs, which results in homoplasmic replacement. T cells that acquire mtDNA mutations from cancer cells exhibit metabolic abnormalities and senescence, with defects in effector functions and memory formation. This in turn leads to impaired antitumour immunity both in vitro and in vivo. Accordingly, the presence of an mtDNA mutation in tumour tissue is a poor prognostic factor for immune checkpoint inhibitors in patients with melanoma or non-small-cell lung cancer. These findings reveal a previously unknown mechanism of cancer immune evasion through mitochondrial transfer and can contribute to the development of future cancer immunotherapies.
en-copyright=
kn-copyright=

en-aut-name=IkedaHideki
en-aut-sei=Ikeda
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

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

en-aut-name=WatanabeTomofumi
en-aut-sei=Watanabe
en-aut-mei=Tomofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakenagaKeizo
en-aut-sei=Takenaga
en-aut-mei=Keizo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=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=AkiSho
en-aut-sei=Aki
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=LinJason
en-aut-sei=Lin
en-aut-mei=Jason
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
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=11
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=12
ORCID=

en-aut-name=SuzukiShinichiro
en-aut-sei=Suzuki
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MakinoshimaHideki
en-aut-sei=Makinoshima
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=ItamiMakiko
en-aut-sei=Itami
en-aut-mei=Makiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=NakamuraYuki
en-aut-sei=Nakamura
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=TatsumiYasutoshi
en-aut-sei=Tatsumi
en-aut-mei=Yasutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=SuenagaYusuke
en-aut-sei=Suenaga
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=MorinagaTakao
en-aut-sei=Morinaga
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
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=20
ORCID=

en-aut-name=OhnumaTakehiro
en-aut-sei=Ohnuma
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
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=22
ORCID=

en-aut-name=UmedaYoshiyasu
en-aut-sei=Umeda
en-aut-mei=Yoshiyasu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
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=24
ORCID=

en-aut-name=KiniwaYukiko
en-aut-sei=Kiniwa
en-aut-mei=Yukiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
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=26
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=27
ORCID=

en-aut-name=IkedaJun-ichiro
en-aut-sei=Ikeda
en-aut-mei=Jun-ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=HanazawaToyoyuki
en-aut-sei=Hanazawa
en-aut-mei=Toyoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
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=30
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=31
ORCID=

en-aut-name=SuzukiTakuji
en-aut-sei=Suzuki
en-aut-mei=Takuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=32
ORCID=

en-aut-name=OsawaTsuyoshi
en-aut-sei=Osawa
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=33
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=34
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=35
ORCID=

affil-num=1
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=2
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
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 Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Division of Innovative Cancer Therapeutics, Chiba Cancer Center Research Institute
kn-affil=

affil-num=6
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
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=Division of Nutriomics and Oncology, RCAST, The University of Tokyo
kn-affil=

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

affil-num=10
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute, Chiba, Japan Department of Dermatology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=11
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=13
en-affil=Department of Medical Oncology, Kindai University Faculty of Medicine
kn-affil=

affil-num=14
en-affil=Tsuruoka Metabolomics Laboratory, National Cancer Center
kn-affil=

affil-num=15
en-affil=Department of Surgical Pathology, Chiba Cancer Center
kn-affil=

affil-num=16
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=17
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=18
en-affil=Laboratory of Evolutionary Oncology, Chiba Cancer Center Research Institute
kn-affil=

affil-num=19
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=20
en-affil=Department of Dermatology, Faculty of Medicine, University of Yamanashi
kn-affil=

affil-num=21
en-affil=Department of Dermatology, Faculty of Medicine, University of Yamanashi
kn-affil=

affil-num=22
en-affil=Department of Dermatology, Faculty of Medicine, University of Yamanashi
kn-affil=

affil-num=23
en-affil=Department of Skin Oncology/Dermatology, Saitama Medical University International Medical Center
kn-affil=

affil-num=24
en-affil=Department of Skin Oncology/Dermatology, Saitama Medical University International Medical Center
kn-affil=

affil-num=25
en-affil=Department of Dermatology, Shinshu University School of Medicine
kn-affil=

affil-num=26
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=27
en-affil=Department of Medical Oncology, Kindai University Faculty of Medicine
kn-affil=

affil-num=28
en-affil=Department of Diagnostic Pathology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=29
en-affil=Department of Otorhinolaryngology/Head and Neck Surgery, Chiba University Graduate School of Medicine
kn-affil=

affil-num=30
en-affil=Department of General Thoracic Surgery and Endocrinological Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=31
en-affil=Division of Cellular Signalling, National Cancer Center Research Institute
kn-affil=

affil-num=32
en-affil=Department of Respirology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=33
en-affil=Division of Nutriomics and Oncology, RCAST, The University of Tokyo
kn-affil=

affil-num=34
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=35
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=12
cd-vols=
no-issue=5
article-no=
start-page=271
end-page=277
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240329
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Japan MSA registry: A multicenter cohort study of multiple system atrophy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Multiple system atrophy (MSA) is a neurodegenerative disorder characterized by autonomic failure and various motor symptoms. While MSA-C (cerebellar type) predominates in East Asia, MSA-P (parkinsonian type) predominates in Europe and North America. This nationwide patient registry aimed to (1) conduct a prospective natural history study of MSA in Japan, (2) facilitate patient recruitment for clinical trials, and (3) deposit bioresources and clinical information in a biobank.<br>
Methods: Thirteen institutions participated in this study. Clinical information was obtained by neurologists from the patients visiting the hospital every 12 months to assess the UMSARS Part 2 scores and by telephone interviews by nurses every 6 months to assess UMSARS Part 1 scores and to determine whether clinical events had occurred.<br>
Results: Demographic data from 329 MSA patients (216 MSA-C and 113 MSA-P) were analyzed. The mean age at symptom onset was 58.2 years (standard deviation, 8.9); the mean duration of symptoms at enrollment was 3.5 years (standard deviation, 2.2). The mean 12-month changes in the UMSARS Part 1 and Part 2 scores were 7.9 (standard deviation, 5.6) and 6.4 (standard deviation, 5.9), respectively. The patient registry proved useful in recruiting participants for clinical trials, including those with gene variants. Clinical information and biospecimens were deposited in a biobank.<br>
Discussion: The study highlighted the importance of telephone interviews in minimizing drop-out rates in natural history studies and demonstrated similar MSA progression rates across populations. The deposited bioresources are available to researchers upon request, aiming to contribute to future MSA researches.
en-copyright=
kn-copyright=

en-aut-name=ChikadaAyaka
en-aut-sei=Chikada
en-aut-mei=Ayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OrimoKenta
en-aut-sei=Orimo
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

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

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

en-aut-name=IshiuraHiroyuki
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en-aut-mei=Hiroyuki
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TodaTatsushi
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MizusawaHidehiro
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en-aut-mei=Hidehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakahashiYuji
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KatsunoMasahisa
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en-aut-mei=Masahisa
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HaraKazuhiro
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en-aut-mei=Kazuhiro
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OnoderaOsamu
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en-aut-mei=Osamu
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=IshiharaTomohiko
en-aut-sei=Ishihara
en-aut-mei=Tomohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TadaMasayoshi
en-aut-sei=Tada
en-aut-mei=Masayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KuwabaraSatoshi
en-aut-sei=Kuwabara
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=SugiyamaAtsuhiko
en-aut-sei=Sugiyama
en-aut-mei=Atsuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=YamanakaYoshitaka
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en-aut-mei=Yoshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=TakahashiRyosuke
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=SawamotoNobukatsu
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en-aut-mei=Nobukatsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=SakatoYusuke
en-aut-sei=Sakato
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=IshimotoTomoyuki
en-aut-sei=Ishimoto
en-aut-mei=Tomoyuki
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=HanajimaRitsuko
en-aut-sei=Hanajima
en-aut-mei=Ritsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=WatanabeYasuhiro
en-aut-sei=Watanabe
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=TakigawaHiroshi
en-aut-sei=Takigawa
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=AdachiTadashi
en-aut-sei=Adachi
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
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=25
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=26
ORCID=

en-aut-name=TakashimaHiroshi
en-aut-sei=Takashima
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=HigashiKeiko
en-aut-sei=Higashi
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=KiraJunichi
en-aut-sei=Kira
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
ORCID=

en-aut-name=YabeIchiro
en-aut-sei=Yabe
en-aut-mei=Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

en-aut-name=MatsushimaMasaaki
en-aut-sei=Matsushima
en-aut-mei=Masaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=31
ORCID=

en-aut-name=OgataKatsuhisa
en-aut-sei=Ogata
en-aut-mei=Katsuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=32
ORCID=

en-aut-name=IshikawaKinya
en-aut-sei=Ishikawa
en-aut-mei=Kinya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=33
ORCID=

en-aut-name=NishidaYoichiro
en-aut-sei=Nishida
en-aut-mei=Yoichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=34
ORCID=

en-aut-name=IshiguroTaro
en-aut-sei=Ishiguro
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=35
ORCID=

en-aut-name=OzakiKokoro
en-aut-sei=Ozaki
en-aut-mei=Kokoro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=36
ORCID=

en-aut-name=NagataTetsuya
en-aut-sei=Nagata
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=37
ORCID=

en-aut-name=TsujiShoji
en-aut-sei=Tsuji
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=38
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

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

affil-num=6
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=8
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=9
en-affil=Department of Neurology, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=10
en-affil=Department of Neurology, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=11
en-affil=Department of Neurology, Brain Research Institute, Niigata University
kn-affil=

affil-num=12
en-affil=Department of Neurology, Brain Research Institute, Niigata University
kn-affil=

affil-num=13
en-affil=Department of Neurology, Brain Research Institute, Niigata University
kn-affil=

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

affil-num=15
en-affil=Department of Neurology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=16
en-affil=Department of Neurology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=17
en-affil=Department of Neurology, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=18
en-affil=Department of Human Health Sciences, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=19
en-affil=Department of Neurology, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=20
en-affil=Department of Neurology, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=21
en-affil=Division of Neurology, Department of Brain and Neurosciences, Faculty of Medicine, Tottori University
kn-affil=

affil-num=22
en-affil=Division of Neurology, Department of Brain and Neurosciences, Faculty of Medicine, Tottori University
kn-affil=

affil-num=23
en-affil=Division of Neurology, Department of Brain and Neurosciences, Faculty of Medicine, Tottori University
kn-affil=

affil-num=24
en-affil=Division of Neurology, Department of Brain and Neurosciences, Faculty of Medicine, Tottori University
kn-affil=

affil-num=25
en-affil=Department of Neurology, Okayama University Graduate School of Medicine and Dentistry
kn-affil=

affil-num=26
en-affil=Department of Neurology, Okayama University Graduate School of Medicine and Dentistry
kn-affil=

affil-num=27
en-affil=Department of Neurology and Geriatrics, Graduate School of Medical and Dental Sciences, Kagoshima University
kn-affil=

affil-num=28
en-affil=Department of Neurology and Geriatrics, Graduate School of Medical and Dental Sciences, Kagoshima University
kn-affil=

affil-num=29
en-affil=Department of Neurology, Graduate School of Medical Sciences, Kyushu University
kn-affil=

affil-num=30
en-affil=Department of Neurology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University
kn-affil=

affil-num=31
en-affil=Department of Neurology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University
kn-affil=

affil-num=32
en-affil=Department of Neurology, Higashi-Saitama National Hospital
kn-affil=

affil-num=33
en-affil=Department of Neurology and Neurological Science, Tokyo Medical and Dental University
kn-affil=

affil-num=34
en-affil=Department of Neurology and Neurological Science, Tokyo Medical and Dental University
kn-affil=

affil-num=35
en-affil=Department of Neurology and Neurological Science, Tokyo Medical and Dental University
kn-affil=

affil-num=36
en-affil=Department of Neurology and Neurological Science, Tokyo Medical and Dental University
kn-affil=

affil-num=37
en-affil=Department of Neurology and Neurological Science, Tokyo Medical and Dental University
kn-affil=

affil-num=38
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
en-keyword=multicenter cohort study
kn-keyword=multicenter cohort study
en-keyword=multiple system atrophy
kn-keyword=multiple system atrophy
en-keyword=natural history
kn-keyword=natural history
en-keyword=patient registry
kn-keyword=patient registry
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=10
article-no=
start-page=1215
end-page=1227
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241121
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Enhanced design of pCMViR-TSC plasmid vector for sustainably high cargo gene expression in mammalian cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The first-generation pCMViR-TSC, implemented through the promoter sandwich rule, yields 10- to 100-fold higher gene expression than the standard plasmid used with the CMV (cytomegalovirus) or CAG promoter. However, the vector’s shortcomings limit its utility to transient expression only, as it is not suitable for establishing stable transformants in mammalian cells. To overcome this weakness, we here introduce the improved plasmid vector pSAKA-4B, derived from pCMViR-TSC as a second-generation chromosome-insertable vector. This vector facilitates the linear entry of the expression unit into the TTAA site of DNA universally with transposase assistance. The vector is helpful for the indefinite expression of our target gene. The new vector system is proven here to be efficient in establishing stable transformants with a high likelihood of positive clones that exhibit significantly elevated expression levels of the delivered foreign gene. This system, alongside the first-generation vector, is therefore instrumental for diverse basic research endeavors concerning genes, proteins, cells, and animals, and potentially for clinical applications such as gene therapy.
en-copyright=
kn-copyright=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=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=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=SakaguchiYoshihiko
en-aut-sei=Sakaguchi
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
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=6
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=7
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=8
ORCID=

en-aut-name=TakahashiTetta
en-aut-sei=Takahashi
en-aut-mei=Tetta
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=JiangFan
en-aut-sei=Jiang
en-aut-mei=Fan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=13
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=14
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=15
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=16
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=17
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=18
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=19
ORCID=

en-aut-name=SagayamaKazumi
en-aut-sei=Sagayama
en-aut-mei=Kazumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
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=21
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=22
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=23
ORCID=

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

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

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

affil-num=4
en-affil=Department of Microbiology, Tokushima Bunri University
kn-affil=

affil-num=5
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Biochemistry, Kawasaki Medical School
kn-affil=

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

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

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

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

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

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

affil-num=13
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=14
en-affil=Department of Breast Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine
kn-affil=

affil-num=15
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=16
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=17
en-affil=Medical Oncology Department of Gastrointestinal Tumors, Liaoning Cancer Hospital & Institute, Cancer Hospital of the Dalian University of Technology
kn-affil=

affil-num=18
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=19
en-affil=Department of Biochemistry, Kawasaki Medical School
kn-affil=

affil-num=20
en-affil=Organization for Research and Innovation Strategy, Okayama University
kn-affil=

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

affil-num=22
en-affil=Division of Tumor Pathology, Near InfraRed Photo-Immuno-Therapy Research Institute, Kansai Medical University
kn-affil=

affil-num=23
en-affil=Faculty of Science and Technology, Division of Molecular Science, Gunma University
kn-affil=
en-keyword=Plasmid
kn-keyword=Plasmid
en-keyword=Gene engineering
kn-keyword=Gene engineering
en-keyword=Cancer
kn-keyword=Cancer
en-keyword=Cell culture
kn-keyword=Cell culture
END

start-ver=1.4
cd-journal=joma
no-vol=150
cd-vols=
no-issue=1
article-no=
start-page=19
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250813
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Biallelic variants in DNAJC7 cause familial amyotrophic lateral sclerosis with the TDP-43 pathology
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the progressive degeneration of motor neurons. ALS pathology primarily involves the failure of protein quality control mechanisms, leading to the accumulation of misfolded proteins, particularly TAR DNA-binding protein 43 (TDP-43). TDP-43 aggregation is a central pathological feature of ALS. Maintaining protein homeostasis is critical and facilitated by heat shock proteins (HSPs), particularly the HSP40 family, which includes co-chaperones such as DNAJC7. Here, we report a family with three siblings affected by ALS who carry a homozygous c.518dupC frameshift variant in DNAJC7, a member of the HSP40 family. All three patients exhibited progressive muscle weakness, limb atrophy, bulbar palsy, and respiratory failure. Pathological examination revealed degeneration of both upper and lower motor neurons, with phosphorylated TDP-43-positive neuronal cytoplasmic inclusions in the frontal and temporal cortices. Immunoblot analysis were consistent with a type B pattern of phosphorylated TDP-43 in the precentral gyrus. Immunohistochemistry and RNA sequencing analyses demonstrated a substantial reduction in DNAJC7 expression at both the protein and RNA levels in affected brain regions. In a TDP-43 cell model, DNAJC7 knockdown impaired the disassembly of TDP-43 following arsenite-induced stress, whereas DNAJC7 overexpression suppressed the assembly and promoted the disassembly of arsenite-induced TDP-43 condensates. Furthermore, in a zebrafish ALS model, dnajc7 knockdown resulted in increased TDP-43 aggregation in motor neurons and reduced survival. To the best of our knowledge, this study provides the first evidence linking biallelic loss-of-function variants in DNAJC7 to familial ALS with TDP-43 pathology.
en-copyright=
kn-copyright=

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

en-aut-name=YokotaOsamu
en-aut-sei=Yokota
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OusakaDaiki
en-aut-sei=Ousaka
en-aut-mei=Daiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=HaraguchiTakashi
en-aut-sei=Haraguchi
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

en-aut-name=MatsuokaChika
en-aut-sei=Matsuoka
en-aut-mei=Chika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KawanoTomohito
en-aut-sei=Kawano
en-aut-mei=Tomohito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=Nakashima-YasudaHanae
en-aut-sei=Nakashima-Yasuda
en-aut-mei=Hanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
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=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=HasegawaMasato
en-aut-sei=Hasegawa
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=HosonoYasuyuki
en-aut-sei=Hosono
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=TeradaSeishi
en-aut-sei=Terada
en-aut-mei=Seishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
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=16
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=17
ORCID=

