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=100
cd-vols=
no-issue=1
article-no=
start-page=219
end-page=228
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240625
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Novel Peptidome Technology for the Diagnosis of Mild Cognitive Impairment and Alzheimer’s Disease by Selected Reaction Monitoring
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background:With the aging of populations worldwide, Alzheimer’s disease (AD) has become a concern due to its high prevalence and the continued lack of established treatments. Early diagnosis is required as a preventive intervention to modify the disease’s progression. In our previous study, we performed peptidomic analysis of serum samples obtained from AD patients and age-matched healthy subjects to seek peptide biomarker candidates for AD by using BLOTCHIP-MS analysis, and identified four peptides as AD biomarker candidates.
Objective:The objective was to validate the serum biomarker peptides to distinguish mild cognitive impairment (MCI) and AD in comparison to cognitively healthy controls using a new peptidome technology, the Dementia Risk Test.
Methods:We enrolled 195 subjects with normal cognitive function (NC; n?=?70), MCI (n?=?55), and AD (n?=?70), The concentrations of cognitive impairment marker peptides (Fibrinogen α chain (FAC), Fibrinogen β chain (FBC), Plasma protease C1 inhibitor (PPC1I), α2-HS-glycoprotein (AHSG)) were quantified by using a selected reaction monitoring assay based on liquid chromatography-MS/MS.
Results:The present study confirmed that three peptides, FAC, FBC, and PPC1I, were significantly upregulated during the onset of AD. This three-peptide set was both highly sensitive in determining AD (sensitivity: 85.7%, specificity: 95.7%, AUC: 0.900) and useful in distinguishing MCI (sensitivity: 61.8%, specificity: 98.6%, AUC: 0.824) from NC.
Conclusions:In this validation study, we confirmed the high diagnostic potential of the three peptides identified in our previous study as candidate serum biomarkers for AD. The Dementia Risk Test may be a powerful tool for detecting AD-related pathological changes.
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=TadokoroKoh
en-aut-sei=Tadokoro
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=HamadaMinaki
en-aut-sei=Hamada
en-aut-mei=Minaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=AsadaKyoichi
en-aut-sei=Asada
en-aut-mei=Kyoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=LeeLyang-Ja
en-aut-sei=Lee
en-aut-mei=Lyang-Ja
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=TachikiHidehisa
en-aut-sei=Tachiki
en-aut-mei=Hidehisa
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=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=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=Protosera, Inc.
kn-affil=
affil-num=4
en-affil=Protosera, Inc.
kn-affil=
affil-num=5
en-affil=Protosera, Inc.
kn-affil=
affil-num=6
en-affil=Protosera, Inc.
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, National Center of Neurology and Psychiatry
kn-affil=
affil-num=9
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Alzheimer’s disease
kn-keyword=Alzheimer’s disease
en-keyword=biochemical marker
kn-keyword=biochemical marker
en-keyword=dementia risk test
kn-keyword=dementia risk test
en-keyword=liquid chromatography-MS/MS
kn-keyword=liquid chromatography-MS/MS
en-keyword=mild cognitive impairment
kn-keyword=mild cognitive impairment
en-keyword=peptidome
kn-keyword=peptidome
en-keyword=selected reaction monitoring
kn-keyword=selected reaction monitoring
END
start-ver=1.4
cd-journal=joma
no-vol=1828
cd-vols=
no-issue=
article-no=
start-page=148790
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202404
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Protective effect of scallop-derived plasmalogen against vascular dysfunction, via the pSTAT3/PIM1/NFATc1 axis, in a novel mouse model of Alzheimer’s disease with cerebral hypoperfusion
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A strong relationship between Alzheimer’s disease (AD) and vascular dysfunction has been the focus of increasing attention in aging societies. In the present study, we examined the long-term effect of scallop-derived plasmalogen (sPlas) on vascular remodeling-related proteins in the brain of an AD with cerebral hypoperfusion (HP) mouse model. We demonstrated, for the first time, that cerebral HP activated the axis of the receptor for advanced glycation endproducts (RAGE)/phosphorylated signal transducer and activator of transcription 3 (pSTAT3)/provirus integration site for Moloney murine leukemia virus 1 (PIM1)/nuclear factor of activated T cells 1 (NFATc1), accounting for such cerebral vascular remodeling. Moreover, we also found that cerebral HP accelerated pSTAT3-mediated astrogliosis and activation of the nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome, probably leading to cognitive decline. On the other hand, sPlas treatment attenuated the activation of the pSTAT3/PIM1/NFATc1 axis independent of RAGE and significantly suppressed NLRP3 inflammasome activation, demonstrating the beneficial effect on AD.
en-copyright=
kn-copyright=
en-aut-name=ZhaiYun
en-aut-sei=Zhai
en-aut-mei=Yun
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=FengTian
en-aut-sei=Feng
en-aut-mei=Tian
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=FukuiYusuke
en-aut-sei=Fukui
en-aut-mei=Yusuke
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=BianYuting
en-aut-sei=Bian
en-aut-mei=Yuting
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=SunHongming
en-aut-sei=Sun
en-aut-mei=Hongming
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=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=YunokiTaijun
en-aut-sei=Yunoki
en-aut-mei=Taijun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=TangYing
en-aut-sei=Tang
en-aut-mei=Ying
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
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=14
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=15
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, The First Affiliated Hospital of Harbin Medical University
kn-affil=
affil-num=14
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=15
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Alzheimer's disease
kn-keyword=Alzheimer's disease
en-keyword=Hypoperfusion
kn-keyword=Hypoperfusion
en-keyword=Cerebral vascular remodeling
kn-keyword=Cerebral vascular remodeling
en-keyword=Scallop-derived plasmalogen
kn-keyword=Scallop-derived plasmalogen
en-keyword=pSTAT3/PIM1/NFATc1 axis
kn-keyword=pSTAT3/PIM1/NFATc1 axis
END
start-ver=1.4
cd-journal=joma
no-vol=96
cd-vols=
no-issue=2
article-no=
start-page=609
end-page=622
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231107
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Protective Effects of Rivaroxaban on White Matter Integrity and Remyelination in a Mouse Model of Alzheimer’s Disease Combined with Cerebral Hypoperfusion
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background:Alzheimer’s disease (AD) is characterized by cognitive dysfunction and memory loss that is accompanied by pathological changes to white matter. Some clinical and animal research revealed that AD combined with chronic cerebral hypoperfusion (CCH) exacerbates AD progression by inducing blood-brain barrier dysfunction and fibrinogen deposition. Rivaroxaban, an anticoagulant, has been shown to reduce the rates of dementia in atrial fibrillation patients, but its effects on white matter and the underlying mechanisms are unclear.
Objective:The main purpose of this study was to explore the therapeutic effect of rivaroxaban on the white matter of AD+CCH mice.
Methods:In this study, the therapeutic effects of rivaroxaban on white matter in a mouse AD+CCH model were investigated to explore the potential mechanisms involving fibrinogen deposition, inflammation, and oxidative stress on remyelination in white matter.
Results:The results indicate that rivaroxaban significantly attenuated fibrinogen deposition, fibrinogen-related microglia activation, oxidative stress, and enhanced demyelination in AD+CCH mice, leading to improved white matter integrity, reduced axonal damage, and restored myelin loss.
Conclusions:These findings suggest that long-term administration of rivaroxaban might reduce the risk of dementia.
en-copyright=
kn-copyright=
en-aut-name=BianZhihong
en-aut-sei=Bian
en-aut-mei=Zhihong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=
en-aut-name=LiuXia
en-aut-sei=Liu
en-aut-mei=Xia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=
en-aut-name=BianYuting
en-aut-sei=Bian
en-aut-mei=Yuting
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
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=7
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=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=
en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine
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=
en-keyword=Alzheimer’s disease
kn-keyword=Alzheimer’s disease
en-keyword=cerebral amyloid angiopathy
kn-keyword=cerebral amyloid angiopathy
en-keyword=chronic cerebral hypoperfusion
kn-keyword=chronic cerebral hypoperfusion
en-keyword=rivaroxaban
kn-keyword=rivaroxaban
en-keyword=white matter
kn-keyword=white matter
END
start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=2023
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Safety and Clinical Effects of a Muse Cell-Based Product in Patients With Amyotrophic Lateral Sclerosis: Results of a Phase 2 Clinical Trial
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Amyotrophic lateral sclerosis (ALS) is characterized by progressive loss of motor neurons. Multilineage-differentiating stress-enduring (Muse) cells are unique endogenous stem cells that show therapeutic effects on motor function in ALS mouse models. We conducted a single-center open phase II clinical trial to evaluate the safety and clinical effects of repeated intravenous injections of an allogenic Muse cell-based product, CL2020, in patients with ALS. Five patients with ALS received CL2020 intravenously once a month for a total of six doses. The primary endpoints were safety and tolerability, and the secondary endpoint was the rate of change in the Revised Amyotrophic Lateral Sclerosis Functional Rating Scale (ALSFRS-R) score. In addition, serum tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), sphingosine-1-phosphate (S1P), cerebrospinal fluid chitotriosidase-1 (CHIT-1), and neurofilament light chain (NfL) levels were evaluated. The CL2020 treatment was highly tolerated without serious side effects. The ALSFRS-R score change trended upward at 12 months post-CL2020 treatment compared with that at 3 months pre-administration, but the difference was not statistically significant. Among five patients diagnosed with ALS, three exhibited a decrease in the rate of ALSFRS-R score change, one demonstrated an increase, and another showed no change. In addition, the patients’ serum IL-6 and TNF-α levels and cerebrospinal fluid CHIT-1 and NfL levels increased for up to 6 months post-treatment; however, their serum S1P levels continuously decreased over 12 months. These findings indicate a favorable safety profile of CL2020 therapy. In the near future, a double-blind study of a larger number of ALS patients should be conducted to confirm the efficacy of ALS treatment with CL2020.
en-copyright=
kn-copyright=
en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=NakanoYumiko
en-aut-sei=Nakano
en-aut-mei=Yumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=SasakiRyo
en-aut-sei=Sasaki
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=TadokoroKoh
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en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=OmoteYoshio
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en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=YunokiTaijun
en-aut-sei=Yunoki
en-aut-mei=Taijun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=KawaharaYuko
en-aut-sei=Kawahara
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=MatsumotoNamiko
en-aut-sei=Matsumoto
en-aut-mei=Namiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=TairaYuki
en-aut-sei=Taira
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=MatsuokaChika
en-aut-sei=Matsuoka
en-aut-mei=Chika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
affil-num=1
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=2
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=3
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=4
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=5
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=6
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=7
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=8
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=9
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=10
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=11
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=12
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=amyotrophic lateral sclerosis
kn-keyword=amyotrophic lateral sclerosis
en-keyword=clinical trial
kn-keyword=clinical trial
en-keyword=CL2020
kn-keyword=CL2020
en-keyword=multilineage-differentiating stress-enduring (Muse) cells
kn-keyword=multilineage-differentiating stress-enduring (Muse) cells
en-keyword=intravenous administration
kn-keyword=intravenous administration
END
start-ver=1.4
cd-journal=joma
no-vol=1821
cd-vols=
no-issue=
article-no=
start-page=148565
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231215
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Injection of exogenous amyloid-β oligomers aggravated cognitive deficits, and activated necroptosis, in APP23 transgenic mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Alzheimer's disease (AD) is a neurodegenerative disease that is characterized by the loss of synapses and neurons in the brain, and the accumulation of amyloid plaques. Aβ oligomers (AβO) play a critical role in the pathogenesis of AD. Although there is increasing evidence to support the involvement of necroptosis in the pathogenesis of AD, the exact mechanism remains elusive. In the present study, we explored the effect of exogenous AβO injection on cell necroptosis and cognitive deficits in APP23 transgenic mice. We found that intrahippocampal injection of AβO accelerated the development of AD pathology and caused cognitive impairment in APP23 mice. Specifically, AβO injection significantly accelerated the accumulation of AβO and increased the expression level of phosphorylated-tau, and also induced necroptosis. Behavioral tests showed that AβO injection was associated with cognitive impairment. Furthermore, necroptosis induced by AβO injection occurred predominantly in microglia of the AD brain. We speculate that AβO increased necroptosis by activating microglia, resulting in cognitive deficits. Our results may aid in an understanding of the role played by AβO in AD from an alternative perspective and provide new ideas and evidence for necroptosis as a potential intervention and therapeutic target for AD.
en-copyright=
kn-copyright=
en-aut-name=YuHaibo
en-aut-sei=Yu
en-aut-mei=Haibo
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=Ota-ElliottRicardo
en-aut-sei=Ota-Elliott
en-aut-mei=Ricardo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=
en-aut-name=BianYuting
en-aut-sei=Bian
en-aut-mei=Yuting
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
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=7
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=8
ORCID=
en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
ORCID=
affil-num=1
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=2
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=3
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=4
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=5
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=6
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=7
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=8
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=9
en-affil=National Center Hospital, National Center of Neurology and Psychiatry
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=
en-keyword=Alzheimer's disease (AD)
kn-keyword=Alzheimer's disease (AD)
en-keyword=Amyloid-13 oligomers (A13O)
kn-keyword=Amyloid-13 oligomers (A13O)
en-keyword=Necroptosis
kn-keyword=Necroptosis
en-keyword=Microglia
kn-keyword=Microglia
en-keyword=Neurodegeneration
kn-keyword=Neurodegeneration
END
start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230824
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Human Cord Blood-Endothelial Progenitor Cells Alleviate Intimal Hyperplasia of Arterial Damage in a Rat Stroke Model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Human cord blood-endothelial progenitor cells (hCB-EPCs) isolated from the human umbilical cord can be used to repair damaged arteries. In this study, we used an animal model with pathological changes that mimics artery wall damage caused by stent retrievers in humans. We injected hCB-EPCs to investigate their effect on endothelial hyperplasia and dysfunction during intimal repair. Four groups were established based on the length of reperfusion (3 and 28 days), as well as the presence or absence of hCB-EPC therapy. Damage to the internal carotid artery was evaluated by hematoxylin-eosin and immunohistochemical staining. Stroke volume was not significantly different between non-EPC and EPC groups although EPC treatment alleviated intimal hyperplasia 28 days after intimal damage. Vascular endothelial growth factor (VEGF) and eNOS expression were significantly higher in the EPC-treated group than in the non-EPC group 3 days after intimal damage. In addition, MMP9 and 4HNE expression in the EPC-treated group was significantly lower than in the non-EPC group. Ultimately, this study found that venous transplantation of hCB-EPCs could inhibit neointimal hyperplasia, alleviate endothelial dysfunction, suppress intimal inflammation, and reduce oxidative stress during healing of intimal damage.