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

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

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

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

affil-num=5
en-affil=Department of Neurology, National Hospital Organisation Minami-Okayama Medical Centre
kn-affil=

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

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

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

affil-num=9
en-affil=Department of Psychiatry, Zikei Hospital
kn-affil=

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

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

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

affil-num=13
en-affil=Department of Brain and Neurosciences, Tokyo Metropolitan Institute of Medical Science
kn-affil=

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

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

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

affil-num=17
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Amyotrophic lateral sclerosis
kn-keyword=Amyotrophic lateral sclerosis
en-keyword=Heat shock protein
kn-keyword=Heat shock protein
en-keyword=DNAJC7
kn-keyword=DNAJC7
en-keyword=TDP-43
kn-keyword=TDP-43
en-keyword=Live-cell imaging
kn-keyword=Live-cell imaging
en-keyword=Zebrafish disease model
kn-keyword=Zebrafish disease model
END

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

start-ver=1.4
cd-journal=joma
no-vol=33
cd-vols=
no-issue=3
article-no=
start-page=99
end-page=117
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240429
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Generation and characterization of cerebellar granule neurons specific knockout mice of Golli-MBP
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Golli–myelin basic proteins, encoded by the myelin basic protein gene, are widely expressed in neurons and oligodendrocytes in the central nervous system. Further, prior research has shown that Golli–myelin basic protein is necessary for myelination and neuronal maturation during central nervous system development. In this study, we established Golli–myelin basic protein-floxed mice to elucidate the cell-type-specific effects of Golli–myelin basic protein knockout through the generation of conditional knockout mice (Golli–myelin basic proteinsfl/fl; E3CreN), in which Golli–myelin basic proteins were specifically deleted in cerebellar granule neurons, where Golli–myelin basic proteins are expressed abundantly in wild-type mice. To investigate the role of Golli–myelin basic proteins in cerebellar granule neurons, we further performed histopathological analyses of these mice, with results indicating no morphological changes or degeneration of the major cellular components of the cerebellum. Furthermore, behavioral analysis showed that Golli–myelin basic proteinsfl/fl; E3CreN mice were healthy and did not display any abnormal behavior. These results suggest that the loss of Golli–myelin basic proteins in cerebellar granule neurons does not lead to cerebellar perturbations or behavioral abnormalities. This mouse model could therefore be employed to analyze the effect of Golli–myelin basic protein deletion in specific cell types of the central nervous system, such as other neuronal cells and oligodendrocytes, or in lymphocytes of the immune system.
en-copyright=
kn-copyright=

en-aut-name=MiyazakiHaruko
en-aut-sei=Miyazaki
en-aut-mei=Haruko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishiokaSaki
en-aut-sei=Nishioka
en-aut-mei=Saki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamanakaTomoyuki
en-aut-sei=Yamanaka
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AbeManabu
en-aut-sei=Abe
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ImamuraYukio
en-aut-sei=Imamura
en-aut-mei=Yukio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyasakaTomohiro
en-aut-sei=Miyasaka
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KakudaNobuto
en-aut-sei=Kakuda
en-aut-mei=Nobuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShimogoriTomomi
en-aut-sei=Shimogori
en-aut-mei=Tomomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YamakawaKazuhiro
en-aut-sei=Yamakawa
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=IkawaMasahito
en-aut-sei=Ikawa
en-aut-mei=Masahito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NukinaNobuyuki
en-aut-sei=Nukina
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

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

affil-num=2
en-affil=Department of Experimental Genome Research, Research Institute for Microbial Diseases, Osaka University
kn-affil=

affil-num=3
en-affil=Laboratory of Structural Neuropathology, Graduate School of Brain Science, Doshisha University
kn-affil=

affil-num=4
en-affil=Department of Animal Model Development, Brain Research Institute, Niigata University
kn-affil=

affil-num=5
en-affil=Laboratory of Structural Neuropathology, Graduate School of Brain Science, Doshisha University
kn-affil=

affil-num=6
en-affil=Faculty of Life and Medical Sciences, Doshisha University
kn-affil=

affil-num=7
en-affil=Faculty of Life and Medical Sciences, Doshisha University
kn-affil=

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

affil-num=9
en-affil=Laboratory for Molecular Mechanisms of Brain Development, RIKEN Center for Brain Science
kn-affil=

affil-num=10
en-affil=Laboratory for Neurogenetics, RIKEN Center for Brain Science
kn-affil=

affil-num=11
en-affil=Department of Experimental Genome Research, Research Institute for Microbial Diseases, Osaka University
kn-affil=

affil-num=12
en-affil=Laboratory of Structural Neuropathology, Graduate School of Brain Science, Doshisha University
kn-affil=
en-keyword=Golli-MBP
kn-keyword=Golli-MBP
en-keyword=Cerebellar granule neuron
kn-keyword=Cerebellar granule neuron
en-keyword=CRISPR/Cas9
kn-keyword=CRISPR/Cas9
en-keyword=Conditional knockout
kn-keyword=Conditional knockout
END

start-ver=1.4
cd-journal=joma
no-vol=218
cd-vols=
no-issue=
article-no=
start-page=104922
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202509
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Alteration of perineuronal nets and parvalbumin interneurons in prefrontal cortex and hippocampus, and correlation with blood corticosterone in activity-based anorexia model mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Anorexia nervosa (AN) is an eating disorder characterized by restricted energy intake, severely underweight status, and frequent hyperactivity. Previous research has shown structural and functional alterations in the medial prefrontal cortex (mPFC) and hippocampus of AN patients. To investigate the pathological mechanism of AN, we analyzed the expression and distribution of parvalbumin (PV) interneurons and perineuronal nets (PNNs), which are implicated in the pathology of neuropsychiatric disorders, in the mPFC and hippocampus dorsal (HPCd) and ventral (HPCv) using an activity-based anorexia (ABA) mouse model. We found that PNN expression and density increased in the mPFC, with minor alterations in the HPCd and HPCv of ABA mice. The expression and distribution of PV neurons were unchanged in the brains of ABA mice, except for a regional decrease in PV-expressing neuron density in the HPCd. Co-localization analysis showed an increased number of PNNs enwrapping PV-negative neurons in the mPFC of ABA mice. Furthermore, the upregulation of PNN expression in the mPFC was positively correlated with elevated blood corticosterone levels, a well-known stress indicator, in ABA mice. Our findings suggest that the increased expression and distribution of PNNs surrounding PV-negative neurons in the mPFC may indicate the pathological mechanisms of AN.
en-copyright=
kn-copyright=

en-aut-name=NguyenHoang Duy
en-aut-sei=Nguyen
en-aut-mei=Hoang Duy
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyazakiHaruko
en-aut-sei=Miyazaki
en-aut-mei=Haruko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KawaiHiroki
en-aut-sei=Kawai
en-aut-mei=Hiroki
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=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=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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 Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Neuropsychiatry, 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 Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

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

affil-num=7
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=anorexia nervosa
kn-keyword=anorexia nervosa
en-keyword=activity-based anorexia
kn-keyword=activity-based anorexia
en-keyword=perineuronal nets
kn-keyword=perineuronal nets
en-keyword=parvalbumin
kn-keyword=parvalbumin
en-keyword=corticosterone
kn-keyword=corticosterone
en-keyword=prefrontal cortex
kn-keyword=prefrontal cortex
en-keyword=hippocampus
kn-keyword=hippocampus
END

start-ver=1.4
cd-journal=joma
no-vol=38
cd-vols=
no-issue=9
article-no=
start-page=e70105
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250724
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Ultrahigh‐Field MR‐Compatible Mechanical Tactile Stimulator for Investigating Somatosensory Processing in Small‐Bodied Animals
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Common marmosets (Callithrix jacchus), small-bodied New World primates that share similar sensory processing pathways with human beings, have gained great interests. Their small body size allows imaging of brain activity with high spatial resolution and on a whole-brain scale using ultrahigh-field (UHF) magnetic resonance imaging (MRI) scanners. However, the strong magnetic field and the small size of the hand and forearm pose challenges in delivering tactile stimulation during fMRI experiments. In the present study, we developed an MR-compatible tactile dual-point stimulator to provide high-precision mechanical stimulation for exploring somatosensory processing in small-bodied animals. The study population consisted of a water phantom and three male common marmosets. Cerebral blood volume (CBV) weighted fMRI data were obtained with a gradient echo (GE), echo-planar imaging (EPI) sequence at 7T scanner. The output performance of the device was tested by a pressure sensor. The MR compatibility of the device was verified by measuring the temporal signal-to-noise ratio (tSNR) of a water phantom. To test the effectiveness of tactile stimulation, we conducted block designed tactile stimulation experiments on marmosets. A one-way repeated measures ANOVA was conducted for comparing the tSNR results. We performed one-sample t-tests to investigate the negative response of the forearm and hand stimulation with a threshold of t > 1.96 (p < 0.05). Performance tests revealed that mechanical stimulation (averaged force: 31.69 g) was applied with a delay of 12 ms. Phantom experiments confirmed that there was no significant difference in the tSNR among three (10 Hz, 1 Hz, and no-stimulus) conditions (F (2, 798) = 0.71, p = 0.49). The CBV activity results showed that the stimulator successfully elicited hand and forearm somatosensory activations in primary somatosensory areas. These results indicated that the device is well suited for small-bodied animal somatosensory studies.
en-copyright=
kn-copyright=

en-aut-name=WangChenyu
en-aut-sei=Wang
en-aut-mei=Chenyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ImaiHirohiko
en-aut-sei=Imai
en-aut-mei=Hirohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FukunagaMasaki
en-aut-sei=Fukunaga
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamamotoHiroki
en-aut-sei=Yamamoto
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YuYinghua
en-aut-sei=Yu
en-aut-mei=Yinghua
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SekiKazuhiko
en-aut-sei=Seki
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HanakawaTakashi
en-aut-sei=Hanakawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UmedaTatsuya
en-aut-sei=Umeda
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YangJiajia
en-aut-sei=Yang
en-aut-mei=Jiajia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=Innovation Research Center for Quantum Medicine, Gifu University School of Medicine
kn-affil=

affil-num=3
en-affil=Section of Brain Function Information, National Institute for Physiological Sciences
kn-affil=

affil-num=4
en-affil=Graduate School of Human and Environmental Studies, Kyoto 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=Department of Neurophysiology, National Center of Neurology and Psychiatry
kn-affil=

affil-num=7
en-affil=Department of Integrated Neuroanatomy and Neuroimaging, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Integrated Neuroanatomy and Neuroimaging, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=9
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=primary somatosensory cortex
kn-keyword=primary somatosensory cortex
en-keyword=small-bodied animals
kn-keyword=small-bodied animals
en-keyword=tactile stimulation device
kn-keyword=tactile stimulation device
en-keyword=ultrahigh-field magnetic resonance imaging
kn-keyword=ultrahigh-field magnetic resonance imaging
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=5
article-no=
start-page=594
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Review Article: Diagnostic Paradigm Shift in Spine Surgery
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Meticulous clinical examination is essential for spinal disorders to utilize the diagnostic methods and technologies that strongly support physicians and enhance clinical practice. A significant change in the approach to diagnosing spinal disorders has occurred in the last three decades, which has enhanced a more nuanced understanding of spine pathology. Traditional radiographic methods such as conventional and functional X-rays and CT scans are still the first line in the diagnosis of spinal disorders due to their low cost and accessibility. As more advanced imaging technologies become increasingly available worldwide, there is a constantly increasing trend in MRI scans for detecting spinal pathologies and making treatment decisions. Not only do MRI scans have superior diagnostic capabilities, but they also assist surgeons in performing meticulous preoperative planning, making them currently the most widely used diagnostic tool for spinal disorders. Positron Emission Tomography (PET) can help detect inflammatory lesions, infections, and tumors. Other advanced diagnostic tools such as CT/MRI fusion image, Functional Magnetic Resonance Imaging (fMRI), Upright and Kinetic MRI, magnetic resonance spectroscopy (MRS), diffusion-weighted imaging (DWI), and diffusion tensor imaging (DTI) could play an important role when it comes to detecting more special pathologies. However, some technical difficulties in the daily praxis and their high costs act as obstacles to their further spread. Integrating artificial intelligence and advancements in data analytics and virtual reality promises to enhance spinal procedures’ precision, safety, and efficacy. As these technologies continue to develop, they will play a critical role in transforming spinal surgery. This paradigm shift emphasizes the importance of continuous innovation and adaptability in improving the diagnosis and treatment of spinal disorders.
en-copyright=
kn-copyright=

en-aut-name=LeventAras Efe
en-aut-sei=Levent
en-aut-mei=Aras Efe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanakaMasato
en-aut-sei=Tanaka
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KumawatChetan
en-aut-sei=Kumawat
en-aut-mei=Chetan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HengChristian
en-aut-sei=Heng
en-aut-mei=Christian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NikolaosSalamalikis
en-aut-sei=Nikolaos
en-aut-mei=Salamalikis
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=LatkaKajetan
en-aut-sei=Latka
en-aut-mei=Kajetan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MiyamotoAkiyoshi
en-aut-sei=Miyamoto
en-aut-mei=Akiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KomatsubaraTadashi
en-aut-sei=Komatsubara
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=AratakiShinya
en-aut-sei=Arataki
en-aut-mei=Shinya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OdaYoshiaki
en-aut-sei=Oda
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=ShinoharaKensuke
en-aut-sei=Shinohara
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=UotaniKoji
en-aut-sei=Uotani
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=2
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=3
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=4
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=5
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=6
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=7
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=8
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=9
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

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

affil-num=11
en-affil=Department of Orthopedic Surgery, Okayama University Hospital
kn-affil=

affil-num=12
en-affil=Department of Orthopedic Surgery, Okayama University Hospital
kn-affil=
en-keyword=diagnosis
kn-keyword=diagnosis
en-keyword=spine surgery
kn-keyword=spine surgery
en-keyword=innovative technique
kn-keyword=innovative technique
en-keyword=MRI
kn-keyword=MRI
en-keyword=myelography
kn-keyword=myelography
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=12
article-no=
start-page=2429
end-page=2437
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=Discovery of a Compound That Inhibits IRE1α S-Nitrosylation and Preserves the Endoplasmic Reticulum Stress Response under Nitrosative Stress
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Inositol-requiring enzyme 1α (IRE1α) is a sensor of endoplasmic reticulum (ER) stress and drives ER stress response pathways. Activated IRE1α exhibits RNase activity and cleaves mRNA encoding X-box binding protein 1, a transcription factor that induces the expression of genes that maintain ER proteostasis for cell survival. Previously, we showed that IRE1α undergoes S-nitrosylation, a post-translational modification induced by nitric oxide (NO), resulting in reduced RNase activity. Therefore, S-nitrosylation of IRE1α compromises the response to ER stress, making cells more vulnerable. We conducted virtual screening and cell-based validation experiments to identify compounds that inhibit the S-nitrosylation of IRE1α by targeting nitrosylated cysteine residues. We ultimately identified a compound (1ACTA) that selectively inhibits the S-nitrosylation of IRE1α and prevents the NO-induced reduction of RNase activity. Furthermore, 1ACTA reduces the rate of NO-induced cell death. Our research identified S-nitrosylation as a novel target for drug development for IRE1α and provides a suitable screening strategy.
en-copyright=
kn-copyright=

en-aut-name=KurogiHaruna
en-aut-sei=Kurogi
en-aut-mei=Haruna
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=KubotaSho
en-aut-sei=Kubota
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KumarAshutosh
en-aut-sei=Kumar
en-aut-mei=Ashutosh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SuzukiTakehiro
en-aut-sei=Suzuki
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

en-aut-name=SawadaDaisuke
en-aut-sei=Sawada
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ZhangKam Y.J.
en-aut-sei=Zhang
en-aut-mei=Kam Y.J.
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=Laboratory for Structural Bioinformatics, Center for Biosystems Dynamics Research, RIKEN
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=Biomolecular Characterization Unit, Technology Platform Division, RIKEN Center for Sustainable Resource Science
kn-affil=

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

affil-num=8
en-affil=Laboratory for Structural Bioinformatics, Center for Biosystems Dynamics Research, RIKEN
kn-affil=