en-copyright=
kn-copyright=
en-aut-name=SunHongming
en-aut-sei=Sun
en-aut-mei=Hongming
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=FengTian
en-aut-sei=Feng
en-aut-mei=Tian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=5
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=6
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=7
ORCID=
en-aut-name=BianYuting
en-aut-sei=Bian
en-aut-mei=Yuting
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=SasakiRyo
en-aut-sei=Sasaki
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=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=TakemotoMami
en-aut-sei=Takemoto
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
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=12
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=13
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=14
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=15
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=National Center Hospital, National Center of Neurology and Psychiatry
kn-affil=
affil-num=15
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=ischemic stroke
kn-keyword=ischemic stroke
en-keyword=human cord blood-endothelial progenitor cells
kn-keyword=human cord blood-endothelial progenitor cells
en-keyword=mechanical thrombectomy
kn-keyword=mechanical thrombectomy
en-keyword=intimal hyperplasia
kn-keyword=intimal hyperplasia
END
start-ver=1.4
cd-journal=joma
no-vol=135
cd-vols=
no-issue=1
article-no=
start-page=34
end-page=35
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Hereditary diffuse leukoencephalopathy with spheroids
kn-title=神経軸索スフェロイド形成を伴う遺伝性びまん性白質脳症について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=
en-aut-name=YunokiTaijun
en-aut-sei=Yunoki
en-aut-mei=Taijun
kn-aut-name=柚木太淳
kn-aut-sei=柚木
kn-aut-mei=太淳
aut-affil-num=1
ORCID=
en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=山下徹
kn-aut-sei=山下
kn-aut-mei=徹
aut-affil-num=2
ORCID=
affil-num=1
en-affil=Department of Neurology, Okayama University Hospital
kn-affil=岡山大学病院 脳神経内科
affil-num=2
en-affil=Department of Neurology, Okayama University Hospital
kn-affil=岡山大学病院 脳神経内科
en-keyword=神経軸索スフェロイド形成を伴う遺伝性びまん性白質脳症
kn-keyword=神経軸索スフェロイド形成を伴う遺伝性びまん性白質脳症
en-keyword=若年性認知症
kn-keyword=若年性認知症
en-keyword=大脳白質病変
kn-keyword=大脳白質病変
END
start-ver=1.4
cd-journal=joma
no-vol=447
cd-vols=
no-issue=
article-no=
start-page=120608
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230415
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
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=Carnosine (β-alanyl-L-histidine) is a natural dipeptide with multiple neuroprotective properties. Previous studies have advertised that carnosine scavenges free radicals and displays anti-inflammatory activity. However, the underlying mechanism and the efficacies of its pleiotropic effect on prevention remained obscure. In this study, we aimed to investigate the anti-oxidative, anti-inflammative, and anti-pyroptotic effects of carnosine in the transient middle cerebral artery occlusion (tMCAO) mouse model. After a daily pre-treatment of saline or carnosine (1000 mg / kg / day) for 14 days, mice (n = 24) were subjected to tMCAO for 60 min and continuously treated with saline or carnosine for additional 1 and 5 days after reperfusion. The administration of carnosine significantly decreased infarct volume 5 days after the tMCAO (*p < 0.05) and effectively suppressed the expression of 4-HNE, 8-OHdG, Nitrotyrosine 5 days, and RAGE 5 days after tMCAO. Moreover, the expression of IL-1β was also significantly suppressed 5 days after tMCAO. Our present findings demonstrated that carnosine effectively relieves oxidative stress caused by ischemic stroke and significantly attenuates neuroinflammatory responses related to IL-1β, suggesting that carnosine can be a promising therapeutic strategy for ischemic stroke.
en-copyright=
kn-copyright=
en-aut-name=HuXinran
en-aut-sei=Hu
en-aut-mei=Xinran
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=FengTian
en-aut-sei=Feng
en-aut-mei=Tian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=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=HuXiao
en-aut-sei=Hu
en-aut-mei=Xiao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=BianYuting
en-aut-sei=Bian
en-aut-mei=Yuting
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
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=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=YunokiTaijun
en-aut-sei=Yunoki
en-aut-mei=Taijun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=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=Ischemic stroke
kn-keyword=Ischemic stroke
en-keyword=Carnosine
kn-keyword=Carnosine
en-keyword=Middle cerebral artery occlusion
kn-keyword=Middle cerebral artery occlusion
en-keyword=Oxidative stress
kn-keyword=Oxidative stress
en-keyword=Inflammation
kn-keyword=Inflammation
en-keyword=Pyroptosis
kn-keyword=Pyroptosis
END
start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=3
article-no=
start-page=e36104
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230313
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Case of Drug-Resistant Myoclonus Improved by Only Slight Adjustment to the Hemodialysis Setting
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Myoclonus, a rare complication in patients with end-stage renal disease, is typically ameliorated through hemodialysis. The present case concerns an 84-year-old male with chronic renal failure undergoing hemodialysis, presenting involuntary movements in his limbs, which gradually worsened from the initiation of hemodialysis without constant elevation of serum blood urea nitrogen and electrolytes levels. Surface electromyography revealed characteristic findings consistent with myoclonus. He was diagnosed with subcortical-nonsegmental myoclonus related to hemodialysis, and the myoclonus was significantly alleviated after slightly increasing the post-dialysis target weight even though drug treatment was ineffective. This case suggests that drug-resistant myoclonus in patients with renal failure may be improved by adjusting hemodialysis settings, even in cases of atypical dialysis disequilibrium syndrome.
en-copyright=
kn-copyright=
en-aut-name=SasakiRyo
en-aut-sei=Sasaki
en-aut-mei=Ryo
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=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=KinomuraMasaru
en-aut-sei=Kinomura
en-aut-mei=Masaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=
affil-num=1
en-affil=Department of Neurology, Okayama University
kn-affil=
affil-num=2
en-affil=Department of Neurology, Hiroshima City Hiroshima Citizens Hospital
kn-affil=
affil-num=3
en-affil=Department of Neurology, Okayama University
kn-affil=
affil-num=4
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University
kn-affil=
affil-num=5
en-affil=Department of Neurology, National Center of Neurology and Psychiatry
kn-affil=
en-keyword=dialysis disequilibrium syndrome
kn-keyword=dialysis disequilibrium syndrome
en-keyword=involuntary movement
kn-keyword=involuntary movement
en-keyword=renal failure
kn-keyword=renal failure
en-keyword=myoclonus
kn-keyword=myoclonus
en-keyword=hemodialysis
kn-keyword=hemodialysis
END
start-ver=1.4
cd-journal=joma
no-vol=62
cd-vols=
no-issue=3
article-no=
start-page=365
end-page=371
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Actual Telemedicine Needs of Japanese Patients with Neurological Disorders in the COVID-19 Pandemic
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective During the coronavirus disease 2019 (COVID-19) pandemic, many social activities have moved online using applications for digital devices (e.g. computers, smartphones). We investigated the needs of telemedicine and trends in medical status and social care situations of Japanese patients with neurological disorders in order to estimate their affinity for an online telemedicine application. Methods We designed an original questionnaire for the present study that asked participants what problems they had with hospital visits, how the COVID-19 pandemic had affected their lives, and whether or not they would like to receive telemedicine.Patients The present study included volunteer caregivers, participants with Parkinson's disease (PD), epiamyotrophic lateral sclerosis (ALS), headache, myopathy, and other neurological diseases from Okayama University Hospital. Results A total of 29.6% of patients wanted to use telemedicine. Patients with ultheadaches (60.0%) and epilepsy (38.1%) were more likely to want to use telemedicine than patients with PD (17.8%) or stroke (19.0%). Almost 90% of patients had access to a digital device, and there was no association between favoring telemedicine, ownership of a digital device, hospital visiting time, or waiting time at the hospital, although age was associated with motivation to telemedicine use (52.6 vs. 62.2 years old, p < 0.001). Conclusion We can contribute to the management of the COVID-19 pandemic and the medical economy by promoting telemedicine, especially for young patients with headaches or epilepsy.
en-copyright=
kn-copyright=
en-aut-name=SasakiRyo
en-aut-sei=Sasaki
en-aut-mei=Ryo
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=NakanoYumiko
en-aut-sei=Nakano
en-aut-mei=Yumiko
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=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=telemedicine
kn-keyword=telemedicine
en-keyword=neurological disorder
kn-keyword=neurological disorder
en-keyword=COVID-19
kn-keyword=COVID-19
en-keyword=headache
kn-keyword=headache
en-keyword=epilepsy
kn-keyword=epilepsy
END
start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=1
article-no=
start-page=58
end-page=60
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20221017
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Novel ABCD1 mutation detected in a symptomatic female carrier of adrenoleukodystrophy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=X-linked adrenoleukodystrophy (ALD) is a major peroxisomal disorder, in which abnormal accumulation of very long-chain fatty acids (VLCFA) caused by ABCD1 gene mutation results in damage to the peripheral and central nervous system and adrenal gland. While affected male patients with ALD present severe neurological symptoms, some female carriers slowly develop spastic gait and urinary incontinence. We report a case of a symptomatic female ALD carrier with a novel ABCD1 gene mutation. She has developed progressive gait disturbance since age 40, and her father and sister had similar symptoms. When admitted to our hospital at age 66, blood analysis showed slight increase of VLCFA, and DNA analysis of ABCD1 gene revealed a novel heterozygous missense mutation (c.1700 A>C, p.Gln567Pro). The genetic testing for ABCD1 gene can be considered in female patients over middle age presenting spastic gait, because female ALD carriers tend to be symptomatic beyond age 60.
en-copyright=
kn-copyright=
en-aut-name=NakanoYumiko
en-aut-sei=Nakano
en-aut-mei=Yumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=TairaYuki
en-aut-sei=Taira
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=SasakiRyo
en-aut-sei=Sasaki
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=TadokoroKoh
en-aut-sei=Tadokoro
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=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=NomuraEmi
en-aut-sei=Nomura
en-aut-mei=Emi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
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=8
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=9
ORCID=
en-aut-name=ShimozawaNobuyuki
en-aut-sei=Shimozawa
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
ORCID=
affil-num=1
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=2
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=3
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=4
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=5
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=6
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=7
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=8
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=9
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=10
en-affil=Division of Genomics Research, Life Science Research Center, Gifu university
kn-affil=
affil-num=11
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=adrenoleukodystrophy
kn-keyword=adrenoleukodystrophy
en-keyword=symptomatic female carriers
kn-keyword=symptomatic female carriers
en-keyword=spastic paraplegia
kn-keyword=spastic paraplegia
en-keyword=ABCD1
kn-keyword=ABCD1
END
start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=5
article-no=
start-page=266
end-page=268
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220815
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Japanese case of Charcot?Marie?Tooth disease type 2Z with severe retinitis pigmentosa
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Charcot-Marie-Tooth disease type 2Z (CMT2Z) shows highly variable clinical features. We report the first Japanese CMT2Z patient with a c.754C>T (p.R252W) substitution of the MORC2 gene, complicating severe retinitis pigmentosa. The MORC2 mutants were involved in a decrease in cell survival through induction of apoptosis. Thus, the MORC2 mutation might be involved in the degeneration of photoreceptors and the development of retinitis pigmentosa.
en-copyright=
kn-copyright=
en-aut-name=NomuraEmi
en-aut-sei=Nomura
en-aut-mei=Emi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=TadokoroKoh
en-aut-sei=Tadokoro
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=SasakiRyo
en-aut-sei=Sasaki
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=NakataYumi
en-aut-sei=Nakata
en-aut-mei=Yumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=
en-aut-name=YunokiTaijun
en-aut-sei=Yunoki
en-aut-mei=Taijun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=TakemotoMami
en-aut-sei=Takemoto
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=
en-aut-name=AndoMasahiro
en-aut-sei=Ando
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
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=11
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 and Geriatrics, Graduate School of Medical and Dental Sciences, Kagoshima University
kn-affil=
affil-num=10
en-affil=Department of Neurology and Geriatrics, Graduate School of Medical and Dental Sciences, Kagoshima University
kn-affil=
affil-num=11
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Charcot-Marie-Tooth disease type 2Z
kn-keyword=Charcot-Marie-Tooth disease type 2Z
en-keyword=MORC2
kn-keyword=MORC2
en-keyword=retinitis pigmentosa
kn-keyword=retinitis pigmentosa
END
start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=5
article-no=
start-page=255
end-page=258
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220615
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Japanese case of successful surgical resection of cerebral cavernous malformations with a CCM2 mutation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cerebral cavernous malformations (CCMs) are congenital abnormalities of cerebral vessels. Surgical resection is rarely considered for the control of epilepsy in a first seizure patient with vascular malformation. In contrast, lesions that produce repetitive or progressive symptoms should be considered for surgical resection as treatment. Herein, we report a Japanese patient with a CCM2 mutation, c.609G>A (p.K203K) substitution, who showed drug-resistant epilepsy and dramatic improvement after surgical resection.
en-copyright=
kn-copyright=
en-aut-name=NomuraEmi
en-aut-sei=Nomura
en-aut-mei=Emi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=OmoteYoshio
en-aut-sei=Omote
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=
en-aut-name=YunokiTaijun
en-aut-sei=Yunoki
en-aut-mei=Taijun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=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=SasakiTatsuya
en-aut-sei=Sasaki
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=AkagawaHiroyuki
en-aut-sei=Akagawa
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
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=11
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 Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=9
en-affil=Tokyo Women's Medical University Institute for Integrated Medical Sciences
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=
en-keyword=CCM2
kn-keyword=CCM2
en-keyword=cerebral cavernous malformation
kn-keyword=cerebral cavernous malformation
en-keyword=drug-resistant epilepsy
kn-keyword=drug-resistant epilepsy
END
start-ver=1.4
cd-journal=joma
no-vol=86
cd-vols=
no-issue=1
article-no=
start-page=111
end-page=123
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202238
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Protective Effect of Rivaroxaban Against Amyloid Pathology and Neuroinflammation Through Inhibiting PAR-1 and PAR-2 in Alzheimer’s Disease Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Recent studies have revealed that atrial fibrillation (AF) patients have a high risk of developing cognitive impairment, vascular dementia, and Alzheimer’s disease (AD). Some reports suggest that the application of oral anticoagulant with an appropriate dose may have a preventive effect on AD. However, which oral anticoagulant drug is more appropriate for preventing AD and the underlying mechanism(s) is still unknown. Objective: The aim of the present study was to assess the treatment effect of rivaroxaban administration as well as investigate the roles of PAR-1 and PAR-2 in the AD?+?CAA mice model. Methods: In the present study, we compared a traditional oral anticoagulant, warfarin, and a direct oral anticoagulant (DOAC), rivaroxaban, via long-term administration to an AD with cerebral amyloid angiopathy (CAA) mice model. Results: Rivaroxaban treatment attenuated neuroinflammation, blood-brain barrier dysfunction, memory deficits, and amyloid-β deposition through PAR-1/PAR-2 inhibition in the AD?+?CAA mice model compared with warfarin and no-treatment groups. Conclusion: The present study demonstrates that rivaroxaban can attenuate AD progress and can be a potential choice to prevent AD.
en-copyright=
kn-copyright=
en-aut-name=BianZhihong
en-aut-sei=Bian
en-aut-mei=Zhihong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=LiuXia
en-aut-sei=Liu
en-aut-mei=Xia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=FengTian
en-aut-sei=Feng
en-aut-mei=Tian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=5
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=6
ORCID=
en-aut-name=BianYuting
en-aut-sei=Bian
en-aut-mei=Yuting
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=
en-aut-name=TadokoroKoh
en-aut-sei=Tadokoro
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
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=11
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=12
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=13
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=14
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=15
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=16
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=
affil-num=15
en-affil=National Center Hospital, National Center of Neurology and Psychiatry
kn-affil=
affil-num=16
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Alzheimer’s disease
kn-keyword=Alzheimer’s disease
en-keyword=cerebral amyloid angiopathy chronic cerebral hypoperfusion
kn-keyword=cerebral amyloid angiopathy chronic cerebral hypoperfusion
en-keyword=rivaroxaban
kn-keyword=rivaroxaban
en-keyword=warfarin
kn-keyword=warfarin
END
start-ver=1.4
cd-journal=joma
no-vol=353
cd-vols=
no-issue=1-2
article-no=
start-page=185
end-page=186
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=20156
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Selective disappearance of medial back muscles in a case of myotonic dystrophy type 1
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Here, we report a unique case of late-onset myotonic dystrophy type 1 in a 64-year-old woman, with selective disappearance of the medial lower back muscles. We compared the clinical features of this patient with those of a cohort of 29 patients with myotonic dystrophy type 1 to clarify the correlation between clinical features and lower back muscle atrophy. After classification into three subgroups according to muscle atrophy pattern, medial muscle atrophy was present in 17.2% of the patients. Affected patients were older at onset than non-affected patients, and limb muscle power and respiratory function decreased with atrophy progression.
en-copyright=
kn-copyright=
en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=
en-aut-name=KurataTomoko
en-aut-sei=Kurata
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=
affil-num=1
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=2
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=3
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=4
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=5
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=6
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
en-keyword=Myotonic dystrophy type 1
kn-keyword=Myotonic dystrophy type 1
en-keyword=Paraspinal muscles
kn-keyword=Paraspinal muscles
en-keyword=Late onset
kn-keyword=Late onset
END
start-ver=1.4
cd-journal=joma
no-vol=387
cd-vols=
no-issue=15
article-no=
start-page=70
end-page=74
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2018
dt-pub=20184
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Familial and sporadic chronic progressive degenerative parietal ataxia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background & objective: Parietal ataxia has been mainly reported as a consequence of acute ischemic stroke, while degenerative parietal ataxia has not been reported.