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

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=11
article-no=
start-page=4984
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250522
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Induced Pluripotent Stem Cells in Cardiomyopathy: Advancing Disease Modeling, Therapeutic Development, and Regenerative Therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cardiomyopathies are a heterogeneous group of heart muscle diseases that can lead to heart failure, arrhythmias, and sudden cardiac death. Traditional animal models and in vitro systems have limitations in replicating the complex pathology of human cardiomyopathies. Induced pluripotent stem cells (iPSCs) offer a transformative platform by enabling the generation of patient-specific cardiomyocytes, thus opening new avenues for disease modeling, drug discovery, and regenerative therapy. This process involves reprogramming somatic cells into iPSCs and subsequently differentiating them into functional cardiomyocytes, which can be characterized using techniques such as electrophysiology, contractility assays, and gene expression profiling. iPSC-derived cardiomyocyte (iPSC-CM) platforms are also being explored for drug screening and personalized medicine, including high-throughput testing for cardiotoxicity and the identification of patient-tailored therapies. While iPSC-CMs already serve as valuable models for understanding disease mechanisms and screening drugs, ongoing advances in maturation and bioengineering are bringing iPSC-based therapies closer to clinical application. Furthermore, the integration of multi-omics approaches and artificial intelligence (AI) is enhancing the predictive power of iPSC models. iPSC-based technologies are paving the way for a new era of personalized cardiology, with the potential to revolutionize the management of cardiomyopathies through patient-specific insights and regenerative strategies.
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=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
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=6
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 Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=induced pluripotent stem cells
kn-keyword=induced pluripotent stem cells
en-keyword=cardiomyopathy
kn-keyword=cardiomyopathy
en-keyword=disease modeling
kn-keyword=disease modeling
en-keyword=drug screening
kn-keyword=drug screening
en-keyword=regenerative therapy
kn-keyword=regenerative therapy
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=27163
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250725
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Eosinophils as a predictive marker of treatment-related adverse events in mRCC patients treated with first-line immune-checkpoint inhibitor combination therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Immune checkpoint inhibitors (ICIs) are a key component of first-line treatment for metastatic renal cell carcinoma (mRCC). However, predicting treatment-related adverse events (TRAEs) remains challenging. This study investigated the utility of eosinophil-related biomarkers as predictors of Common Terminology Criteria for Adverse Events grade ≥ 3 TRAEs in mRCC patients undergoing ICI combination therapy. In this retrospective analysis across 21 hospitals in Japan, we examined 180 patients treated with ICI/ICI therapy and 216 patients treated with ICI/tyrosine kinase inhibitor (TKI) therapy. Grade ≥ 3 TRAEs occurred in 39.4% and 31.9% of patients in the ICI/ICI and ICI/TKI groups, respectively. An elevated eosinophil proportion of ≥ 2.0% (odds ratio [OR]: 2.36; 95% CI [confidence interval] 1.23–4.54, p = 0.01) and a low neutrophil/eosinophil ratio (NER) of ≤ 40.0 (OR: 2.78, 95% CI 1.39–5.53, p = 0.004) were significant predictors of severe TRAEs in the ICI/ICI group. However, no significant associations were found in the ICI/TKI group. These findings may help identify patients who suffer from grade ≥ 3 TRAEs and help determine individualized treatment strategies in patients with mRCC.
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=KatayamaSatoshi
en-aut-sei=Katayama
en-aut-mei=Satoshi
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=MoriKeiichiro
en-aut-sei=Mori
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FukuokayaWataru
en-aut-sei=Fukuokaya
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KomuraKazumasa
en-aut-sei=Komura
en-aut-mei=Kazumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TsujinoTakuya
en-aut-sei=Tsujino
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MaenosonoRyoichi
en-aut-sei=Maenosono
en-aut-mei=Ryoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TakaharaKiyoshi
en-aut-sei=Takahara
en-aut-mei=Kiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NukayaTakuhisa
en-aut-sei=Nukaya
en-aut-mei=Takuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=InokiLan
en-aut-sei=Inoki
en-aut-mei=Lan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=ToyodaShingo
en-aut-sei=Toyoda
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=HashimotoTakeshi
en-aut-sei=Hashimoto
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=HirasawaYosuke
en-aut-sei=Hirasawa
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
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=15
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=16
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=17
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=18
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=19
ORCID=

en-aut-name=SadahiraTakuya
en-aut-sei=Sadahira
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=TominagaYusuke
en-aut-sei=Tominaga
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=YamanoiTomoaki
en-aut-sei=Yamanoi
en-aut-mei=Tomoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=YoshinagaKasumi
en-aut-sei=Yoshinaga
en-aut-mei=Kasumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
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=24
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=25
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=26
ORCID=

en-aut-name=KuroseKyohei
en-aut-sei=Kurose
en-aut-mei=Kyohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=KimuraTakahiro
en-aut-sei=Kimura
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=AzumaHaruhito
en-aut-sei=Azuma
en-aut-mei=Haruhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
ORCID=

en-aut-name=ShirokiRyoichi
en-aut-sei=Shiroki
en-aut-mei=Ryoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

en-aut-name=FujitaKazutoshi
en-aut-sei=Fujita
en-aut-mei=Kazutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=31
ORCID=

en-aut-name=OhnoYoshio
en-aut-sei=Ohno
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=32
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=33
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, The Jikei University School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Urology, The Jikei University School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Urology, The Jikei University School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Urology, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=7
en-affil=Department of Urology, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=8
en-affil=Department of Urology, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=9
en-affil=Department of Urology, Fujita Health University School of Medicine
kn-affil=

affil-num=10
en-affil=Department of Urology, Fujita Health University School of Medicine
kn-affil=

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

affil-num=12
en-affil=Department of Urology, Kindai University Faculty of Medicine
kn-affil=

affil-num=13
en-affil=Department of Urology, Tokyo Medical University
kn-affil=

affil-num=14
en-affil=Department of Urology, Tokyo Medical University
kn-affil=

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

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

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

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

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

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

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

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

affil-num=23
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=24
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=25
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=26
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=27
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=28
en-affil=Department of Urology, The Jikei University School of Medicine
kn-affil=

affil-num=29
en-affil=Department of Urology, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=30
en-affil=Department of Urology, Fujita Health University School of Medicine
kn-affil=

affil-num=31
en-affil=Department of Urology, Kindai University Faculty of Medicine
kn-affil=

affil-num=32
en-affil=Department of Urology, Tokyo Medical University
kn-affil=

affil-num=33
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Renal cell carcinoma
kn-keyword=Renal cell carcinoma
en-keyword=Immune checkpoint inhibitor
kn-keyword=Immune checkpoint inhibitor
en-keyword=ICI
kn-keyword=ICI
en-keyword=Eosinophil
kn-keyword=Eosinophil
en-keyword=Immune-related adverse event
kn-keyword=Immune-related adverse event
en-keyword=Treatment-related adverse event
kn-keyword=Treatment-related adverse event
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=10
article-no=
start-page=1444
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250516
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Canine c-kit Novel Mutation Isolated from a Gastrointestinal Stromal Tumor (GIST) Retains the Ability to Form Dimers but Lacks Autophosphorylation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Gastrointestinal stromal tumors (GISTs) are mesenchymal tumors that develop in the gastrointestinal tract; KIT mutations are present in both canine and human GISTs. In this study, genomic DNA was extracted from formalin-fixed paraffin-embedded (FFPE) sections of 55 canine GIST cases, and mutation searches were performed for exons 8, 9, and 11. The results revealed novel mutations, A434T and F436S, in exon 8. In contrast to the A434T mutation without functional changes, the F436S mutant retained its dimerization ability, but lost its phosphorylation function and attenuated downstream Akt signaling, which is reflected in wound healing and migration activities. A comparison of the subcellular localization of WT KIT and the F436S mutant revealed no differences. In silico simulations indicated that the F436S mutation alters the structure of the near-membrane region and that its effects may extend to the transmembrane and intracellular domains compared to the WT. F436S is a point mutation that affects the entire molecule because co-mutation with the F436S mutation and the known autophosphorylation mutation reduces the autophosphorylation abilities.
en-copyright=
kn-copyright=

en-aut-name=ShimakawaKei
en-aut-sei=Shimakawa
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=DogeSo
en-aut-sei=Doge
en-aut-mei=So
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MichishitaMasaki
en-aut-sei=Michishita
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TanabeEri
en-aut-sei=Tanabe
en-aut-mei=Eri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TajimaTsuyoshi
en-aut-sei=Tajima
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KobayashiMasato
en-aut-sei=Kobayashi
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=BonkobaraMakoto
en-aut-sei=Bonkobara
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

en-aut-name=OchiaiKazuhiko
en-aut-sei=Ochiai
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TanakaYoshikazu
en-aut-sei=Tanaka
en-aut-mei=Yoshikazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Laboratory of Veterinary Hygiene, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=2
en-affil=Laboratory of Veterinary Pathology, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=3
en-affil=Laboratory of Veterinary Pathology, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=4
en-affil=Laboratory of Veterinary Hygiene, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=5
en-affil=Laboratory of Veterinary Pharmacology, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=6
en-affil=Laboratory of Veterinary Reproduction, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=7
en-affil=Laboratory of Veterinary Clinical Pathology, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

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

affil-num=9
en-affil=Laboratory of Veterinary Hygiene, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=10
en-affil=Laboratory of Veterinary Hygiene, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=
en-keyword=autophosphorylation
kn-keyword=autophosphorylation
en-keyword=canine
kn-keyword=canine
en-keyword=c-kit
kn-keyword=c-kit
en-keyword=GIST
kn-keyword=GIST
en-keyword=KIT
kn-keyword=KIT
en-keyword=loss-of-function mutation
kn-keyword=loss-of-function mutation
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=1
article-no=
start-page=2
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250128
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of temperature cycles on the sleep-like state in Hydra vulgaris
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Sleep is a conserved physiological phenomenon across species. It is mainly controlled by two processes: a circadian clock that regulates the timing of sleep and a homeostat that regulates the sleep drive. Even cnidarians, such as Hydra and jellyfish, which lack a brain, display sleep-like states. However, the manner in which environmental cues affect sleep-like states in these organisms remains unknown. In the present study, we investigated the effects of light and temperature cycles on the sleep-like state in Hydra vulgaris.<br>
Results Our findings indicate that Hydra responds to temperature cycles with a difference of up to 5° C, resulting in decreased sleep duration under light conditions and increased sleep duration in dark conditions. Furthermore, our results reveal that Hydra prioritizes temperature changes over light as an environmental cue. Additionally, our body resection experiments show tissue-specific responsiveness in the generation ofthe sleep-like state under different environmental cues. Specifically, the upper body can generate the sleep-like state in response to a single environmental cue. In contrast, the lower body did not respond to 12-h light–dark cycles at a constant temperature.<br>
Conclusions These findings indicate that both light and temperature influence the regulation of the sleep-like state in Hydra. Moreover, these observations highlight the existence of distinct regulatory mechanisms that govern patterns of the sleep-like state in brainless organisms, suggesting the potential involvement of specific regions for responsiveness of environmental cues for regulation of the sleep-like state.
en-copyright=
kn-copyright=

en-aut-name=SatoAya
en-aut-sei=Sato
en-aut-mei=Aya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SekiguchiManabu
en-aut-sei=Sekiguchi
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakadaKoga
en-aut-sei=Nakada
en-aut-mei=Koga
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=ItohTaichi Q.
en-aut-sei=Itoh
en-aut-mei=Taichi Q.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Faculty of Arts and Science, Kyushu 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 Systems Life Sciences, Kyushu University
kn-affil=

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

affil-num=5
en-affil=Faculty of Arts and Science, Kyushu University
kn-affil=
en-keyword=Hydra
kn-keyword=Hydra
en-keyword=Sleep
kn-keyword=Sleep
en-keyword=Temperature
kn-keyword=Temperature
en-keyword=Environmental cues
kn-keyword=Environmental cues
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=10819
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A high-protein diet-responsive gut hormone regulates behavioral and metabolic optimization in Drosophila melanogaster
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Protein is essential for all living organisms; however, excessive protein intake can have adverse effects, such as hyperammonemia. Although mechanisms responding to protein deficiency are well-studied, there is a significant gap in our understanding of how organisms adaptively suppress excessive protein intake. In the present study, utilizing the fruit fly, Drosophila melanogaster, we discover that the peptide hormone CCHamide1 (CCHa1), secreted by enteroendocrine cells in response to a high-protein diet (HPD), is vital for suppressing overconsumption of protein. Gut-derived CCHa1 is received by a small subset of enteric neurons that produce short neuropeptide F, thereby modulating protein-specific satiety. Importantly, impairment of the CCHa1-mediated gut-enteric neuronal axis results in ammonia accumulation and a shortened lifespan under HPD conditions. Collectively, our findings unravel the crosstalk of gut hormone and neuronal pathways that orchestrate physiological responses to prevent and adapt to dietary protein overload.
en-copyright=
kn-copyright=

en-aut-name=YoshinariYuto
en-aut-sei=Yoshinari
en-aut-mei=Yuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishimuraTakashi
en-aut-sei=Nishimura
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
ORCID=

en-aut-name=KondoShu
en-aut-sei=Kondo
en-aut-mei=Shu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TanimotoHiromu
en-aut-sei=Tanimoto
en-aut-mei=Hiromu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KobayashiTomoe
en-aut-sei=Kobayashi
en-aut-mei=Tomoe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsuyamaMakoto
en-aut-sei=Matsuyama
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NiwaRyusuke
en-aut-sei=Niwa
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Metabolic Regulation and Genetics, Institute for Molecular and Cellular Regulation, Gunma University
kn-affil=

affil-num=2
en-affil=Metabolic Regulation and Genetics, Institute for Molecular and Cellular Regulation, Gunma 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=Department of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science
kn-affil=

affil-num=5
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=

affil-num=6
en-affil=Division of Molecular Genetics, Shigei Medical Research Institute
kn-affil=

affil-num=7
en-affil=Division of Molecular Genetics, Shigei Medical Research Institute
kn-affil=

affil-num=8
en-affil=Life Science Center for Survival Dynamics, Tsukuba Advanced Research Alliance (TARA), University of Tsukuba
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250710
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neurotransmitter and Receptor Mapping in Drosophila Circadian Clock Neurons via T2A-GAL4 Screening
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The circadian neuronal network in the brain comprises central pacemaker neurons and associated input and output pathways. These components work together to generate coherent rhythmicity, synchronize with environmental time cues, and convey circadian information to downstream neurons that regulate behaviors such as the sleep/wake cycle. To mediate these functions, neurotransmitters and neuromodulators play essential roles in transmitting and modulating signals between neurons. In Drosophila melanogaster, approximately 240 brain neurons function as clock neurons. Previous studies have identified several neurotransmitters and neuromodulators, including the Pigment-dispersing factor (PDF) neuropeptide, along with their corresponding receptors in clock neurons. However, our understanding of the neurotransmitters and receptors involved in the circadian system remains incomplete. In this study, we conducted a T2A-GAL4-based screening for neurotransmitter and receptor genes expressed in clock neurons. We identified 2 neurotransmitter-related genes and 22 receptor genes. Notably, while previous studies had reported the expression of 6 neuropeptide receptor genes in large ventrolateral neurons (l-LNv), we also found that 14 receptor genes—including those for dopamine, serotonin, and γ-aminobutyric acid—are expressed in l-LNv neurons. These findings suggest that l-LNv neurons serve as key integrative hubs within the circadian network, receiving diverse external signals.
en-copyright=
kn-copyright=

en-aut-name=FukudaAyumi
en-aut-sei=Fukuda
en-aut-mei=Ayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SaitoAika
en-aut-sei=Saito
en-aut-mei=Aika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
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 Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=clock neurons
kn-keyword=clock neurons
en-keyword=neurotransmitter
kn-keyword=neurotransmitter
en-keyword=T2A-GAL4
kn-keyword=T2A-GAL4
en-keyword=immunostaining
kn-keyword=immunostaining
en-keyword=Drosophila
kn-keyword=Drosophila
END

start-ver=1.4
cd-journal=joma
no-vol=35
cd-vols=
no-issue=12
article-no=
start-page=2916
end-page=2926.e3
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Oxytocin facilitates human touch-induced play behavior in rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pleasant touch sensations play a fundamental role in social bonding, yet the neural mechanisms underlying affinity-like behaviors remain poorly understood. Here, we demonstrate that juvenile-adolescent rats, which naturally engage in social play with peers characterized by rough-and-tumble interactions and 50 kHz ultrasonic vocalizations indicating pleasant sensations, develop a strong affinity for human hands through similar playful contact achieved by repeated tickling with human hands. Using this rat with tickling-induced high affinity for human hands, we discovered that repeated tickling mimicking rough-and-tumble play led to increased oxytocin receptor (OTR) expression in the ventrolateral part of the ventromedial hypothalamus (VMHvl). Inhibition of oxytocin signaling in the VMHvl reduced affinity-like behaviors from rats to human hands. These findings suggest that OTR neurons in VMHvl play an important role in the increase in affinity for human hands induced by pleasant touch sensation with human touch-induced play behavior. Based on retrograde and anterograde tracing studies examining the supraoptic nucleus (SON) and the paraventricular nucleus (PVN) as primary sources of oxytocin, we demonstrate that a subset of oxytocin fibers in the VMHvl originate from the SON, suggesting that affinity-like behavior from rats to human hands may be controlled by oxytocin signaling from magnocellular neurons. Together, this work advances our understanding of how oxytocin shapes social behavior and may inform the development of therapeutic strategies to promote positive social interactions.
en-copyright=
kn-copyright=

en-aut-name=HayashiHimeka
en-aut-sei=Hayashi
en-aut-mei=Himeka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TateishiSayaka
en-aut-sei=Tateishi
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=InutsukaAyumu
en-aut-sei=Inutsuka
en-aut-mei=Ayumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MaejimaSho
en-aut-sei=Maejima
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HagiwaraDaisuke
en-aut-sei=Hagiwara
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SakumaYasuo
en-aut-sei=Sakuma
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OnakaTatsushi
en-aut-sei=Onaka
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=GrinevichValery
en-aut-sei=Grinevich
en-aut-mei=Valery
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
ORCID=

affil-num=1
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University,
kn-affil=

affil-num=2
en-affil=Ushimado Marine Institute (UMI), Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Division of Brain and Neurophysiology, Department of Physiology, Jichi Medical University
kn-affil=

affil-num=4
en-affil=Ushimado Marine Institute (UMI), Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Neuropeptide Research in Psychiatry, Central Institute of Mental Health, German Center for Psychiatry (DZPG), Medical Faculty Mannheim, University of Heidelberg
kn-affil=

affil-num=6
en-affil=Department of Anatomy and Neurobiology, Graduate School of Medical Sciences, Nippon Medical School
kn-affil=

affil-num=7
en-affil=Division of Brain and Neurophysiology, Department of Physiology, Jichi Medical University
kn-affil=

affil-num=8
en-affil=Department of Neuropeptide Research in Psychiatry, Central Institute of Mental Health, German Center for Psychiatry (DZPG), Medical Faculty Mannheim, University of Heidelberg
kn-affil=

affil-num=9
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University,
kn-affil=
en-keyword=tickling
kn-keyword=tickling
en-keyword=oxytocin
kn-keyword=oxytocin
en-keyword=oxytocin receptor
kn-keyword=oxytocin receptor
en-keyword=ventrolateral part of the ventromedial hypothalamus
kn-keyword=ventrolateral part of the ventromedial hypothalamus
en-keyword=affinity-like behaviors
kn-keyword=affinity-like behaviors
END

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250624
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dual functions of SNAP25 in mouse taste buds
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Type III cells in mouse taste buds are considered to transmit aversive stimuli, such as sourness, to the gustatory nerve through vesicular synapses. Synaptosome-associated protein 25 (SNAP25) might contribute to synaptic vesicular release in sour sensation, although direct evidence has been lacking. Here, we demonstrated that epithelia-specific Snap25 conditional knockout (cKO) mice exhibited a significant reduction in the number of type III cells. Notably, the proportion of 5-ethynyl 2′-deoxyuridine-positive post-mitotic type III cells in Snap25 cKO mice was significantly lower on tracing day 14, but not at day 7, which suggests that SNAP25 contributes to the maintenance of type III cells. In a short-term lick test, Snap25 cKO (sour taste absent) and Snap25/ transient receptor potential vanilloid 1 double KO (sour taste and somatosensory absent) mice exhibit a significantly higher lick response to sour tastants, confirming the role of SNAP25 for sour sensation. Electrophysiological recordings of the chorda tympani nerve reveal nearly abolished ammonium and sour taste responses in Snap25 cKO mice, which concludes sour-dependent synapse transmission in type III cells. Overall, these data suggest that vesicular synapses in taste buds are indispensable for transmission of information from, and the replenishment of, sour-sensitive type III taste cells.
en-copyright=
kn-copyright=

en-aut-name=HorieKengo
en-aut-sei=Horie
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WangKuanyu
en-aut-sei=Wang
en-aut-mei=Kuanyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
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=4
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=5
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=6
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=7
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=Tokyo Dental Junior College
kn-affil=

affil-num=5
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
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=
en-keyword=sour taste
kn-keyword=sour taste
en-keyword=synapse
kn-keyword=synapse
en-keyword=taste buds
kn-keyword=taste buds
en-keyword=taste nerve
kn-keyword=taste nerve
en-keyword=Type III cells
kn-keyword=Type III cells
END

start-ver=1.4
cd-journal=joma
no-vol=166
cd-vols=
no-issue=8
article-no=
start-page=bqaf102
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250605
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neuromedin U Deficiency Disrupts Daily Testosterone Fluctuation and Reduces Wheel-running Activity in Rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The objective of this study was to elucidate the role of endogenous Neuromedin U (NMU) in rats by performing NMU knockout (KO). Male, but not female NMU KO rats exhibited decreased wheel-running activity vs wildtype (WT), although overall home cage activity was not affected. Plasma testosterone in WT rats varied significantly over the course of a day, with a peak at ZT1 and a nadir at ZT18, whereas in NMU KO rats testosterone remained stable throughout the day. Chronic administration of testosterone restored wheel-running activity in NMU KO rats to the same level as in WT rats, suggesting that the decrease in wheel-running activity in NMU KO rats is due to the disruption of the diurnal change of testosterone. Accordingly, expression of the luteinizing hormone beta subunit (Lhb) mRNA in the pars distalis of anterior pituitary was significantly lower in NMU KO rats; immunostaining revealed that the size of luteinizing hormone (LH)–expressing cells was also relatively small in those animals. In the brain of male WT rats, Nmu was highly expressed in the pars tuberalis, and the NMU receptor Nmur2 was highly expressed in the ependymal cell layer of the third ventricle. This study reveals a novel function of NMU and indicates that endogenous NMU in rats plays a role in the regulation of motivated activity via regulation of testosterone.
en-copyright=
kn-copyright=

en-aut-name=OtsukaMai
en-aut-sei=Otsuka
en-aut-mei=Mai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakeuchiYu
en-aut-sei=Takeuchi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoriyamaMaho
en-aut-sei=Moriyama
en-aut-mei=Maho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=EgoshiSakura
en-aut-sei=Egoshi
en-aut-mei=Sakura
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=GotoYuki
en-aut-sei=Goto
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=GuTingting
en-aut-sei=Gu
en-aut-mei=Tingting
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KimuraAtsushi P
en-aut-sei=Kimura
en-aut-mei=Atsushi P
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HaraguchiShogo
en-aut-sei=Haraguchi
en-aut-mei=Shogo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
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=10
ORCID=

en-aut-name=MatsuyamaMakoto
en-aut-sei=Matsuyama
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=BentleyGeorge E
en-aut-sei=Bentley
en-aut-mei=George E
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=13
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 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=Department of Biological Sciences, Faculty of Science, Hokkaido University
kn-affil=

affil-num=8
en-affil=Department of Biochemistry, Showa University School of Medicine
kn-affil=

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

affil-num=10
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=11
en-affil=Division of Molecular Genetics, Shigei Medical Research Institute
kn-affil=

affil-num=12
en-affil=Department of Integrative Biology and Helen Wills Neuroscience Institute, University of California at Berkeley
kn-affil=

affil-num=13
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Neuromedin U
kn-keyword=Neuromedin U
en-keyword=rat
kn-keyword=rat
en-keyword=motivation
kn-keyword=motivation
en-keyword=activity
kn-keyword=activity
en-keyword=testosterone
kn-keyword=testosterone
en-keyword=wheel-running
kn-keyword=wheel-running
END

start-ver=1.4
cd-journal=joma
no-vol=64
cd-vols=
no-issue=5
article-no=
start-page=759
end-page=762
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250301
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Novel De Novo Variant in KCNH5 in a Patient with Refractory Epileptic Encephalopathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We herein report a novel de novo KCNH5 variant in a patient with refractory epileptic encephalopathy. The patient exhibited seizures at 1 year and 7 months old, which gradually worsened, leading to a bedridden status. Brain magnetic resonance imaging (MRI) showed cerebral atrophy and cerebellar hypoplasia. A trio whole-exome sequence analysis identified a de novo heterozygous c.640A>C, p.Lys214Gln variant in KCNH5 that was predicted to be deleterious. Recent studies have linked KCNH5 to various epileptic encephalopathies, with many patients showing normal MRI findings. The present case expands the clinical spectrum of the disease, as it is characterized by severe neurological prognosis, cerebral atrophy, and cerebellar hypoplasia.
en-copyright=
kn-copyright=

en-aut-name=MitsutakeAkihiko
en-aut-sei=Mitsutake
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsukawaTakashi
en-aut-sei=Matsukawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NaitoTatsuhiko
en-aut-sei=Naito
en-aut-mei=Tatsuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=MitsuiJun
en-aut-sei=Mitsui
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HaradaHiroaki
en-aut-sei=Harada
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FujioKeishi
en-aut-sei=Fujio
en-aut-mei=Keishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FujishiroJun
en-aut-sei=Fujishiro
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MoriHarushi
en-aut-sei=Mori
en-aut-mei=Harushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MorishitaShinichi
en-aut-sei=Morishita
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TsujiShoji
en-aut-sei=Tsuji
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
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, The University of Tokyo
kn-affil=

affil-num=6
en-affil=Department of Rheumatology and Allergy, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=7
en-affil=Department of Rheumatology and Allergy, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=8
en-affil=Department of Pediatric Surgery, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=9
en-affil=Department of Radiology, School of Medicine, Jichi Medical University
kn-affil=

affil-num=10
en-affil=Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo
kn-affil=

affil-num=11
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=12
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
en-keyword=epileptic encephalopathy
kn-keyword=epileptic encephalopathy
en-keyword=whole-exome sequencing
kn-keyword=whole-exome sequencing
en-keyword=KCNH5
kn-keyword=KCNH5
en-keyword=de novo variant
kn-keyword=de novo variant
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=20250303
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Recent progress in oculopharyngodistal myopathy research from clinical and genetic viewpoints
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Oculopharyngodistal myopathy (OPDM) is a rare muscular disorder characterized by ocular symptoms, pharyngeal symptoms, facial weakness, and distal predominant limb muscle weakness. The cause of the disease was unknown for a long time. Recently, however, it has been reported that expansions of CGG or CCG repeats in LRP12, LOC642361/NUTM2B-AS1, GIPC1, NOTCH2NLC, RILPL1, and ABCD3 are the causes of the disease. Cases sometimes present with neurological symptoms, and the clinical spectrum of diseases caused by expansions of CGG or CCG repeats has been proposed to be called FNOP-spectrum disorder after the names of fragile X-associated tremor/ataxia syndrome, neuronal intranuclear inclusion disease, oculopharyngeal myopathy with leukoencephalopathy, and OPDM. In this article, the recent progress in the field of OPDM is reviewed, and remaining issues in OPDM are discussed.
en-copyright=
kn-copyright=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=oculopharyngodistal myopathy
kn-keyword=oculopharyngodistal myopathy
en-keyword=CGG repeat
kn-keyword=CGG repeat
en-keyword=CCG repeat
kn-keyword=CCG repeat
en-keyword=repeat motif–phenotype correlation
kn-keyword=repeat motif–phenotype correlation
en-keyword=FNOP-spectrum disorder
kn-keyword=FNOP-spectrum disorder
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=5602-25
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=Two Cases of Autosomal Recessive Spinocerebellar Ataxia-8 Showing Two Novel Variants of SYNE1 in Japanese Families
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Autosomal recessive spinocerebellar ataxia-8 (SCAR8) is a neurodegenerative disorder caused by the biallelic pathogenic variants of SYNE1. It is characterized by slowly progressive cerebellar ataxia and atrophy. We identified two SCAR8 families using exome analyses and two novel variants, c.2127delG (p.Met709Ilefs) and c.15943G>T (p.Gly5315*), in SYNE1 (NM_182961.4). Pathogenic variants of SYNE1 cause various symptoms, including cerebellar ataxia, pyramidal tract disorders, and joint disorders, and the pathogenic variants discovered in this study were located in a region prone to cerebellar ataxia.
en-copyright=
kn-copyright=

en-aut-name=YunokiTaijun
en-aut-sei=Yunoki
en-aut-mei=Taijun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuokaChika
en-aut-sei=Matsuoka
en-aut-mei=Chika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OsakadaYosuke
en-aut-sei=Osakada
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=5
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=6
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=7
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=8
ORCID=

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

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

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

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

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

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

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

affil-num=8
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=SCAR8
kn-keyword=SCAR8
en-keyword=SCAR
kn-keyword=SCAR
en-keyword=cerebellar ataxia
kn-keyword=cerebellar ataxia
en-keyword=whole-exome sequencing analysis
kn-keyword=whole-exome sequencing analysis
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=20250325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=タンパク質の限界発現により引き起こされるタンパク質毒性と細胞表現型の解析
kn-title=Analysis of Protein Toxicity and Cellular Phenotypes Triggered by the Maximum Overexpression of Proteins in Yeast 
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NAMBAShotaro
en-aut-sei=NAMBA
en-aut-mei=Shotaro
kn-aut-name=難波匠太郎
kn-aut-sei=難波
kn-aut-mei=匠太郎
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=岡山大学大学院環境生命自然科学研究科
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=2025
dt-pub=20250325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=ラドン吸入がマウス脳中のタンパク質に及ぼす作用：プロテオーム解析と多変量解析を用いた検討
kn-title=Effect of Radon Inhalation on Murine Brain Proteins : Investigation Using Proteomic and Multivariate Analyses
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NAOEShota
en-aut-sei=NAOE
en-aut-mei=Shota
kn-aut-name=直江翔太
kn-aut-sei=直江
kn-aut-mei=翔太
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=岡山大学大学院保健学研究科
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
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dt-pub-year=2025
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kn-subject=
en-title=ヒトの感覚運動システムにおける体部位局在情報処理機構の解明
kn-title=Study of the Brain Topological Processing Mechanisms in the Human Sensorimotor System
en-subtitle=
kn-subtitle=
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kn-copyright=

en-aut-name=WANGCHENYU
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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

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en-title=注意が聴覚と触覚の多感覚情報処理に与える影響の神経基盤の解明
kn-title=Study on neural mechanisms of attention effects on auditory-tactile multisensory processing
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en-aut-name=ANWEICHAO
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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

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kn-subject=
en-title=物体の弾性が柔らかさと心地よさ知覚に与える影響に関する研究
kn-title=Study on the Influence of Object Compliance on Softness and Pleasantness Perception
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kn-copyright=

en-aut-name=GAOBINYUE
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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

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en-title=行動の社会的要因：歩行者の衝突回避におけるダイナミクスの定量化
kn-title=Social Factors in Motion: Quantifying the Dynamics of Dyad–Individual Collision Avoidance
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kn-subtitle=
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kn-copyright=

en-aut-name=Adrien Thibaud Marie GREGORJ
en-aut-sei=Adrien Thibaud Marie GREGORJ
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kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama university
kn-affil=岡山大学大学院自然科学研究科
END

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en-title=げっ歯類における性的二型行動とそのホルモン調節機構
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en-aut-name=HAYASHIHimeka
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ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama university
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END

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en-title=分光法とペーパー分析デバイスに基づく酵素活性測定法の開発
kn-title=Development of Enzyme Activity Assays Based on Spectrometric Methods and Paper-Based Analytical Devices 
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en-aut-name=RENJIANCHAO
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ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama university
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kn-title=環境中親電子物質によるDNAメチル化制御を介したケモカイン発現誘導機構
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en-aut-name=TSUCHIDATomoki
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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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kn-title=小胞体ストレスセンサー IRE1α に対する S-ニトロシル化阻害薬の同定とその薬効評価
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kn-subtitle=
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kn-copyright=

en-aut-name=KUROGIHaruna
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kn-aut-mei=春那
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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kn-subject=
en-title=マウスにおける発酵乳成分に対する味覚反応と摂取行動
kn-title=Taste Responses and Ingestive Behaviors to Ingredients of Fermented Milk in Mice
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kn-subtitle=
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kn-copyright=

en-aut-name=YAMASEYuko
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kn-aut-mei=裕子
aut-affil-num=1
ORCID=

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

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kn-subject=
en-title=味蕾内の味覚シグナル伝達調節におけるGABAの役割
kn-title=The role of GABA in modulation of taste signaling within the taste bud
en-subtitle=
kn-subtitle=
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kn-copyright=

en-aut-name=MIKAMIAyaka
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en-aut-mei=Ayaka
kn-aut-name=三上彩可
kn-aut-sei=三上
kn-aut-mei=彩可
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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en-title=マウスIII型細胞におけるCcn3の機能の探索
kn-title=Exploring the Role of Ccn3 in Type III Cell of Mice Taste Buds
en-subtitle=
kn-subtitle=
en-abstract=
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kn-copyright=

en-aut-name=Kuanyu Wang
en-aut-sei=Kuanyu Wang
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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

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en-title=COVID-19罹患後症状の患者における就労状況への影響
kn-title=Changes in Working Situations of Employed Long COVID Patients: Retrospective Study in Japanese Outpatient Clinic
en-subtitle=
kn-subtitle=
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en-copyright=
kn-copyright=

en-aut-name=MATSUDAYui
en-aut-sei=MATSUDA
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kn-aut-name=松田祐依
kn-aut-sei=松田
kn-aut-mei=祐依
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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kn-subject=
en-title=LPS誘発不安様行動に対する釣藤散および釣藤鈎の効果に関する検討
kn-title=Ameliorating effect of chotosan and its active component, Uncaria hook, on lipopolysaccharide-induced anxiety-like behavior in mice
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kn-subtitle=
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en-aut-name=OKAWAYasumasa
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kn-aut-mei=恭昌
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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en-title=バソヒビン2を標的としたペプチドワクチンは糖尿病性腎症に対して予防的効果を持つ
kn-title=Preventive effects of vasohibin-2-targeting peptide vaccine for diabetic nephropathy
en-subtitle=
kn-subtitle=
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kn-abstract=
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kn-copyright=

en-aut-name=NAKASHIMAYuri
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kn-aut-mei=有理
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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en-title=精神的ストレスはアドレナリンβ2受容体を介して皮膚アレルギー炎症におけるマクロファージの抗炎症機能を減弱させる
kn-title=Stress-experienced monocytes/macrophages lose anti-inflammatory function via β2-adrenergic receptor in skin allergic inflammation
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kn-subtitle=
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kn-abstract=
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kn-copyright=

en-aut-name=URAKAMIHitoshi
en-aut-sei=URAKAMI
en-aut-mei=Hitoshi
kn-aut-name=浦上仁志
kn-aut-sei=浦上
kn-aut-mei=仁志
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
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kn-subject=
en-title=脳卒中モデルマウスにおけるフラボノイド、スダチチンの神経保護効果　
kn-title=Neuroprotective effect of, a flavonoid, sudachitin in mice stroke model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=OTA ELLIOTT RICARDO SATOSHI
en-aut-sei=OTA ELLIOTT RICARDO SATOSHI
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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
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cd-vols=
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en-article=
kn-article=
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kn-subject=
en-title=腹腔神経節および上腸間膜神経節の除去によるグルコース耐性の改善と膵島サイズの縮小
kn-title=Celiac and superior mesenteric ganglia removal improves glucose tolerance and reduces pancreas islet size
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=XUSHANSHAN
en-aut-sei=XU
en-aut-mei=SHANSHAN
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
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cd-vols=
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dt-received=
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dt-pub-year=2025
dt-pub=20250325
dt-online=
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kn-subject=
en-title=頚部脊髄刺激療法はCCL2を介した経路を抑制することでてんかんモデルラットに対して抗てんかん作用を示す
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=
en-copyright=
kn-copyright=

en-aut-name=OKAZAKIYosuke
en-aut-sei=OKAZAKI
en-aut-mei=Yosuke
kn-aut-name=岡﨑洋介
kn-aut-sei=岡﨑
kn-aut-mei=洋介
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=8
cd-vols=
no-issue=1
article-no=
start-page=715
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250508
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=TRPV2 mediates stress resilience in mouse cardiomyocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The heart dynamically compensates for haemodynamic stress, but how this resilience forms during cardiac growth is not clear. Using a temporally inducible, cardiac-specific knockout in mice we show that the Transient receptor potential vanilloid family 2 (TRPV2) channel is crucial for the maturation of cardiomyocyte stress resilience. TRPV2 defects in growing hearts lead to small morphology, abnormal intercalated discs, weak contractility, and low expression of serum response factor and Insulin-like growth factor-1 (IGF-1) signalling. Individual cardiomyocytes of TRPV2-deficient hearts show reduced contractility with abnormal Ca2+ handling. In cultured neonatal cardiomyocytes, mechanical Ca2+ response, excitation-contraction coupling, sarcoplasmic reticulum Ca2+ content, actin formation, nuclear localisation of Myocyte enhancer factor 2c, and IGF-1 expression require TRPV2. TRPV2-deficient hearts show a defective response to dobutamine stress and no compensatory hypertrophic response to phenylephrine administration, but no stress response to pressure overload. These data suggest TRPV2 mediates the maturation of cardiomyocyte stress resilience, and will advance therapeutic interventions and drug discovery for heart disease.
en-copyright=
kn-copyright=

en-aut-name=DongYubing
en-aut-sei=Dong
en-aut-mei=Yubing
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