Methods: We investigated clinical characteristics, neuroimaging data, and genetic analysis of patients with cerebellar ataxia plus parietal atrophy.
Results: We identified seven patients, including five patients from two families, with chronic progressive cerebellar ataxia due to degenerative parietal atrophy but not stroke. Age at onset of ataxia was 57.6 +/- 6.9 years. All patients showed chronic progressive cerebellar ataxia with severity of ataxic gait > limb ataxia > dysarthria. Patients showed no cognitive dysfunction, muscle weakness, or parkinsonism, and only two patients showed mild sensory disturbances. The seven patients showed lateralized limb ataxia with greater contralateral parietal lobe atrophy by magnetic resonance imaging, and hypoperfusion by single photon emission computed tomography, without any abnormal cerebellar pathology (i.e., crossed cerebellar diaschisis). Pathogenic mutations in the microtubule-associated protein tau gene were not found using two single nucleotide polymorphisms.
Conclusions: This is the first description showing unique clinical features of familial and sporadic chronic progressive degenerative parietal ataxia.
en-copyright=
kn-copyright=
en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
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=3
ORCID=
en-aut-name=KurataTomoko
en-aut-sei=Kurata
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=NomuraEmi
en-aut-sei=Nomura
en-aut-mei=Emi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
ORCID=
en-aut-name=KitaguchiMasataka
en-aut-sei=Kitaguchi
en-aut-mei=Masataka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
affil-num=1
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=2
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=3
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=4
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=5
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=6
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=7
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=8
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=9
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=10
en-affil=Department of Molecular Genetics, Bioresource Science Branch, Center of Bioresource, Brain Research Institute Niigata University
kn-affil=
affil-num=11
en-affil=Department of Neurology, Baba Memorial Hospital
kn-affil=
affil-num=12
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
en-keyword=parietal ataxia
kn-keyword=parietal ataxia
en-keyword=parietal lobe atrophy
kn-keyword=parietal lobe atrophy
en-keyword=crossed cerebellar diaschisis
kn-keyword=crossed cerebellar diaschisis
en-keyword=MAPT
kn-keyword=MAPT
END
start-ver=1.4
cd-journal=joma
no-vol=95
cd-vols=
no-issue=9
article-no=
start-page=1818
end-page=1828
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20161230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Downregulation of PAR-1 and PAR-2 by Rivaroxaban
kn-title=Reduction of intracerebral hemorrhage by rivaroxaban after tPA thrombolysis is associated with downregulation of PAR-1 and PAR-2
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This study aimed to assess the risk of intracerebral hemorrhage (ICH) after tissue-type plasminogen activator (tPA) treatment in rivaroxaban compared with warfarin-pretreated male Wistar rat brain after ischemia in relation to activation profiles of protease-activated receptor-1, -2, -3, and -4 (PAR-1, -2, -3, and -4). After pretreatment with warfarin (0.2?mg/kg/day), low-dose rivaroxaban (60?mg/kg/day), high-dose rivaroxaban (120?mg/kg/day), or vehicle for 14 days, transient middle cerebral artery occlusion was induced for 90?min, followed by reperfusion with tPA (10?mg/kg/10?ml). Infarct volume, hemorrhagic volume, immunoglobulin G leakage, and blood parameters were examined. Twenty-four hours after reperfusion, immunohistochemistry for PARs was performed in brain sections. ICH volume was increased in the warfarin-pretreated group compared with the rivaroxaban-treated group. PAR-1, -2, -3, and -4 were widely expressed in the normal brain, and their levels were increased in the ischemic brain, especially in the peri-ischemic lesion. Warfarin pretreatment enhanced the expression of PAR-1 and PAR-2 in the peri-ischemic lesion, whereas rivaroxaban pretreatment did not. The present study shows a lower risk of brain hemorrhage in rivaroxaban-pretreated compared with warfarin-pretreated rats following tPA administration to the ischemic brain. It is suggested that the relative downregulation of PAR-1 and PAR-2 by rivaroxaban compared with warfarin pretreatment might be partly involved in the mechanism of reduced hemorrhagic complications in patients receiving rivaroxaban in clinical trials. ? 2016 Wiley Periodicals, Inc.
en-copyright=
kn-copyright=
en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=
en-aut-name=KonoSyoichiro
en-aut-sei=Kono
en-aut-mei=Syoichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=ShangJingwei
en-aut-sei=Shang
en-aut-mei=Jingwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=HeitmeierStefan
en-aut-sei=Heitmeier
en-aut-mei=Stefan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=PerzbornElisabeth
en-aut-sei=Perzborn
en-aut-mei=Elisabeth
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
ORCID=
affil-num=1
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=2
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=3
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=4
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=5
en-affil=Departments of Neurology
kn-affil=
affil-num=6
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=7
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=8
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=9
en-affil=Bayer Pharma AG, Drug Discovery - Global Therapeutic Research Groups, Cardiovascular Pharmacology
kn-affil=
affil-num=10
en-affil=Bayer Pharma AG, Drug Discovery - Global Therapeutic Research Groups, Cardiovascular Pharmacology
kn-affil=
affil-num=11
en-affil=Departments of Neurology, Dentistry and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
en-keyword=PAR-3
kn-keyword=PAR-3
en-keyword=PAR-4
kn-keyword=PAR-4
en-keyword=tissue plasminogen activator
kn-keyword=tissue plasminogen activator
en-keyword=warfarin
kn-keyword=warfarin
END
start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Efficacy and safety of spot heating and ultrasound irradiation on in vitro and in vivo thrombolysis models
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= The feasibility of transcranial sonothrombolysis has been demonstrated, although little is known about the relationships between thermal or mechanical mechanisms and thrombolytic outcomes. Therefore, the present study aims to reveal the effect and safety of temperature and ultrasound through in vitro and in vivo thrombolysis models. Artificial clots in microtubes were heated in a water bath or sonicated by ultrasound irradiation, and then clots weight decrease with rising temperature and sonication time was confirmed. In the in vitro thrombotic occlusion model, based on spot heating, clot volume was reduced and clots moved to the distal side, followed by recanalization of the occlusion. In the in vivo study, the common carotid artery of rats was exposed to a spot heater or to sonication. No brain infarct or brain blood barrier disruption was shown, but endothelial junctional dysintegrity and an inflammatory response in the carotid artery were detected. The present spot heating and ultrasound irradiation models seem to be effective for disintegrating clots in vitro, but the safety of the in vivo model was not fully supported by the data. However, the data indicates that a shorter time exposure could be less invasive than a longer exposure.
en-copyright=
kn-copyright=
en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=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=FengTian
en-aut-sei=Feng
en-aut-mei=Tian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
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=6
ORCID=
en-aut-name=TadokoroKoh
en-aut-sei=Tadokoro
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=
en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
affil-num=1
en-affil=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, Okayama, Japan
kn-affil=
affil-num=7
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=8
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=9
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END
start-ver=1.4
cd-journal=joma
no-vol=56
cd-vols=
no-issue=17
article-no=
start-page=2343
end-page=2346
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2017
dt-pub=20170901
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Successful Delayed Aortic Surgery for a Patient with Ischemic Stroke Secondary to Aortic Dissection
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The diagnosis of aortic dissection (AD) is sometimes difficult within the limited time window of recombinant tissue plasminogen activator (tPA) for ischemic stroke (IS). A 60-year-old man developed sudden left hemiparesis due to IS. During tPA infusion, his blood pressure dropped and consciousness declined. After transfer to our hospital, carotid duplex ultrasonography led to a diagnosis of AD. Emergency surgery was postponed because of the risk of hemorrhagic transformation. The patient successfully underwent aortic surgery on day 5 and was discharged with a remarkable improvement in his symptoms. Delayed surgery may avoid hemorrhagic transformation in patients with AD-induced IS who have received tPA.