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

en-aut-name=UjiharaYoshihiro
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en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ChenYanzhu
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en-aut-mei=Yanzhu
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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=NakamuraKazufumi
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kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KatanosakaKimiaki
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kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NaruseKeiji
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KatanosakaYuki
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en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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 Electrical and Mechanical Engineering, Graduate School of Engineering, Nagoya Institute of Technology
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 Chronic Kidney Disease and Cardiovascular Disease, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

affil-num=7
en-affil=Department of Biomedical Sciences, College of Life and Health Sciences, Chubu University
kn-affil=

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

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

start-ver=1.4
cd-journal=joma
no-vol=214
cd-vols=
no-issue=
article-no=
start-page=32
end-page=41
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202505
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Medaka approach to evolutionary social neuroscience
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Previously, the integration of comparative biological and neuroscientific approaches has led to significant advancements in social neuroscience. This review highlights the potential and future directions of evolutionary social neuroscience research utilizing medaka fishes (the family Adrianichthyidae) including Japanese medaka (Oryzias latipes). We focus on medaka social cognitive capabilities and mate choice behavior, particularly emphasizing mate preference using visual cues. Medaka fishes are also advantageous due to their abundant genetic resources, extensive genomic information, and the relative ease of laboratory breeding and genetic manipulation. Here we present some research examples of both the conventional neuroscience approach and evolutionary approach involving medaka fishes and other species. We also discuss the prospects of uncovering the molecular and cellular mechanisms underlying the diversity of visual mate preference among species. Especially, we introduce that the single-cell transcriptome technology, particularly in conjunction with 'Adaptive Circuitry Census', is an innovative tool that bridges comparative biological methods and neuroscientific approaches. Evolutionary social neuroscience research using medaka has the potential to unveil fundamental principles in neuroscience and elucidate the mechanisms responsible for generating diversity in mating strategies.
en-copyright=
kn-copyright=

en-aut-name=AnsaiSatoshi
en-aut-sei=Ansai
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=Hiraki-KajiyamaTowako
en-aut-sei=Hiraki-Kajiyama
en-aut-mei=Towako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UedaRyutaro
en-aut-sei=Ueda
en-aut-mei=Ryutaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SekiTakahide
en-aut-sei=Seki
en-aut-mei=Takahide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YokoiSaori
en-aut-sei=Yokoi
en-aut-mei=Saori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KatsumuraTakafumi
en-aut-sei=Katsumura
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakeuchiHideaki
en-aut-sei=Takeuchi
en-aut-mei=Hideaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Ushimado Marine Institute, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=

affil-num=3
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=

affil-num=4
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=

affil-num=5
en-affil=School of Pharmaceutical Sciences, Hokkaido University
kn-affil=

affil-num=6
en-affil=School of Medicine, Kitasato University
kn-affil=

affil-num=7
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=
en-keyword=Evolutionary neuroscience
kn-keyword=Evolutionary neuroscience
en-keyword=Comparative neuroscience
kn-keyword=Comparative neuroscience
en-keyword=Medaka bioresource
kn-keyword=Medaka bioresource
en-keyword=Visual mate preference
kn-keyword=Visual mate preference
en-keyword=Sexual selection
kn-keyword=Sexual selection
en-keyword=Genetic manipulation
kn-keyword=Genetic manipulation
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=7
article-no=
start-page=2221
end-page=
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=Length Estimation of Pneumatic Artificial Muscle with Optical Fiber Sensor Using Machine Learning
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A McKibben artificial muscle is a soft actuator driven by air pressure, characterized by its flexibility, lightweight design, and high power-to-weight ratio. We have developed a smart artificial muscle that is capable of sensing its motion. To enable this sensing function, an optical fiber was integrated into the sleeve consisting of multiple fibers and serving as a component of the McKibben artificial muscle. By measuring the macrobending loss of the optical fiber, the length of the smart artificial muscle is expected to be estimated. However, experimental results indicated that the sensor's characteristics depend not only on the length but also on the load and the applied air pressure. This dependency arises because the stress applied to the optical fiber increases, causing microbending loss. In this study, we employed a machine learning model, primarily composed of Long Short-Term Memory (LSTM) neural networks, to estimate the length of the smart artificial muscle. The experimental results demonstrate that the length estimation obtained through machine learning exhibits a smaller error. This suggests that machine learning is a feasible approach to enhancing the length measurement accuracy of the smart artificial muscle.
en-copyright=
kn-copyright=

en-aut-name=NiYilei
en-aut-sei=Ni
en-aut-mei=Yilei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WakimotoShuichi
en-aut-sei=Wakimoto
en-aut-mei=Shuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TianWeihang
en-aut-sei=Tian
en-aut-mei=Weihang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TodaYuichiro
en-aut-sei=Toda
en-aut-mei=Yuichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KandaTakefumi
en-aut-sei=Kanda
en-aut-mei=Takefumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamaguchiDaisuke
en-aut-sei=Yamaguchi
en-aut-mei=Daisuke
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 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=
en-keyword=McKibben artificial muscle
kn-keyword=McKibben artificial muscle
en-keyword=machine learning
kn-keyword=machine learning
en-keyword=optical fiber
kn-keyword=optical fiber
en-keyword=motion estimation
kn-keyword=motion estimation
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=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=16
cd-vols=
no-issue=
article-no=
start-page=1537615
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=PARylation-mediated post-transcriptional modifications in cancer immunity and immunotherapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Poly-ADP-ribosylation (PARylation) is a post-translational modification in which ADP-ribose is added to substrate proteins. PARylation is mediated by a superfamily of ADP-ribosyl transferases known as PARPs and influences a wide range of cellular functions, including genome integrity maintenance, and the regulation of proliferation and differentiation. We and others have recently reported that PARylation of SH3 domain-binding protein 2 (3BP2) plays a role in bone metabolism, immune system regulation, and cytokine production. Additionally, PARylation has recently gained attention as a target for cancer treatment. In this review, we provide an overview of PARylation, its involvement in several signaling pathways related to cancer immunity, and the potential of combination therapies with PARP inhibitors and immune checkpoint inhibitors.
en-copyright=
kn-copyright=

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

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
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=
en-keyword=PARylation
kn-keyword=PARylation
en-keyword=cancer
kn-keyword=cancer
en-keyword=post-transcriptional regulation
kn-keyword=post-transcriptional regulation
en-keyword=ubiquitylation
kn-keyword=ubiquitylation
en-keyword=immune system
kn-keyword=immune system
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=6
article-no=
start-page=790
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250320
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Improving Diagnostic Performance for Head and Neck Tumors with Simple Diffusion Kurtosis Imaging and Machine Learning Bi-Parameter Analysis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/Objectives: Mean kurtosis (MK) values in simple diffusion kurtosis imaging (SDI)-a type of diffusion kurtosis imaging (DKI)-have been reported to be useful in the diagnosis of head and neck malignancies, for which pre-processing with smoothing filters has been reported to improve the diagnostic accuracy. Multi-parameter analysis using DKI in combination with other image types has recently been reported to improve the diagnostic performance. The purpose of this study was to evaluate the usefulness of machine learning (ML)-based multi-parameter analysis using the MK and apparent diffusion coefficient (ADC) values-which can be acquired simultaneously through SDI-for the differential diagnosis of benign and malignant head and neck tumors, which is important for determining the treatment strategy, as well as examining the usefulness of filter pre-processing. Methods: A total of 32 pathologically diagnosed head and neck tumors were included in the study, and a Gaussian filter was used for image pre-processing. MK and ADC values were extracted from pixels within the tumor area and used as explanatory variables. Five ML algorithms were used to create models for the prediction of tumor status (benign or malignant), which were evaluated through ROC analysis. Results: Bi-parameter analysis with gradient boosting achieved the best diagnostic performance, with an AUC of 0.81. Conclusions: The usefulness of bi-parameter analysis with ML methods for the differential diagnosis of benign and malignant head and neck tumors using SDI data were demonstrated.
en-copyright=
kn-copyright=

en-aut-name=YoshidaSuzuka
en-aut-sei=Yoshida
en-aut-mei=Suzuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KurodaMasahiro
en-aut-sei=Kuroda
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraYoshihide
en-aut-sei=Nakamura
en-aut-mei=Yoshihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FukumuraYuka
en-aut-sei=Fukumura
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakamitsuYuki
en-aut-sei=Nakamitsu
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=Al-HammadWlla E.
en-aut-sei=Al-Hammad
en-aut-mei=Wlla E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KurodaKazuhiro
en-aut-sei=Kuroda
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ShimizuYudai
en-aut-sei=Shimizu
en-aut-mei=Yudai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TanabeYoshinori
en-aut-sei=Tanabe
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OitaMasataka
en-aut-sei=Oita
en-aut-mei=Masataka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SugiantoIrfan
en-aut-sei=Sugianto
en-aut-mei=Irfan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=BarhamMajd
en-aut-sei=Barham
en-aut-mei=Majd
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TekikiNouha
en-aut-sei=Tekiki
en-aut-mei=Nouha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KamaruddinNurul N.
en-aut-sei=Kamaruddin
en-aut-mei=Nurul N.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
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=15
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=16
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=17
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=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
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=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

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

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

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

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

affil-num=10
en-affil=Graduate School of Interdisciplinary Sciences and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Oral Radiology, Faculty of Dentistry, Hasanuddin University
kn-affil=

affil-num=12
en-affil=Department of Dentistry and Dental Surgery, College of Medicine and Health Sciences, An-Najah National University
kn-affil=

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

affil-num=14
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=15
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=16
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=17
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=head and neck tumors
kn-keyword=head and neck tumors
en-keyword=mean kurtosis
kn-keyword=mean kurtosis
en-keyword=simple diffusion kurtosis imaging
kn-keyword=simple diffusion kurtosis imaging
en-keyword=magnetic resonance imaging
kn-keyword=magnetic resonance imaging
en-keyword=apparent diffusion coefficient value
kn-keyword=apparent diffusion coefficient value
en-keyword=diffusion kurtosis imaging
kn-keyword=diffusion kurtosis imaging
en-keyword=machine learning
kn-keyword=machine learning
en-keyword=bi-parameter analysis
kn-keyword=bi-parameter analysis
en-keyword=gradient boosting
kn-keyword=gradient boosting
en-keyword=differential diagnosis of benign and malignant
kn-keyword=differential diagnosis of benign and malignant
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=15
cd-vols=
no-issue=1
article-no=
start-page=7506
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250303
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A glucocorticoid-regulating molecule, Fkbp5, may interact with mitogen-activated protein kinase signaling in the organ of Corti of mice cochleae
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=FKBP5 is a 51-Da FK506-binding protein and member of the immunophilin family involved in controlling the signaling of glucocorticoid receptor from the cytosol to nucleus. Fkbp5 has previously been shown to be expressed in murine cochlear tissue, including the organ of Corti (i.e., the sensory epithelium of the cochlea). Fkbp5-/- mice as used in this study show hearing loss in the low-frequency (8-kHz) range and click-evoked auditory brainstem response (ABR) threshold compared to wild-type mice. Both Fkbp5-/- and wild-type mice showed hearing loss at all frequencies and click-ABR thresholds at 24 h and 14 days following acoustic overexposure (AO). Tissues of the organ of Corti were subjected to RNA sequencing and KEGG pathway analysis. In Fkbp5-/- mice before AO, the mitogen-activated protein kinase (MAPK) signaling pathway was dysregulated compared to wild-type mice. In wild-type mice at 12 h following AO, the most significantly modulated KEGG pathway was the TNF signaling pathway and major MAPK molecules p38 and Jun were involved in the TNF signaling pathway. In Fkbp5-/- mice at 12 h following AO, the MAPK signaling pathway was dysregulated compared to wild-type mice following AO. In conclusion, Fkbp5 interacts with MAPK signaling in the organ of Corti in mice cochleae.
en-copyright=
kn-copyright=

en-aut-name=SatoAsuka
en-aut-sei=Sato
en-aut-mei=Asuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=MaedaYukihide
en-aut-sei=Maeda
en-aut-mei=Yukihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

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

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

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

affil-num=4
en-affil=Department of Otolaryngology-Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=The organ of Corti
kn-keyword=The organ of Corti
en-keyword=Acoustic trauma
kn-keyword=Acoustic trauma
en-keyword=RNA sequencing
kn-keyword=RNA sequencing
en-keyword=51-Da FK506-binding protein
kn-keyword=51-Da FK506-binding protein
en-keyword=Mitogen-activated protein kinase signaling
kn-keyword=Mitogen-activated protein kinase signaling
en-keyword=Tumor necrosis factor signaling
kn-keyword=Tumor necrosis factor signaling
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=4
article-no=
start-page=1391
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250219
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Course of General Fatigue in Patients with Post-COVID-19 Conditions Who Were Prescribed Hochuekkito: A Single-Center Exploratory Pilot Study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: After the start of the COVID-19 pandemic, general fatigue in patients with long COVID and post-COVID-19 conditions (PCC) became a medical issue. Although there is a lack of evidence-based treatments, Kampo medicine (traditional Japanese medicine) has gained attention in Japan. At an outpatient clinic in Japan specializing in long COVID, 24% of all prescriptions were Kampo medicines, and 72% of Kampo medicine prescriptions were hochuekkito. However, there has been no prospective, quantitative study on the course of fatigue in patients with long COVID and PCC who were prescribed hochuekkito. The aim of this study was to clarify the course of fatigue in those patients. Methods: This study included patients aged 18 years or older with general fatigue who visited the long COVID specialized outpatient clinic at Okayama University Hospital and consented to participate after being prescribed hochuekkito. We reviewed the backgrounds of the patients, and we evaluated the patients' fatigue assessment scale in person or online. Results: Twenty patients were enrolled in this study from September to December in 2023. The average age of the patients was 42.9 years (SD: 15.8 years) and 12 patients (60%) were female. After hochuekkito administration, the fatigue assessment scale score decreased from 35.9 (SD: 5.9) at the initial visit to 31.2 (SD: 9.4) after 8 weeks, indicating a trend for improvement in fatigue (difference: 4.7; 95% CI: 0.5-8.9). Conclusions: A trend for improvement in fatigue was observed in patients with long COVID and PCC who were prescribed hochuekkito, indicating a potential benefit of hochuekkito for general fatigue in such patients. General fatigue in patients with long COVID or PCC can be classified as post-infectious fatigue syndrome and is considered a condition of qi deficiency in Kampo medicine, for which hochuekkito is appropriately indicated.
en-copyright=
kn-copyright=

en-aut-name=TokumasuKazuki
en-aut-sei=Tokumasu
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsukiNobuyoshi
en-aut-sei=Matsuki
en-aut-mei=Nobuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
ORCID=

en-aut-name=SakamotoYoko
en-aut-sei=Sakamoto
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=

en-aut-name=MatsudaYui
en-aut-sei=Matsuda
en-aut-mei=Yui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakuradaYasue
en-aut-sei=Sakurada
en-aut-mei=Yasue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HondaHiroyuki
en-aut-sei=Honda
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
ORCID=

en-aut-name=HasegawaToru
en-aut-sei=Hasegawa
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakaseRyosuke
en-aut-sei=Takase
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OmuraDaisuke
en-aut-sei=Omura
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=13
ORCID=

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

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

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

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

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

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

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

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

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

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

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

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

affil-num=13
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=fatigue assessment scale (FAS)
kn-keyword=fatigue assessment scale (FAS)
en-keyword= general fatigue
kn-keyword= general fatigue
en-keyword= hochuekkito
kn-keyword= hochuekkito
en-keyword= kampo medicine
kn-keyword= kampo medicine
en-keyword= long COVID
kn-keyword= long COVID
en-keyword= post-COVID-19 condition
kn-keyword= post-COVID-19 condition
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=
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=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=114
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=裏表紙・英文目次
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=
article-no=
start-page=27
end-page=38
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The List of Published by Members of the Faculty From January to December 2024.
kn-title=公表学術論文等リスト　2024
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=
article-no=
start-page=11
end-page=20
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Uncovering the role of arcuate kisspeptin neurons as a source of the gonadotropin-releasing hormone pulse generator using gene-modified rats
kn-title=遺伝子改変ラットを用いた弓状核キスペプチンニューロンの性腺刺激ホルモン放出ホルモンパルスジェネレーターとしての役割解明
en-subtitle=
kn-subtitle=
en-abstract=　世界において，乳牛の受胎率（妊娠率）が低下しており，家畜の繁殖成績向上のための効果的な治療法が必要とされている．家畜を含む哺乳類において，生殖機能は視床下部－下垂体－性腺軸から分泌されるホルモンによって制御されている．これらのホルモンのうち，性腺刺激ホルモン放出ホルモン（GnRH）のパルス状分泌（GnRH パルス）は，性腺刺激ホルモン分泌と性腺機能に本質的に重要である．したがって，GnRH パルスを制御するメカニズム（GnRH パルスジェネレーター）を解明することは，家畜の生殖技術を向上させるために不可欠である．本総説では，著者らの遺伝子改変ラットモデルを用いた弓状核キスペプチンニューロン（ΚNDy ニューロンとしても知られる）がGnRH パルスジェネレーターの本体であることの直接的な証拠を示した研究を中心として，過去20年間の研究を概説した．また，ΚNDy ニューロンが分泌するニューロキニンB，グルタミン酸，ダイノルフィンA がΚNDy ニューロンの神経活動を同期させ，GnRH パルスを発生させるメカニズムについて論じた．遺伝子改変ラットモデルから得られた知識は，GnRH/ 性腺刺激ホルモンパルスを刺激して，家畜の繁殖能力を向上させる新規繁殖促進剤開発に寄与すると期待できる．
kn-abstract=　Strategies for increasing reproductive performance are needed for domestic animals because for example the conception (pregnancy) rate has decreased in dairy cows around the world. Reproductive function is controlled by hormones released by the hypothalamus-pituitary-gonadal axis in mammals, including domestic animals. Of those hormones, tonic (pulsatile) gonadotropin-releasing hormone (GnRH) release is fundamentally important for gonadotropin release and gonadal activity. Therefore, uncovering the mechanism controlling GnRH pulses, that is GnRH pulse generator, is essential to improve reproductive technologies for domestic animals. The present review is focused on the indispensable role of arcuate nucleus (ARC) kisspeptin neurons (also known as KNDy neurons) as the GnRH pulse generator in mammals. First, we give a brief overview of studies on hypothalamic kisspeptin neurons throughout the past two decades. Second, we review studies that have provided direct evidence that ARC kisspeptin neurons serve as the GnRH pulse generator, with a special focus on our gene-modified rat models. Finally, we discuss the mechanism underlying GnRH pulse generation. The knowledge obtained from gene-modified rat models should be clinically important and could be adapted to new tools to improve reproductive performance in livestock by stimulating GnRH/gonadotropin pulses.
en-copyright=
kn-copyright=

en-aut-name=NagaeMayuko
en-aut-sei=Nagae
en-aut-mei=Mayuko
kn-aut-name=長江麻佑子
kn-aut-sei=長江
kn-aut-mei=麻佑子
aut-affil-num=1
ORCID=

en-aut-name=UenoyamaYoshihisa
en-aut-sei=Uenoyama
en-aut-mei=Yoshihisa
kn-aut-name=上野山賀久
kn-aut-sei=上野山
kn-aut-mei=賀久
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=岡山大学大学院環境生命自然科学研究科

affil-num=2
en-affil=Graduate School of Bioagricultural Sciences, Nagoya University
kn-affil=名古屋大学大学院生命農学研究科
en-keyword=gene-modified rats
kn-keyword=gene-modified rats
en-keyword=GnRH
kn-keyword=GnRH
en-keyword=kisspeptin
kn-keyword=kisspeptin
en-keyword=LH
kn-keyword=LH
en-keyword=pulse generator
kn-keyword=pulse generator
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=63
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250113
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Impact of Task Context on Pleasantness and Softness Estimations: A Study Based on Three Touch Strategies
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This study investigated the two distinct perceptions (pleasantness and softness) of deformable stimuli with different degrees of compliance under conditions with and without a contextual task. Three tactile strategies-grasping, pinching, and pressing-were used to perceive the stimuli. In Experiment 1 (without a contextual task), participants estimated the perceived intensity of softness or pleasantness for each stimulus. In Experiment 2 (with a contextual task), the participants sequentially perceived two stimuli with different compliance levels and indicated which stimulus they perceived as softer and pleasant. The results showed that the psychophysical relationship between compliance and perceived softness was consistent across all tactile strategies in both experiments, with softness estimates increasing as compliance increased. However, the relationship between compliance and pleasantness differed between the two experiments. In Experiment 1, pleasantness estimates increased monotonically with increased compliance. However, in Experiment 2, across all tactile strategies, pleasantness began to decrease within the compliance range of 0.25-2.0 cm2/N, exhibiting an inverted U-shaped trend. These findings indicate that the relationship between compliance and pleasantness is task-dependent, particularly demonstrating significantly different trends when a contextual task is introduced. In contrast, the relationship between compliance and softness remained consistently monotonic.
en-copyright=
kn-copyright=

en-aut-name=GaoBinyue
en-aut-sei=Gao
en-aut-mei=Binyue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YuYinghua
en-aut-sei=Yu
en-aut-mei=Yinghua
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EjimaYoshimichi
en-aut-sei=Ejima
en-aut-mei=Yoshimichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WuJinglong
en-aut-sei=Wu
en-aut-mei=Jinglong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YangJiajia
en-aut-sei=Yang
en-aut-mei=Jiajia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

affil-num=2
en-affil=Graduate School of 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=
en-keyword=pleasantness
kn-keyword=pleasantness
en-keyword=softness
kn-keyword=softness
en-keyword=touch strategy
kn-keyword=touch strategy
en-keyword=task context
kn-keyword=task context
en-keyword=psychophysics
kn-keyword=psychophysics
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=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=18
cd-vols=
no-issue=2
article-no=
start-page=125
end-page=132
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=ナトリウムチャネル異常とてんかん
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=大守（川﨑）伊織
kn-aut-sei=大守（川﨑）
kn-aut-mei=伊織
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学学術研究院教育学域
END

start-ver=1.4
cd-journal=joma
no-vol=326
cd-vols=
no-issue=6
article-no=
start-page=F1054
end-page=F1065
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=Preventive effects of vasohibin-2-targeting peptide vaccine for diabetic nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Diabetic nephropathy remains the leading cause of end-stage kidney disease in many countries, and additional therapeutic targets are needed to prevent its development and progression. Some angiogenic factors are involved in the pathogenesis of diabetic nephropathy. Vasohibin-2 (VASH2) is a novel proangiogenic factor, and our previous study showed that glomerular damage is inhibited in diabetic Vash2 homozygous knockout mice. Therefore, we established a VASH2-targeting peptide vaccine as a tool for anti-VASH2 therapy in diabetic nephropathy. In this study, the preventive effects of the VASH2-targeting peptide vaccine against glomerular injury were examined in a streptozotocin (STZ)-induced diabetic mouse model. The mice were subcutaneously injected with the vaccine at two doses 2 wk apart and then intraperitoneally injected with 50 mg/kg STZ for 5 consecutive days. Glomerular injury was evaluated 20 wk after the first vaccination. Treatment with the VASH2-targeting peptide vaccine successfully induced circulating anti-VASH2 antibody without inflammation in major organs. Although the vaccination did not affect blood glucose levels, it significantly prevented hyperglycemia-induced increases in urinary albumin excretion and glomerular volume. The vaccination did not affect increased VASH2 expression but significantly inhibited renal angiopoietin-2 (Angpt2) expression in the diabetic mice. Furthermore, it significantly prevented glomerular macrophage infiltration. The preventive effects of vaccination on glomerular injury were also confirmed in db/db mice. Taken together, the results of this study suggest that the VASH2-targeting peptide vaccine may prevent diabetic glomerular injury in mice by inhibiting Angpt2-mediated microinflammation.
en-copyright=
kn-copyright=

en-aut-name=NakashimaYuri
en-aut-sei=Nakashima
en-aut-mei=Yuri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanabeKatsuyuki
en-aut-sei=Tanabe
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MifuneTomoyo
en-aut-sei=Mifune
en-aut-mei=Tomoyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=5
ORCID=

en-aut-name=NakagamiHironori
en-aut-sei=Nakagami
en-aut-mei=Hironori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SatoYasufumi
en-aut-sei=Sato
en-aut-mei=Yasufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
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 Health Development and Medicine, Osaka University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Health Development and Medicine, Osaka University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=New Industry Creation Hatchery Center, Tohoku University
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=
en-keyword=albuminuria
kn-keyword=albuminuria
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
en-keyword=macrophages
kn-keyword=macrophages
en-keyword=peptide vaccine
kn-keyword=peptide vaccine
en-keyword=vasohibin-2
kn-keyword=vasohibin-2
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=3
article-no=
start-page=198
end-page=200
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250108
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Long-Term Follow-Up of a Patient With SPG11
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We present a case of a male patient with disease-causing variants in SPG11, a causative gene for autosomal recessive spastic paraplegia with a thin corpus callosum (ARHSP-TCC), as well as juvenile amyotrophic lateral sclerosis (ALS5) and Charcot–Marie–Tooth disease (CMT2X). A neurological examination at age 18 revealed dysarthria, muscle weakness in bilateral lower extremities, hyperreflexia in patellar reflex, hyporeflexia in Achilles reflex with an extensor plantar reflex, and intellectual disability. Magnetic resonance imaging revealed a thin corpus callosum and ears of the lynx sign. At the age of 26, weakness and muscle atrophy progressed. While no sensory disturbances were noted, there was a mild decrease in sensory nerve action potentials of the sural nerve over the 8 years between 18 and 26. Clinicians should be aware that SPG11 belongs to the same spectrum of disorders as ALS5 and CMT2X and presents various phenotypes depending on the stage of the disease.
en-copyright=
kn-copyright=

en-aut-name=OsakadaYosuke
en-aut-sei=Osakada
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=MatsuokaChika
en-aut-sei=Matsuoka
en-aut-mei=Chika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=

en-aut-name=TsunodaKeiichiro
en-aut-sei=Tsunoda
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=DeguchiKentaro
en-aut-sei=Deguchi
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=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=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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, Tsuyama Chuo Hospital
kn-affil=

affil-num=6
en-affil=Department of Neurology, Okayama City Hospital
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=
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=17
cd-vols=
no-issue=3-4
article-no=
start-page=116
end-page=125
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Deep Reinforcement Learning Enabled Adaptive Virtual Machine Migration Control in Multi-Stage Information Processing Systems
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This paper tackles a Virtual Machine (VM) migration control problem to maximize the progress (accuracy) of information processing tasks in multi-stage information processing systems. The conventional methods for this problem are effective only for specific situations, such as when the system load is high. In this paper, in order to adaptively achieve high accuracy in various situations, we propose a VM migration method using a Deep Reinforcement Learning (DRL) algorithm. It is difficult to directly apply a DRL algorithm to the VM migration control problem because the size of the solution space of the problem dynamically changes according to the number of VMs staying in the system while the size of the agent’s action space is fixed in DRL algorithms. To cope with this difficulty, the proposed method divides the VM migration control problem into two problems: the problem of determining only the VM distribution (i.e., the proportion of the number of VMs deployed on each edge server) and the problem of determining the locations of all the VMs so that it follows the determined VM distribution. The former problem is solved by a DRL algorithm, and the latter by a heuristic method. This approach makes it possible to apply a DRL algorithm to the VM migration control problem because the VM distribution is expressed by a vector with a fixed number of dimensions and can be directly outputted by the agent. The simulation results confirm that our proposed method can adaptively achieve quasi-optimal accuracy in various situations with different link delays, types of the information processing tasks and the number of VMs.
en-copyright=
kn-copyright=

en-aut-name=FukushimaYukinobu
en-aut-sei=Fukushima
en-aut-mei=Yukinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KoujitaniYuki
en-aut-sei=Koujitani
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakaneKazutoshi
en-aut-sei=Nakane
en-aut-mei=Kazutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TarutaniYuya
en-aut-sei=Tarutani
en-aut-mei=Yuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WuCelimuge
en-aut-sei=Wu
en-aut-mei=Celimuge
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=JiYusheng
en-aut-sei=Ji
en-aut-mei=Yusheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YokohiraTokumi
en-aut-sei=Yokohira
en-aut-mei=Tokumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MuraseTutomu
en-aut-sei=Murase
en-aut-mei=Tutomu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Faculty 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 Information Science Nagoya University
kn-affil=

affil-num=4
en-affil=Graduate School of Engineering Osaka University
kn-affil=

affil-num=5
en-affil=Graduate School of Informatics and Engineering The Univ. of Electro-Commun.
kn-affil=

affil-num=6
en-affil=Information Systems Architecture Research Division National Institute of Informatics
kn-affil=

affil-num=7
en-affil=Faculty of Interdisciplinary Science and Engineering in Health Systems Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Information Science Nagoya University
kn-affil=
en-keyword=Multi-stage information processing system
kn-keyword=Multi-stage information processing system
en-keyword=VM migration control
kn-keyword=VM migration control
en-keyword=Deep reinforcement learning
kn-keyword=Deep reinforcement learning
en-keyword=Deep Deterministic Policy Gradient (DDPG)
kn-keyword=Deep Deterministic Policy Gradient (DDPG)
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=3
article-no=
start-page=769
end-page=774
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230519
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Review: Nicotinic acetylcholine receptors to regulate important brain activity—what occurs at the molecular level?
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Herein, we briefly review the role of nicotinic acetylcholine receptors in regulating important brain activity by controlled release of acetylcholine from subcortical neuron groups, focusing on a microscopic viewpoint and considering the nonlinear dynamics of biological macromolecules associated with neuron activity and how they give rise to advanced brain functions of brain.
en-copyright=
kn-copyright=

en-aut-name=NaraShigetoshi
en-aut-sei=Nara
en-aut-mei=Shigetoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamagutiYutaka
en-aut-sei=Yamaguti
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TsudaIchiro
en-aut-sei=Tsuda
en-aut-mei=Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

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

affil-num=2
en-affil=Faculty of Information Engineering, Fukuoka Institute of Technology
kn-affil=

affil-num=3
en-affil=Chubu University Academy of Emerging Sciences/Center for Mathematical Science and Artificial Intelligence, Chubu University
kn-affil=
en-keyword=Neuromodulator
kn-keyword=Neuromodulator
en-keyword=Nichotinic
kn-keyword=Nichotinic
en-keyword=Acetylcholine
kn-keyword=Acetylcholine
en-keyword=Receptors
kn-keyword=Receptors
en-keyword=Brain activity
kn-keyword=Brain activity
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=12
article-no=
start-page=e0315385
end-page=
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=Phase-dependent trends in the prevalence of myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) related to long COVID: A criteria-based retrospective study in Japan
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background <br>
The characteristics of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) related to COVID-19 have remained uncertain. To elucidate the clinical trend of ME/CFS induced by long COVID, we examined data for patients who visited our outpatient clinic established in a university hospital during the period from Feb 2021 to July 2023.<br>
<br>
Methods <br>
Long COVID patients were classified into two groups, an ME/CFS group and a non-ME/CFS group, based on three diagnostic criteria.<br>
<br>
Results <br>
The prevalence of ME/CFS in the long COVID patients was 8.4% (62 of 739 cases; female: 51.6%) and factors related to ME/CFS were severe illness, smoking and alcohol drinking habits, and fewer vaccinations. The frequency of ME/CFS decreased from 23.9% in the Preceding period to 13.7% in the Delta-dominant period and to 3.3% in the Omicron-dominant period. Fatigue and headache were commonly frequent complaints in the ME/CFS group, and the frequency of poor concentration in the ME/CFS group was higher in the Omicron period. Serum ferritin levels were significantly higher in female patients in the ME/CFS group infected in the Preceding period. In the ME/CFS group, the proportion of patients complaining of brain fog significantly increased from 22.2% in the Preceding period to 47.9% in the Delta period and to 81.3% in the Omicron period. The percentage of patients who had received vaccination was lower in the ME/CFS group than the non-ME/CFS group over the study period, whereas there were no differences in the vaccination rate between the groups in each period.<br>
<br>
Conclusion <br>
The proportion of long COVID patients who developed ME/CFS strictly diagnosed by three criteria was lower among patients infected in the Omicron phase than among patients infected in the other phases, while the proportion of patients with brain fog inversely increased. Attention should be paid to the variant-dependent trends of ME/CFS triggered by long COVID (300 words).
en-copyright=
kn-copyright=

en-aut-name=MoritaSatoru
en-aut-sei=Morita
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
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=3
ORCID=

en-aut-name=HondaHiroyuki
en-aut-sei=Honda
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=

en-aut-name=SunadaNaruhiko
en-aut-sei=Sunada
en-aut-mei=Naruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakuradaYasue
en-aut-sei=Sakurada
en-aut-mei=Yasue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MatsudaYui
en-aut-sei=Matsuda
en-aut-mei=Yui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SoejimaYoshiaki
en-aut-sei=Soejima
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
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=11
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 General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=
article-no=
start-page=1468230
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=Perspectives of traditional herbal medicines in treating retinitis pigmentosa
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Medicinal plants, also known as herbs, have been discovered and utilized in traditional medical practice since prehistoric times. Medicinal plants have been proven rich in thousands of natural products that hold great potential for the development of new drugs. Previously, we reviewed the types of Chinese traditional medicines that a Tang Dynasty monk Jianzhen (Japanese: Ganjin) brought to Japan from China in 742. This article aims to review the origin of Kampo (Japanese traditional medicine), and to present the overview of neurodegenerative diseases and retinitis pigmentosa as well as medicinal plants in some depth. Through the study of medical history of the origin of Kampo, we found that herbs medicines contain many neuroprotective ingredients. It provides us a new perspective on extracting neuroprotective components from herbs medicines to treat neurodegenerative diseases. Retinitis pigmentosa (one of the ophthalmic neurodegenerative diseases) is an incurable blinding disease and has become a popular research direction in global ophthalmology. To date, treatments for retinitis pigmentosa are very limited worldwide. Therefore, we intend to integrate the knowledge and skills from different disciplines, such as medical science, pharmaceutical science and plant science, to take a new therapeutic approach to treat neurodegenerative diseases. In the future, we will use specific active ingredients extracted from medicinal plants to treat retinitis pigmentosa. By exploring the potent bioactive ingredients present in medicinal plants, a valuable opportunity will be offered to uncover novel approaches for the development of drugs which target for retinitis pigmentosa.
en-copyright=
kn-copyright=