en-copyright=
kn-copyright=
en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
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=3
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=4
ORCID=
en-aut-name=ManabeYasuhiro
en-aut-sei=Manabe
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=TakahashiYoshiaki
en-aut-sei=Takahashi
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
ORCID=
en-aut-name=KonoSyoichiro
en-aut-sei=Kono
en-aut-mei=Syoichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=13
ORCID=
affil-num=1
en-affil=Departments of Neurology, Dentistry, and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=2
en-affil=Departments of Neurology, Dentistry, and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University
kn-affil=
affil-num=3
en-affil=Departments of Neurology, Dentistry, and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University, Japan
kn-affil=
affil-num=4
en-affil=Departments of Neurology, Dentistry, and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University, Japan
kn-affil=
affil-num=5
en-affil=Department of Neurology, Okayama National Hospital Medical Center, Japan
kn-affil=
affil-num=6
en-affil=Department of Neurology, Okayama National Hospital Medical Center, Japan
kn-affil=
affil-num=7
en-affil=Departments of Neurology, Dentistry, and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University, Japan
kn-affil=
affil-num=8
en-affil=Departments of Neurology, Dentistry, and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University, Japan
kn-affil=
affil-num=9
en-affil=Departments of Neurology, Dentistry, and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University, Japan
kn-affil=
affil-num=10
en-affil=Department of Neurology, Okayama National Hospital Medical Center, Japan
kn-affil=
affil-num=11
en-affil=Departments of Neurology, Dentistry, and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University, Japan
kn-affil=
affil-num=12
en-affil=Departments of Neurology, Dentistry, and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University, Japan
kn-affil=
affil-num=13
en-affil=Departments of Neurology, Dentistry, and Pharmaceutical Sciences, Graduate School of Medicine, Okayama University, Japan
kn-affil=
END
start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=
article-no=
start-page=98
end-page=101
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202224
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A case of a heterozygous ABCC6 mutation showing recurrent ischemic strokes and intracranial hemorrhages
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Mutations in the ATP-binding cassette subfamily C member 6 (ABCC6) gene are responsible for pseudoxanthoma elasticum (PXE). PXE is a rare genetic metabolic disease with autosomal recessive inheritance that shows ectopic mineralization in skin, eyes and blood vessels, and causes cerebrovascular disease. There are few reports of intracranial hemorrhages in patients with the ABCC6 mutation. We report the first Japanese case with a heterozygous ABCC6 mutation displaying recurrent ischemic strokes and intracranial hemorrhages. We propose that the ABCC6 mutation may be one cause of neurovascular diseases with a family history.
en-copyright=
kn-copyright=
en-aut-name=NomuraEmi
en-aut-sei=Nomura
en-aut-mei=Emi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=KawaharaYuko
en-aut-sei=Kawahara
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=OmoteYoshio
en-aut-sei=Omote
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=TakahashiYoshiaki
en-aut-sei=Takahashi
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=MatsumotoNamiko
en-aut-sei=Matsumoto
en-aut-mei=Namiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=IkegamiKen
en-aut-sei=Ikegami
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
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=10
ORCID=
en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=UemuraMasahiro
en-aut-sei=Uemura
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=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, Brain Research Institute, Niigata 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=ATP-binding cassette subfamily C member 6 (ABCC6)
kn-keyword=ATP-binding cassette subfamily C member 6 (ABCC6)
en-keyword=neurovascular diseases
kn-keyword=neurovascular diseases
en-keyword=pseudoxanthoma elasticum (PXE)
kn-keyword=pseudoxanthoma elasticum (PXE)
END
start-ver=1.4
cd-journal=joma
no-vol=58
cd-vols=
no-issue=21
article-no=
start-page=3163
end-page=3165
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20191101
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Spastic Paraplegia Accompanied by Extrapyramidal Sign and Frontal Cognitive Dysfunction
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A complicated form of spastic paraplegia is a neurodegenerative disorder presenting as progressive spasticity in the bilateral lower limbs accompanied by some clinical features. The present case showed spastic paralysis and hyperreflexia in all extremities as well as lead pipe rigidity in the neck and bilateral upper extremities (R < L), decreased scores on frontal cognitive tests, a decreased accumulation of the right dorsal putamen on a DAT scan, and hypoperfusion of the bilateral frontal lobes on 99mTc-ECD single photon emission computed tomography (SPECT). The present case provides a new spectrum of spastic paraplegia based on the evidence of clinical scores and the findings of brain functional imaging.
en-copyright=
kn-copyright=
en-aut-name=SasakiRyo
en-aut-sei=Sasaki
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=TadokoroKoh
en-aut-sei=Tadokoro
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=TakahashiYoshiaki
en-aut-sei=Takahashi
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=ShangJingwei
en-aut-sei=Shang
en-aut-mei=Jingwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
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=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=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
affil-num=1
en-affil=Department of Neurology, 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, The University of Tokyo Hospital
kn-affil=
affil-num=11
en-affil=Department of Molecular Neurology, The University of Tokyo Hospital, Japan Institute of Medical Genomics, International University of Health and Welfare
kn-affil=
affil-num=12
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=spastic paraplegia
kn-keyword=spastic paraplegia
en-keyword=extrapyramidal sign
kn-keyword=extrapyramidal sign
en-keyword=frontal cognitive dysfunction
kn-keyword=frontal cognitive dysfunction
END
start-ver=1.4
cd-journal=joma
no-vol=58
cd-vols=
no-issue=7
article-no=
start-page=1033
end-page=1036
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Characteristic Clinical Features of Werner Syndrome with a Novel Compound Heterozygous WRN Mutation c.1720+1G>A Plus c.3139-1G>C
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Werner syndrome (WS) is an autosomal recessive progeroid disorder caused by mutations in the WRN gene (WRN). Most Japanese WS patients are born from a consanguineous marriage with homozygous WRN mutations. We herein report a rare WS patient born from non-consanguineous parents with compound heterozygous WRN mutations with a novel heterogeneous c.1720+1G>A substitution plus the most frequent heterogeneous c.3139-1G>C substitution among Japanese. Although the present case showed clinical characteristics common to previous Japanese WS patients, he had not developed any malignant tumors as of 43 years of age, suggesting that WS patients with this particular genetic mutation have a different phenotype than others.
en-copyright=
kn-copyright=
en-aut-name=MatsumotoNamiko
en-aut-sei=Matsumoto
en-aut-mei=Namiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
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=4
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=ShangJingwei
en-aut-sei=Shang
en-aut-mei=Jingwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
ORCID=
en-aut-name=WatanabeAki
en-aut-sei=Watanabe
en-aut-mei=Aki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=YokoteKoutaro
en-aut-sei=Yokote
en-aut-mei=Koutaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=TakemotoMinoru
en-aut-sei=Takemoto
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=OshimaJunko
en-aut-sei=Oshima
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
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=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, Okayama Citizen's Hospital
kn-affil=
affil-num=4
en-affil=Department of General Internal Medicine, Okayama Citizen's Hospital
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 Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University
kn-affil=
affil-num=11
en-affil=Department of Clinical Cell Biology and Medicine, Graduate School of Medicine, Chiba University
kn-affil=
affil-num=12
en-affil=Department of Diabetes, Metabolism and Endocrinology, School of Medicine, International University of Health and Welfare
kn-affil=
affil-num=13
en-affil=Department of Pathology, University of Washington
kn-affil=
affil-num=14
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=werner syndrome
kn-keyword=werner syndrome
en-keyword=compound heterozygous
kn-keyword=compound heterozygous
en-keyword=Japanese
kn-keyword=Japanese
END
start-ver=1.4
cd-journal=joma
no-vol=58
cd-vols=
no-issue=3
article-no=
start-page=437
end-page=440
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Rare Case of Klinefelter Syndrome Accompanied by Spastic Paraplegia and Peripheral Neuropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Klinefelter syndrome is a chromosomal disorder with a typical karyotype of 47, XXY, accompanied by various neurological symptoms. We herein report the first case of Klinefelter syndrome with a rare mosaic form of 47, XXY and 48, XXXY, combined with both spastic paraplegia and peripheral motor neuropathy. This case showed spasticity and hyperreflexia with pathological reflexes and ankle clonus as well as muscle weakness in all extremities. A motor nerve conduction study and the magnetic motor evoked potential suggested motor axonal neuropathy and corticospinal tract disorders. The present case suggests that Klinefelter syndrome can present with both upper and lower motor neuron degeneration.
en-copyright=
kn-copyright=
en-aut-name=SasakiRyo
en-aut-sei=Sasaki
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=TakahashiYoshiaki
en-aut-sei=Takahashi
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=
en-aut-name=TadokoroKoh
en-aut-sei=Tadokoro
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=ShangJingwei
en-aut-sei=Shang
en-aut-mei=Jingwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
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=11
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=
en-keyword=Klinefelter syndrome
kn-keyword=Klinefelter syndrome
en-keyword=mosaic form
kn-keyword=mosaic form
en-keyword=peripheral neuropathy
kn-keyword=peripheral neuropathy
en-keyword=spastic paraplegia
kn-keyword=spastic paraplegia
END
start-ver=1.4
cd-journal=joma
no-vol=58
cd-vols=
no-issue=8
article-no=
start-page=1081
end-page=1085
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190415
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Improving Anxiety in Subacute Myelo-optico-neuropathy (SMON) after an Automated Telephone Call Service
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective We evaluated the clinical effects of a telephone call service for psychological symptoms such as anxiety, depression or apathy in subacute myelo-optico-neuropathy (SMON) patients living alone or with a single caregiver.
Methods Up to 16 SMON patients (4 men, 12 women) and 32 control subjects were evaluated by the geriatric depression scale (GDS), apathy scale (AS) and state and trait anxiety inventory (STAI) forms X-I, including the P and A values for depression, apathy and state anxiety including disturbed peace of mind and enhanced anxiety, respectively, before (pre) and three months after (post) the telephone call service.
Results The SMON patients, especially women, had significantly worse baseline scores in GDS (depression), AS (apathy) and STAI (state anxiety) than control subjects. The automated telephone call service significantly improved the high baseline STAI scores, including the P and A scores (disturbed peace of mind and enhanced anxiety), of SMON patients but not the GDS or AS scores.
Conclusion SMON patients, especially women, living alone or with a single caregiver showed higher baseline depression, apathy and anxiety scores than the control subjects. The present automated telephone call service proved to be a useful care tool for improving the anxiety of SMON patients with high STAI P and A scores.
en-copyright=
kn-copyright=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=5
ORCID=
en-aut-name=DoutareShinji
en-aut-sei=Doutare
en-aut-mei=Shinji
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=
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=Doutare Medical Clinic
kn-affil=
affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=anxiety
kn-keyword=anxiety
en-keyword=SMON
kn-keyword=SMON
en-keyword=STAI
kn-keyword=STAI
en-keyword=telephone call service
kn-keyword=telephone call service
END
start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=2
article-no=
start-page=305
end-page=308
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210115
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Oldest Japanese Case of Combined Central and Peripheral Demyelination, which Developed Nine Years After the First Instance of Optic Neuritis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Combined central and peripheral demyelination (CCPD) causes demyelination in both the central and peripheral nervous systems. Anti-neurofascin 155 antibody plays an important pathogenic role in CCPD, but evidence concerning an association between this antibody and CCPD remains inconclusive. Although there have been no reports of precedent optic neuritis developing into CCPD, we herein report a Japanese man in whom optic neuritis recurred four times over nine years and who developed CCPD without positive antineurofascin 155 antibody. This case suggests the possibility of developing CCPD after optic nerve neuritis and the existence of an unknown antibody that induces CCPD.
en-copyright=
kn-copyright=
en-aut-name=NomuraEmi
en-aut-sei=Nomura
en-aut-mei=Emi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=KawaharaYuko
en-aut-sei=Kawahara
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=OmoteYoshio
en-aut-sei=Omote
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=TadokoroKoh
en-aut-sei=Tadokoro
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=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=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
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=OgataHidenori
en-aut-sei=Ogata
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
affil-num=1
en-affil=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, Neurological Institute, Graduate School of Medical Sciences, Kyushu University
kn-affil=
affil-num=9
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Combined central and peripheral demyclination (CCPD)
kn-keyword=Combined central and peripheral demyclination (CCPD)
en-keyword=recurrent optic neuritis
kn-keyword=recurrent optic neuritis
END
start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=1
article-no=
start-page=19
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210206
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of edaravone on pregnant mice and their developing fetuses subjected to placental ischemia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Growing evidence indicates that reduced uterine perfusion pressure (RUPP) triggers the cascade of events leading to preeclampsia. Edaravone is a powerful free radical scavenger used for the treatment of ischemia/reperfusion diseases due to its anti-oxidative stress and anti-inflammatory properties. Here we investigate the effect of edaravone (3 mg/kg) on different maternal and fetal outcomes of RUPP-induced placental ischemia mice model. RUPP surgery was performed on gestation day (GD) 13 followed by edaravone injection from GD14 to GD18, sacrifice day. The results showed that edaravone injection significantly decreased the maternal blood pressure (113.2 +/- 2.3 mmHg) compared with RUPP group (131.5 +/- 1.9 mmHg). Edaravone increased fetal survival rate (75.4%) compared with RUPP group (54.4%), increased fetal length, weights, and feto-placental ratio (7.2 and 5.7 for RUPP and RUPP-Edaravone groups, respectively) compared with RUPP group. In addition, RUPP resulted in many fetal morphological abnormalities as well as severe delayed ossification, however edaravone decreased the morphological abnormalities and increased the ossification of the fetal endoskeleton. Edaravone improved the histopathological structure of the maternal kidney and heart as well as decreased the elevated blood urea and creatinine levels (31.5 +/- 0.15 mg/dl (RUPP), 25.6 +/- 0.1 mg/dl (RUPP+edaravone) for urea and 5.4 +/- 0.1 mg/dl (RUPP), 3.5 +/- 0.1 mg/dl (RUPP+edaravone) for creatinine) and decreased cleaved caspase-3 expression in the maternal kidney. In conclusion, this study demonstrated that our RUPP mice model recapitulated preeclampsia symptoms and edaravone injection ameliorated most of these abnormalities suggesting its effectiveness and potential application in preeclampsia treatment regimes.
en-copyright=
kn-copyright=
en-aut-name=AtallahMarwa
en-aut-sei=Atallah
en-aut-mei=Marwa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
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=3
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=
en-keyword=Preeclampsia
kn-keyword=Preeclampsia
en-keyword=RUPP
kn-keyword=RUPP
en-keyword=Edaravone
kn-keyword=Edaravone
en-keyword=Placental ischemia
kn-keyword=Placental ischemia
en-keyword=Endoskeleton
kn-keyword=Endoskeleton
en-keyword=Fetal growth restriction
kn-keyword=Fetal growth restriction
END
start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=2
article-no=
start-page=166
end-page=170
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20201214
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A new telestroke network system in northern area of Okayama prefecture
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background
Telestroke network can provide rapid access to specialized treatment and improves on‐site management of acute stroke patients through the “hub‐and‐spoke” model. In the northern part of Okayama Prefecture, there has been a regional gap of stroke care due to the shortage of stroke specialists and facilities. In addition, due to the novel coronavirus disease 2019 (COVID‐19), it is required to reduce the unnecessary contact with stroke patients from other hospitals.
Aim
We organized a novel cost‐free telestroke network with an image and video sharing for neurological diseases in the northern part of Okayama Prefecture to improve the stroke management in the area.
Method
We prepared the tablet device on which Skype? application was installed for each hospital and recruited the patients who visited or hospitalized in the spoke hospitals and were suspected to have some neurological diseases from April 2019 to May 2020. The patient's clinical data were recorded and analyzed.
Results
During the study period, 5 patients were recruited including the cases with the initial diagnosis of stroke or brain tumor. Among them, 2 cases were transferred to the hub hospital, 2 cases were transferred to other hospitals, and 1 case was treated on site under specialist's advice.