en-aut-name=LiuShihui
en-aut-sei=Liu
en-aut-mei=Shihui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuoToshihiko
en-aut-sei=Matsuo
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MatsuoChie
en-aut-sei=Matsuo
en-aut-mei=Chie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AbeTakumi
en-aut-sei=Abe
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ChenJinghua
en-aut-sei=Chen
en-aut-mei=Jinghua
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SunChi
en-aut-sei=Sun
en-aut-mei=Chi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ZhaoQing
en-aut-sei=Zhao
en-aut-mei=Qing
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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 Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Ophthalmology, University of Florida, College of Medicine
kn-affil=

affil-num=6
en-affil=Department of Ophthalmology and Visual Sciences, Washington University in St. Louis
kn-affil=

affil-num=7
en-affil=National Key Laboratory of Plant Molecular Genetics, CAS Center for Excellence in Molecular Plant Sciences, Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences
kn-affil=
en-keyword=retinitis pigmentosa
kn-keyword=retinitis pigmentosa
en-keyword=ophthalmology
kn-keyword=ophthalmology
en-keyword=botany
kn-keyword=botany
en-keyword=pharmacology
kn-keyword=pharmacology
en-keyword=medical history
kn-keyword=medical history
en-keyword=compound
kn-keyword=compound
en-keyword=drug discovery
kn-keyword=drug discovery
en-keyword=degenerative diseases
kn-keyword=degenerative diseases
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=ラットモデルにおけるくも膜下出血発症後急性期における脳波抑制は早期脳損傷の重要なマーカーである
kn-title=Power suppression in EEG after the onset of SAH is a significant marker of early brain injury in rat models
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TAKASUGIYuji
en-aut-sei=TAKASUGI
en-aut-mei=Yuji
kn-aut-name=髙杉祐二
kn-aut-sei=髙杉
kn-aut-mei=祐二
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=時間予測が触覚知覚の形成に与える影響の神経基盤の解明
kn-title=The neural substrates of temporal prediction forming tactile perception in humans
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=RENRONGXIA
en-aut-sei=REN
en-aut-mei=RONGXIA
kn-aut-name=任栄霞
kn-aut-sei=任
kn-aut-mei=栄霞
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=主観的認知機能の低下が視聴覚統合とクロスモーダルトレーニングに与える影響
kn-title=Effects of Subjective Cognitive Decline on Audiovisual Integration and Cross-modal Training
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=LISHENGNAN
en-aut-sei=LI
en-aut-mei=SHENGNAN
kn-aut-name=李勝楠
kn-aut-sei=李
kn-aut-mei=勝楠
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=Go/No-Go課題を用いた運動抑制の神経基盤の解明
kn-title=The neural substrates of motion inhibitory control during Go/No-Go response inhibition task
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=ZHANGNAN
en-aut-sei=ZHANG
en-aut-mei=NAN
kn-aut-name=張楠
kn-aut-sei=張
kn-aut-mei=楠
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=コンピュータービジョンによる食事摂取量推定技術
kn-title=Computer Vision Systems for Estimating Food Consumption in a Hospital Setting
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=YUITA ARUM SARI
en-aut-sei=YUITA ARUM SARI
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=コンピュータ・ビジョンによる動物体検出技術と精子品質推定への応用
kn-title=Computer Vision-based Motion Segmentation and Its Application for Sperm Quality Estimation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SIGIT ADINUGROHO
en-aut-sei=SIGIT ADINUGROHO
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=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=IoTアプリケーション・システムのための統合サーバ・プラットフォームに関する研究
kn-title=A Study of Integrated Server Platform for IoT Application Systems
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=YOHANES YOHANIE FRIDELIN PANDUMAN
en-aut-sei=YOHANES YOHANIE FRIDELIN PANDUMAN
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 Natural Science and Technology, Okayama university
kn-affil=岡山大学大学院自然科学研究科
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=
kn-title=キイロショウジョウバエ概日時計を制御する時計神経回路の網羅的機能解析
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SEKIGUCHIManabu
en-aut-sei=SEKIGUCHI
en-aut-mei=Manabu
kn-aut-name=関口学
kn-aut-sei=関口
kn-aut-mei=学
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama university
kn-affil=岡山大学大学院自然科学研究科
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=女性の新型コロナウイルス感染症罹患後症状にみられる月経関連症状の検討
kn-title=Clinical characteristics of female long COVID patients with menstrual symptoms: a retrospective study from a Japanese outpatient clinic
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SAKURADAYasue
en-aut-sei=SAKURADA
en-aut-mei=Yasue
kn-aut-name=櫻田泰江
kn-aut-sei=櫻田
kn-aut-mei=泰江
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=酸化ストレスと炎症反応に関するマウス脳卒中モデルにおけるカルノシンの神経保護効果
kn-title=Neuroprotective effects of carnosine in a mice stroke model concerning oxidative stress and inflammatory response
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=HUXINRAN
en-aut-sei=HU
en-aut-mei=XINRAN
kn-aut-name=胡欣冉
kn-aut-sei=胡
kn-aut-mei=欣冉
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においてPRRX1とTOP2Aのタンパク質間相互作用は悪性化を促進させる
kn-title=PRRX1-TOP2A interaction is a malignancy-promoting factor in human malignant peripheral nerve sheath tumours
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TAKIHIRAShota
en-aut-sei=TAKIHIRA
en-aut-mei=Shota
kn-aut-name=棏平将太
kn-aut-sei=棏平
kn-aut-mei=将太
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=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=12
cd-vols=
no-issue=
article-no=
start-page=78366
end-page=78378
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=Aromug: A Mug-Type Olfactory Interface to Enhance the Sweetness Perception of Beverages
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sugary beverages are a significant contributor to sugar consumption, and their excessive consumption is associated with increased risks of elevated blood glucose levels and diabetes. Many individuals have a strong preference for sugary beverages and often find beverages with lower sugar content to be less satisfying. Attempts to switch to less sugary options are frequently short-lived, leading to a return to higher-sugar beverages. Recognizing that 75 – 95% of taste perception is influenced by scent, we investigated a scent-based approach to reduce sugar intake while preserving the perception of sweetness. This study introduces an olfactory interface in the form of a mug named “Aromug,” designed to emit a sweet scent in sync with the drinking action. Aromug incorporates motion sensing and scent presentation functions to enhance the perceived sweetness of a beverage, thereby encouraging a gradual reduction in sugar intake. Our experiments, involving 33 participants, demonstrated that the combined scents of sugar-free coffee and chocolate increased the perception of sweetness (p =1.641×10−2 ). The study also found that the simultaneous presentation of scent and visual cues improved taste satisfaction and sweetness perception. Additionally, we observed variations in sweetness preference related to age and frequency of coffee consumption. It was particularly observed that people in their 20s and those who frequently drink coffee tend to perceive the taste of beverages as sweeter. This suggests a potential for Aromug to customize the scent experience based on individual preferences, offering a novel way to encourage healthier beverage choices.
en-copyright=
kn-copyright=

en-aut-name=MayumiDaiki
en-aut-sei=Mayumi
en-aut-mei=Daiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraYugo
en-aut-sei=Nakamura
en-aut-mei=Yugo
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=MisakiShinya
en-aut-sei=Misaki
en-aut-mei=Shinya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YasumotoKeiichi
en-aut-sei=Yasumoto
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Graduate School of Science and Technology, Nara Institute of Science and Technology
kn-affil=

affil-num=2
en-affil=Faculty of Information Science and Electrical Engineering, Kyushu University
kn-affil=

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

affil-num=4
en-affil=Graduate School of Science and Technology, Nara Institute of Science and Technology
kn-affil=

affil-num=5
en-affil=Graduate School of Science and Technology, Nara Institute of Science and Technology
kn-affil=
en-keyword=Olfaction
kn-keyword=Olfaction
en-keyword=olfactory interfaces
kn-keyword=olfactory interfaces
en-keyword=olfactory display
kn-keyword=olfactory display
en-keyword=scents
kn-keyword=scents
en-keyword=taste evaluation
kn-keyword=taste evaluation
en-keyword=smell
kn-keyword=smell
en-keyword=olfactory perception
kn-keyword=olfactory perception
en-keyword=behavior change support
kn-keyword=behavior change support
END

start-ver=1.4
cd-journal=joma
no-vol=63
cd-vols=
no-issue=19
article-no=
start-page=2655
end-page=2660
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=A Prompt Diagnosis and Treatment of a Case of Nuclear Protein of the Testis Carcinoma Characterized by a Bronchial Lesion and High Serum Alpha-fetoprotein Level Following Genomic Testing
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Nuclear protein of the testis carcinoma (NUTC) is a rare and aggressive malignancy. We herein report a case of NUTC in the lung characterized by a bronchial lesion and elevated alpha-fetoprotein levels. A 35-year-old Japanese man presented to our institution with suspected advanced lung cancer based on a histological examination. Subsequently, next-generation sequencing (NGS) yielded a positive BRD4-NUTM1 fusion. In addition, positive NUT immunostaining of the lung biopsy specimen confirmed NUTC in the lungs. Systemic chemotherapy and radiotherapy showed a temporary response, with decreased serum alpha-fetoprotein levels. We highlight this case of a prompt diagnosis by NGS of NUTC in a young individual with a rapidly progressing tumor.
en-copyright=
kn-copyright=

en-aut-name=MatsuuraHiroaki
en-aut-sei=Matsuura
en-aut-mei=Hiroaki
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=OdaNaohiro
en-aut-sei=Oda
en-aut-mei=Naohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=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=RaiKammei
en-aut-sei=Rai
en-aut-mei=Kammei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
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=9
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=10
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=11
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

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, Fukuyama City 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=Center for Innovative Clinical 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=Department of Respiratory Medicine, Okayama University Hospital
kn-affil=

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

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

affil-num=12
en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=NUT carcinoma
kn-keyword=NUT carcinoma
en-keyword=BRD4-NUTM1
kn-keyword=BRD4-NUTM1
en-keyword=lung cancer
kn-keyword=lung cancer
en-keyword=alpha-fetoprotein (AFP)
kn-keyword=alpha-fetoprotein (AFP)
en-keyword=immune checkpoint inhibitor
kn-keyword=immune checkpoint inhibitor
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=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=12
cd-vols=
no-issue=
article-no=
start-page=142592
end-page=142605
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=MUSIC Spectrum Based Interference Detection, Localization, and Interference Arrival Prediction for mmWave IRS-MIMO System
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=For a millimeter wave (mmWave) intelligent re-configurable surface (IRS)-MIMO system, if it can correctly detect the interference occurrence and their locations, the patterns of interference signal can be collected and learned using machine learning for the prediction of interference arrival. With the information of interference location and activity pattern, the capacity of the system can be largely improved using many techniques such as beamforming, interference cancellation, and transmission scheduling. This paper aims to detect interference occurrence using a low-complexity MUSIC (MUSIC: multiple signal classification) spectrum-based method, and then localize their sources for mmWave IRS-MIMO system. The MUSIC spectrum of wireless system can be regarded as somehow the 'signature' related to the signals transmitted from different users or interference. We utilize such property to detect the occurrence of interference, and then localize their sources in a low-complexity way. Finally, the pattern of interference occurrence can be learned to predict the interference arrival from the collected data. This paper also proposed an efficient probabilistic neural network (PNN)-based predictor for the interference arrival prediction and showed its prediction accuracy. From simulated results, our proposed method can achieve the correct results with the accuracy near to 100% when the fingerprint samples is over 10. In addition, the localization error can be within 1 m with more than 65% and 43% for Y-axis and X-axis, respectively. Finally, based on the results of the interference occurrence, the proposed PNN-based predictor for the interference arrival prediction can capture correctly the similar distribution function of the coming continuous idle status.
en-copyright=
kn-copyright=

en-aut-name=HouYafei
en-aut-sei=Hou
en-aut-mei=Yafei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YanoKazuto
en-aut-sei=Yano
en-aut-mei=Kazuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SugaNorisato
en-aut-sei=Suga
en-aut-mei=Norisato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WebberJulian
en-aut-sei=Webber
en-aut-mei=Julian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=DennoSatoshi
en-aut-sei=Denno
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SakanoToshikazu
en-aut-sei=Sakano
en-aut-mei=Toshikazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

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

affil-num=2
en-affil=Wave Engineering Laboratories, Advanced Telecommunications Research Institute International
kn-affil=

affil-num=3
en-affil=Wave Engineering Laboratories, Advanced Telecommunications Research Institute International
kn-affil=

affil-num=4
en-affil=Wave Engineering Laboratories, Advanced Telecommunications Research Institute International
kn-affil=

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

affil-num=6
en-affil=Wave Engineering Laboratories, Advanced Telecommunications Research Institute International
kn-affil=
en-keyword=Interference detection
kn-keyword=Interference detection
en-keyword=MUSIC spectrum
kn-keyword=MUSIC spectrum
en-keyword=interference localization
kn-keyword=interference localization
en-keyword=prediction of interference arrival
kn-keyword=prediction of interference arrival
en-keyword=probabilistic neural network
kn-keyword=probabilistic neural network
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=5
article-no=
start-page=413
end-page=421
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=Focal Cerebral Hypoperfusion Detected by Arterial Spin-Labeled Magnetic Resonance Imaging in Patients with Migraine Presenting with Neurological Symptoms Concomitant with or without Headache
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We investigated patients with migraine or migraine variants who exhibited focal cerebral hypoperfusion on arterial spin-labeled (ASL) magnetic resonance (MR) imaging along with neurological symptoms. Fourteen patients with migraine demonstrated focal cerebral hypoperfusion. Three other patients did not have a history of recurrent headaches but exhibited comparable cerebral hypoperfusion to migraine patients on ASL-MRI in addition to neurological symptoms. Patients with migraine may present with neurological symptoms associated with cortical spreading depression during, after, or even without a headache phase. Additionally, the isolated neurological symptoms may be caused by a pathophysiology identical to that of migraine but without presenting with recurrent headaches.
en-copyright=
kn-copyright=

en-aut-name=KashiharaKenichi
en-aut-sei=Kashihara
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IrisawaMinoru
en-aut-sei=Irisawa
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakaoWataru
en-aut-sei=Takao
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Okayama Neurology Clinic
kn-affil=

affil-num=2
en-affil=Department of Radiology, Okayama Kyokuto Hospital
kn-affil=

affil-num=3
en-affil=Division of Radiology, Okayama Kyokuto Hospital
kn-affil=
en-keyword=arterial spin-labeled magnetic resonance imaging
kn-keyword=arterial spin-labeled magnetic resonance imaging
en-keyword=cortical spreading depression
kn-keyword=cortical spreading depression
en-keyword=migraine complex
kn-keyword=migraine complex
en-keyword=migraine without headache
kn-keyword=migraine without headache
en-keyword=vertigo
kn-keyword=vertigo
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=60
cd-vols=
no-issue=5
article-no=
start-page=6736
end-page=6751
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=Superior Efficiency Under PWM Harmonic Current in an Axial-Flux PM Machine for HEV/EV Traction: Comparison With a Radial-Flux PM Machine
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This paper evaluates the harmonic current caused by a pulse width modulation (PWM) inverter and how it affects the efficiency of a novel axial-flux permanent-magnet machine using a ferrite permanent magnet (AF-FePM) in traction applications. First, differences between the finite element analysis (FEA) and experimental results are discussed using a prototype of the proposed AF-FePM. Second, the AF-FePM is compared with a commercially available radial-flux permanent-magnet machine using a Nd-sintered magnet (RF-NdPM). For both machines, the efficiency and loss are calculated using FEA when applying the sinusoidal and harmonic currents. Additionally, we present the superior efficiency of the AF-FePM under the PWM harmonic current during a WLTC driving cycle because the designed model employs the ferrite magnet and a round copper wire, unlike the RF-NdPM. Finally, motor and inverter losses at different switching frequencies are also evaluated. This paper eventually shows that the proposed AF-FePM would be one of the suitable candidates to enhance high efficiency under PWM harmonic current condition based on comprehensive discussion.
en-copyright=
kn-copyright=

en-aut-name=TsunataRen
en-aut-sei=Tsunata
en-aut-mei=Ren
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakemotoMasatsugu
en-aut-sei=Takemoto
en-aut-mei=Masatsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ImaiJun
en-aut-sei=Imai
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SaitoTatsuya
en-aut-sei=Saito
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UenoTomoyuki
en-aut-sei=Ueno
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

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

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

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

affil-num=4
en-affil=Sumitomo Electric Industries Ltd.
kn-affil=

affil-num=5
en-affil=Sumitomo Electric Industries Ltd.
kn-affil=
en-keyword=Axial gap motor
kn-keyword=Axial gap motor
en-keyword=axial-flux machine
kn-keyword=axial-flux machine
en-keyword=carbon-fiber-reinforced plastic
kn-keyword=carbon-fiber-reinforced plastic
en-keyword=ferrite magnet
kn-keyword=ferrite magnet
en-keyword=iron loss
kn-keyword=iron loss
en-keyword=PWM drive
kn-keyword=PWM drive
en-keyword=PWM harmonic current
kn-keyword=PWM harmonic current
en-keyword=radial-flux machine
kn-keyword=radial-flux machine
en-keyword=soft magnetic composite
kn-keyword=soft magnetic composite
en-keyword=switching frequency
kn-keyword=switching frequency
en-keyword=WLTC drive
kn-keyword=WLTC drive
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=10
article-no=
start-page=1600
end-page=1609
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=Molecular Diversity of Photosensitive Protein Opsins and Their High Potential for Optogenetic Applications
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Because G protein coupled receptors (GPCRs) represent the largest family of drug targets in clinical trials, GPCR signaling cascades are closely related to various physiological phenomena, attracting significant attention in pharmaceutical science. Opsins (also known as animal rhodopsins) are photoreceptive proteins containing retinal as a chromophore, which function as GPCRs and underlie the molecular basis of photoreception in animals. Recently, opsins have been progressively applied in an innovative technology called optogenetics to regulate biological activities using light. A wide variety of opsins have been identified in metazoans and characterized at the molecular and physiological levels, providing a foundation for their optogenetic applications. In this review, I briefly introduce the diversity of opsins in terms of their molecular functions, including G protein selectivity and photoreaction properties. This diversity provides a significant advantage for optically manipulating a wide variety of GPCR signaling cascades with high temporal resolution. Additionally, I discuss the rich array of opsin-based optogenetic tools used to control various physiological processes and their potential as therapeutic tools for vision restoration. Based on the introduction, I expect that the optogenetic approach will offer powerful tools to provide valuable insights into the molecular mechanisms of various physiological phenomena and next-generation treatment options for diseases beyond the capacity of traditional drugs.
en-copyright=
kn-copyright=

en-aut-name=KojimaKeiichi
en-aut-sei=Kojima
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

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

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=
article-no=
start-page=1471602
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Ameliorating effect of chotosan and its active component, Uncaria hook, on lipopolysaccharide-induced anxiety-like behavior in mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction: In this study, we aimed to examine the effects of chotosan, a traditional Japanese botanical drug, and its active component, Uncaria hook, on anxiety-like behaviors induced by systemic inflammation in mice. <br>
Methods: To induce systemic inflammation, the mice were treated with lipopolysaccharide (LPS), a bacterial endotoxin. Prior to LPS treatment, the mice were administered chotosan or Uncaria hook orally each day for 14 days. Anxiety-like behavior of the mice was evaluated using the light-dark test 24 h after LPS treatment.<br>
Results: Repeated administration of chotosan prevented anxiety-like behavior in both normal and LPS-treated mice. Similarly, administration of Uncaria hook suppressed LPS-induced anxiety-like behavior in mice. Furthermore, treatment with tandospirone, a 5-HT1A receptor agonist, alleviated anxiety-like behavior in mice, whereas treatment with DOI, a 5-HT2A receptor agonist, enhanced anxiety-like behavior in mice. LPS treatment significantly increased serotonin (5-HT)(2A) receptor mRNA expression in the frontal cortex, whereas 5-HT1A receptor mRNA expression remained unchanged in the hippocampus. Notably, chotosan significantly suppressed the mRNA expression of 5-HT2A receptor. <br>
Discussion: These findings indicate that chotosan exerts anxiolytic-like effects in the context of inflammation-induced anxiety, potentially mediated by the inhibition of 5-HT2A receptor hyperfunction in LPS-treated mice. Consequently, we postulate that chotosan may be effective in managing inflammation-induced anxiety-like behaviors.
en-copyright=
kn-copyright=

en-aut-name=OkawaYasumasa
en-aut-sei=Okawa
en-aut-mei=Yasumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

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

en-aut-name=IzushiYasuhisa
en-aut-sei=Izushi
en-aut-mei=Yasuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KitamuraYoshihisa
en-aut-sei=Kitamura
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
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=6
ORCID=

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

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

affil-num=3
en-affil=Department of Pharmacotherapy, School of Pharmacy, Shujitsu University
kn-affil=

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

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

affil-num=6
en-affil=Department of Clinical Pharmacy, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=anxiolytic
kn-keyword=anxiolytic
en-keyword=chotosan
kn-keyword=chotosan
en-keyword=inflammation
kn-keyword=inflammation
en-keyword=serotonin receptor
kn-keyword=serotonin receptor
en-keyword=Uncaria hook
kn-keyword=Uncaria hook
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=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=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=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=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 µM) > 2C-T-2 (150 µM), 2C-T-4 (200 µM) > 2C-I (250 µM) in CATH.a cells and 2C-T-7, 2C-I (150 µM) > 2C-T-2 (250 µM) > 2C-C, 2C-T-4 (300 µM) 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=12
cd-vols=
no-issue=1
article-no=
start-page=121
end-page=
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=Pure argyrophilic grain disease revisited: independent effects on limbic, neocortical, and striato-pallido-nigral degeneration and the development of dementia in a series with a low to moderate Braak stage
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Agyrophilic grains (AGs) are age-related limbic-predominant lesions in which four-repeat tau is selectively accumulated. Because previous methodologically heterogeneous studies have demonstrated inconsistent findings on the relationship between AGs and dementia, whether AGs affect cognitive function remains unclear. To address this question, we first comprehensively evaluated the distribution and quantity of Gallyas-positive AGs and the severity of neuronal loss in the limbic, neocortical, and subcortical regions in 30 cases of pure argyrophilic grain disease (pAGD) in Braak stages I-IV and without other degenerative diseases, and 34 control cases that had only neurofibrillary tangles with Braak stages I-IV and no or minimal A beta deposits. Then, we examined whether AGs have independent effects on neuronal loss and dementia by employing multivariate ordered logistic regression and binomial logistic regression. Of 30 pAGD cases, three were classified in diffuse form pAGD, which had evident neuronal loss not only in the limbic region but also in the neocortex and subcortical nuclei. In all 30 pAGD cases, neuronal loss developed first in the amygdala, followed by temporo-frontal cortex, hippocampal CA1, substantia nigra, and finally, the striatum and globus pallidus with the progression of Saito AG stage. In multivariate analyses of 30 pAGD and 34 control cases, the Saito AG stage affected neuronal loss in the amygdala, hippocampal CA1, temporo-frontal cortex, striatum, globus pallidus, and substantia nigra independent of the age, Braak stage, and limbic-predominant age-related TDP-43 encephalopathy (LATE-NC) stage. In multivariate analyses of 23 pAGD and 28 control cases that lacked two or more lacunae and/or one or more large infarctions, 100 or more AGs per x 400 visual field in the amygdala (OR 10.02, 95% CI 1.12-89.43) and hippocampal CA1 (OR 12.22, 95% CI 1.70-87.81), and the presence of AGs in the inferior temporal cortex (OR 8.18, 95% CI 1.03-65.13) affected dementia independent of age, moderate Braak stages (III-IV), and LATE-NC. Given these findings, the high density of limbic AGs and the increase of AGs in the inferior temporal gyrus may contribute to the occurrence of dementia through neuronal loss, at least in cases in a low to moderate Braak stage.
en-copyright=
kn-copyright=

en-aut-name=YokotaOsamu
en-aut-sei=Yokota
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MikiTomoko
en-aut-sei=Miki
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Nakashima-YasudaHanae
en-aut-sei=Nakashima-Yasuda
en-aut-mei=Hanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshizuHideki
en-aut-sei=Ishizu
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HaraguchiTakashi
en-aut-sei=Haraguchi
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IkedaChikako
en-aut-sei=Ikeda
en-aut-mei=Chikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HasegawaMasato
en-aut-sei=Hasegawa
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MiyashitaAkinori
en-aut-sei=Miyashita
en-aut-mei=Akinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IkeuchiTakeshi
en-aut-sei=Ikeuchi
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NishikawaNaoto
en-aut-sei=Nishikawa
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakenoshitaShintaro
en-aut-sei=Takenoshita
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SudoKoichiro
en-aut-sei=Sudo
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TeradaSeishi
en-aut-sei=Terada
en-aut-mei=Seishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
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=14
ORCID=

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

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

affil-num=3
en-affil=Okayama University Medical School 
kn-affil=

affil-num=4
en-affil=Okayama University Medical School 
kn-affil=

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

affil-num=6
en-affil=Okayama University Medical School 
kn-affil=

affil-num=7
en-affil=Dementia Research Project, Tokyo Metropolitan Institute of Medical Science
kn-affil=

affil-num=8
en-affil=Department of Molecular Genetics, Brain Research Institute, Niigata University
kn-affil=

affil-num=9
en-affil=Department of Molecular Genetics, Brain Research Institute, Niigata University
kn-affil=

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

affil-num=11
en-affil=Department of Neuropsychiatry, Okayama University Hospital
kn-affil=

affil-num=12
en-affil=Department of Psychiatry, Tosa Hospital
kn-affil=

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

affil-num=14
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Argyrophilic grain
kn-keyword=Argyrophilic grain
en-keyword=Globus pallidus
kn-keyword=Globus pallidus
en-keyword=Hippocampal sclerosis
kn-keyword=Hippocampal sclerosis
en-keyword=Striatum
kn-keyword=Striatum
en-keyword=Substantia nigra
kn-keyword=Substantia nigra
en-keyword=Subthalamic nucleus
kn-keyword=Subthalamic nucleus
END

start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=1
article-no=
start-page=341
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240813
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pathological findings in enucleated eyes of patients with neurofibromatosis type 1: report of a case with 15-year follow-up and review of 14 patients in the literature
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Backgrounds Iris nodules are frequently noted as clinical manifestations of neurofibromatosis type 1 but the other intraocular manifestations are rare. The purpose of this study is to present a patient with a phthisic eye who underwent enucleation for a cosmetic reason after 15-year follow-up and also to review 14 patients with enucleation described in the literature.<br>
Case presentation A 17-year-old man with neurofibromatosis type 1 from infancy underwent the enucleation of phthisic left eye and also had the resection of eyelid subcutaneous mass lesions on the left side for a cosmetic reason. He had undergone four-time preceding surgeries for eyelid and orbital mass reduction on the left side in childhood and had developed total retinal detachment 10 years previously. Pathologically, the enucleated eye showed massive retinal gliosis positive for both S-100 and glial fibrillary acidic protein (GFAP) in the area with involvement of the detached retinal neuronal layer, together with a more fibrotic lesion along the choroid which were, in contrast, negative for both S-100 and GFAP. The choroid, ciliary body, and iris did not show apparent neurofibroma while episcleral neurofibroma was present.<br>
Literature review In review of enucleated eyes of 14 patients in the literature, buphthalmic eyes with early-onset glaucoma on the unilateral side was clinically diagnosed in 9 patients who frequently showed varying extent of hemifacial neurofibromatosis which involved the eyelid and orbit on the same side. Pathologically, neurofibromas in varying extent were found in the choroid of 12 patients. One patient showed choroidal malignant melanoma on the left side and fusiform enlargement of the optic nerve on the right side suspected of optic nerve glioma. The phthisic eye in another patient showed massive retinal gliosis similar to the present patient.<br>
Conclusions In summary of the 15 patients with neurofibromatosis type 1, including the present patient, buphthalmic or phthisic eyes with no vision were enucleated for cosmetic reasons and showed choroidal neurofibroma in most patients and massive retinal gliosis in two patients including the present patient.
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=NishidaKenji
en-aut-sei=Nishida
en-aut-mei=Kenji
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=SenoTakaya
en-aut-sei=Seno
en-aut-mei=Takaya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=

en-aut-name=OnoShigeki
en-aut-sei=Ono
en-aut-mei=Shigeki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

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

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

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

affil-num=6
en-affil=Department of Neurological Surgery, General Medical Center, Kawasaki Medical School
kn-affil=
en-keyword=Neurofibromatosis type 1
kn-keyword=Neurofibromatosis type 1
en-keyword=Enucleation
kn-keyword=Enucleation
en-keyword=Eye
kn-keyword=Eye
en-keyword=Pathology
kn-keyword=Pathology
en-keyword=Massive retinal gliosis
kn-keyword=Massive retinal gliosis
en-keyword=Choroidal neurofibroma
kn-keyword=Choroidal neurofibroma
en-keyword=Phthisis
kn-keyword=Phthisis
en-keyword=Buphthalmos
kn-keyword=Buphthalmos
en-keyword=Malignant melanoma
kn-keyword=Malignant melanoma
en-keyword=Cosmetic surgery
kn-keyword=Cosmetic surgery
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=14
article-no=
start-page=4099
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240713
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Importance of Blood Glucose Measurement for Predicting the Prognosis of Long COVID: A Retrospective Study in Japan
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose: The present study aimed to clarify the effects of a hyperglycemic condition on the clinical consequences of long COVID. Methods: Among 643 patients who visited the outpatient clinic of our hospital from February 2021 to September 2023, long COVID patients were classified into a hyperglycemic (HG) group with casual blood glucose levels above 140 mg/dL and a normoglycemic (NG) group. The patients' backgrounds, clinical symptoms, health status including the QOL evaluation scale (EQ-5D-5L), self-rating depression scale (SDS), and F-scale questionnaire (FSSG), blood test data, and recovery periods were analyzed. Results: The NG group included 607 patients with long COVID and the HG group included 36 patients with long COVID. Patients in the HG group were older than those in the NG group (55 vs. 41 years; p < 0.001) and included a larger percentage of males (67% vs. 44%; p = 0.009). The HG group had a larger percentage of patients with moderate-to-severe conditions in the acute infection phase (28% vs. 12%; p = 0.008), a higher BMI (25 vs. 22 kg/m(2); p < 0.001), higher blood pressure (138/81 vs. 122/72 mmHg; p < 0.001), and a larger percentage of patients with an alcohol drinking habit (53% vs. 34%; p = 0.031). Long COVID symptoms and self-rated scales were not differed between the two groups; however, the laboratory data showed that liver and renal functions and metabolic data were significantly worse in the HG group. Although there was no apparent difference between the two groups in duration from the infection to the first visit, the HG group had a significantly longer period of recovery from long COVID (median period of 421 vs. 294 days; p = 0.019). Conclusion: A hyperglycemic state associated with other lifestyle-related diseases is associated with the prolongation of recovery from long COVID.
en-copyright=
kn-copyright=

en-aut-name=YokoyamaSho
en-aut-sei=Yokoyama
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HondaHiroyuki
en-aut-sei=Honda
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OtsukaYuki
en-aut-sei=Otsuka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=5
ORCID=

en-aut-name=SakuradaYasue
en-aut-sei=Sakurada
en-aut-mei=Yasue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsudaYui
en-aut-sei=Matsuda
en-aut-mei=Yui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SunadaNaruhiko
en-aut-sei=Sunada
en-aut-mei=Naruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HasegawaToru
en-aut-sei=Hasegawa
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TakaseRyosuke
en-aut-sei=Takase
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OmuraDaisuke
en-aut-sei=Omura
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SoejimaYoshiaki
en-aut-sei=Soejima
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=13
ORCID=

en-aut-name=KishidaMasayuki
en-aut-sei=Kishida
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
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=15
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 General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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=

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

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

affil-num=15
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=blood glucose
kn-keyword=blood glucose
en-keyword=diabetes mellitus
kn-keyword=diabetes mellitus
en-keyword=long COVID
kn-keyword=long COVID
en-keyword=omicron variant
kn-keyword=omicron variant
en-keyword=post-COVID-19 condition
kn-keyword=post-COVID-19 condition
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=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-FörsterCharlotte
en-aut-sei=Helfrich-Förster
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 Würzburg
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 Würzburg
kn-affil=

affil-num=6
en-affil=Neurobiology and Genetics, Theodor-Boveri Institute, Biocenter, University of Würzburg
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=13
cd-vols=
no-issue=13
article-no=
start-page=3809
end-page=
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=Changes in Working Situations of Employed Long COVID Patients: Retrospective Study in Japanese Outpatient Clinic
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose: The present study aimed to uncover the impact of long COVID on the working situations of Japanese patients. Methods: Changes in the working situations of the patients who visited our long COVID clinic were evaluated from medical records for the aspects of physical status, quality of life (QOL), and mental conditions. <br>
Results: Of 846 long COVID patients who visited our clinic from February 2021 to December 2023, 545 employed patients aged between 18 and 65 years were included in this study. A total of 295 patients (54.1%) with long COVID (median age: 43 years, female: 55.6%) experienced changes in their working status. Those patients included 220 patients (40.4%) who took a leave of absence, 53 patients (9.7%) who retired, and 22 patients (4%) with reduced working hours. Most of the patients (93.2%) with changes in working conditions had mild disease severity in the acute phase of COVID-19. The majority of those patients with mild disease severity (58.8%) were infected in the Omicron-variant phase and included 65.3% of the female patients. The major symptoms in long COVID patients who had changes in their working situations were fatigue, insomnia, headache, and dyspnea. Scores indicating fatigue and QOL were worsened in long COVID patients who had changes in their working situations. In addition, 63.7% of the long COVID patients with changes in their working situations had decreases in their incomes. <br>
Conclusions: Changes in the working situation of long COVID patients who were employed had a negative impact on the maintenance of their QOL.
en-copyright=
kn-copyright=

en-aut-name=MatsudaYui
en-aut-sei=Matsuda
en-aut-mei=Yui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakuradaYasue
en-aut-sei=Sakurada
en-aut-mei=Yasue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
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=4
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=5
ORCID=

en-aut-name=SunadaNaruhiko
en-aut-sei=Sunada
en-aut-mei=Naruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HondaHiroyuki
en-aut-sei=Honda
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HasegawaToru
en-aut-sei=Hasegawa
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TakaseRyosuke
en-aut-sei=Takase
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OmuraDaisuke
en-aut-sei=Omura
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=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, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

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

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

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

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

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

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

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

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

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

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

affil-num=12
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=employment
kn-keyword=employment
en-keyword=job retirement
kn-keyword=job retirement
en-keyword=leave of absence
kn-keyword=leave of absence
en-keyword=long COVID
kn-keyword=long COVID
en-keyword=omicron variant
kn-keyword=omicron variant
en-keyword=post-COVID-19 condition
kn-keyword=post-COVID-19 condition
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