Conclusion
The new telestroke network system may be beneficial for acute stroke management and reducing the unnecessary patient's transfer in the rural area, especially under coexistence with COVID‐19.
en-copyright=
kn-copyright=
en-aut-name=SasakiRyo
en-aut-sei=Sasaki
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=
en-aut-name=OmoteYoshio
en-aut-sei=Omote
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=YunokiTaijun
en-aut-sei=Yunoki
en-aut-mei=Taijun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=KobayashiKazuki
en-aut-sei=Kobayashi
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=SawataTakashi
en-aut-sei=Sawata
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=SatoYuki
en-aut-sei=Sato
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=KubotaJunichi
en-aut-sei=Kubota
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=MizobuchiMasayuki
en-aut-sei=Mizobuchi
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=HayashiTakashi
en-aut-sei=Hayashi
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=13
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, Tsuyama Central Hospital
kn-affil=
affil-num=7
en-affil=Department of Neurosurgery, Tsuyama Central Hospital
kn-affil=
affil-num=8
en-affil=Department of Gastrointestinal Surgery, Tsuyama 1st Hospital
kn-affil=
affil-num=9
en-affil=Department of Internal Medicine, Sato Memorial Hospital
kn-affil=
affil-num=10
en-affil=Department of Internal Medicine, Tajiri Hospital
kn-affil=
affil-num=11
en-affil=Department of Neurosurgery, Kaneda Hospital
kn-affil=
affil-num=12
en-affil=Department of Orthopedics, Sayo Central Hospital
kn-affil=
affil-num=13
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=COVID‐19
kn-keyword=COVID‐19
en-keyword=Okayama
kn-keyword=Okayama
en-keyword=skype
kn-keyword=skype
en-keyword=telemedicine
kn-keyword=telemedicine
en-keyword=telestroke
kn-keyword=telestroke
END
start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=1
article-no=
start-page=217
end-page=227
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200107
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A New Serum Biomarker Set to Detect Mild Cognitive Impairment and Alzheimer’s Disease by Peptidome Technology
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background:
Because dementia is an emerging problem in the world, biochemical markers of cerebrospinal fluid (CSF) and radio-isotopic analyses are helpful for diagnosing Alzheimer’s disease (AD). Although blood sample is more feasible and plausible than CSF or radiological biomarkers for screening potential AD, measurements of serum amyloid- β (Aβ), plasma tau, and serum antibodies for Aβ1 - 42 are not yet well established.
Objective:
We aimed to identify a new serum biomarker to detect mild cognitive impairment (MCI) and AD in comparison to cognitively healthy control by a new peptidome technology.
Methods:
With only 1.5μl of serum, we examined a new target plate “BLOTCHIP?” plus a matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF/MS) to discriminate control (n?=?100), MCI (n?=?60), and AD (n?=?99). In some subjects, cognitive Mini-Mental State Examination (MMSE) were compared to positron emission tomography (PET) with Pittsburgh compound B (PiB) and the serum probability of dementia (SPD). The mother proteins of candidate serum peptides were examined in autopsied AD brains.
Results:
Apart from Aβ or tau, the present study discovered a new diagnostic 4-peptides-set biomarker for discriminating control, MCI, and AD with 87% of sensitivity and 65% of specificity between control and AD (***p?0.001). MMSE score was well correlated to brain Aβ deposition and to SPD of AD. The mother proteins of the four peptides were upregulated for coagulation, complement, and plasticity (three proteins), and was downregulated for anti-inflammation (one protein) in AD brains.
Conclusion:
The present serum biomarker set provides a new, rapid, non-invasive, highly quantitative and low-cost clinical application for dementia screening, and also suggests an alternative pathomechanism of AD for neuroinflammation and neurovascular unit damage.
en-copyright=
kn-copyright=
en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=ShangJingwei
en-aut-sei=Shang
en-aut-mei=Jingwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=ShiXiaowen
en-aut-sei=Shi
en-aut-mei=Xiaowen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=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=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=NakanoYumiko
en-aut-sei=Nakano
en-aut-mei=Yumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
ORCID=
en-aut-name=IkedaMasaki
en-aut-sei=Ikeda
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
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=12
ORCID=
en-aut-name=OkamotoKoichi
en-aut-sei=Okamoto
en-aut-mei=Koichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
en-aut-name=ShojiMikio
en-aut-sei=Shoji
en-aut-mei=Mikio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=
en-aut-name=TakatamaMasamitsu
en-aut-sei=Takatama
en-aut-mei=Masamitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=
en-aut-name=KojoMotohisa
en-aut-sei=Kojo
en-aut-mei=Motohisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=
en-aut-name=KurodaTakeshi
en-aut-sei=Kuroda
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=
en-aut-name=OnoKenjiro
en-aut-sei=Ono
en-aut-mei=Kenjiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=
en-aut-name=KimuraNoriyuki
en-aut-sei=Kimura
en-aut-mei=Noriyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=
en-aut-name=MatsubaraEtsuro
en-aut-sei=Matsubara
en-aut-mei=Etsuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
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=21
ORCID=
en-aut-name=WakutaniYosuke
en-aut-sei=Wakutani
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=
en-aut-name=TakaoYoshiki
en-aut-sei=Takao
en-aut-mei=Yoshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=
en-aut-name=HigashiYasuto
en-aut-sei=Higashi
en-aut-mei=Yasuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=
en-aut-name=AsadaKyoichi
en-aut-sei=Asada
en-aut-mei=Kyoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=
en-aut-name=SengaTakehito
en-aut-sei=Senga
en-aut-mei=Takehito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=
en-aut-name= LeeLyang-Ja
en-aut-sei= Lee
en-aut-mei=Lyang-Ja
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=
en-aut-name=TanakaKenji
en-aut-sei=Tanaka
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=
affil-num=1
en-affil=Department of Neurology, Okayama University
kn-affil=
affil-num=2
en-affil=Department of Neurology, Okayama University
kn-affil=
affil-num=3
en-affil=Department of Neurology, Okayama University
kn-affil=
affil-num=4
en-affil=Department of Neurology, Okayama University
kn-affil=
affil-num=5
en-affil=Department of Neurology, Okayama University
kn-affil=
affil-num=6
en-affil=Department of Neurology, Okayama University
kn-affil=
affil-num=7
en-affil=Department of Neurology, Okayama University
kn-affil=
affil-num=8
en-affil=Department of Neurology, Okayama University
kn-affil=
affil-num=9
en-affil=Department of Neurology, Okayama University
kn-affil=
affil-num=10
en-affil=Department of Neurology, Okayama City Hospital, Okayama
kn-affil=
affil-num=11
en-affil=Department of Neurology, Gunma University, Graduate School of Medicine
kn-affil=
affil-num=12
en-affil=Department of Neurology, Gunma University, Graduate School of Medicine
kn-affil=
affil-num=13
en-affil=Department of Neurology, Geriatrics Research Institute and Hospital
kn-affil=
affil-num=14
en-affil=Department of Neurology, Geriatrics Research Institute and Hospital
kn-affil=
affil-num=15
en-affil=Department of Neurology, Geriatrics Research Institute and Hospital
kn-affil=
affil-num=16
en-affil=Department of Neurology, Ako Chuo Hospital
kn-affil=
affil-num=17
en-affil=Division of Neurology, Department of Medicine, Showa University, School of Medicine
kn-affil=
affil-num=18
en-affil=Division of Neurology, Department of Medicine, Showa University, School of Medicine
kn-affil=
affil-num=19
en-affil=Department of Neurology, Faculty of Medicine, Oita University
kn-affil=
affil-num=20
en-affil=Department of Neurology, Faculty of Medicine, Oita University
kn-affil=
affil-num=21
en-affil=Department of Neurology, Kurashiki Heisei Hospital
kn-affil=
affil-num=22
en-affil=Department of Neurology, Kurashiki Heisei Hospital
kn-affil=
affil-num=23
en-affil=Department of Neurology, Kurashiki Heisei Hospital
kn-affil=
affil-num=24
en-affil=Department of Neurology, Himeji Central Hospital
kn-affil=
affil-num=25
en-affil=Membrane Protein and Ligand Analysis Center, Protosera Inc.,
kn-affil=
affil-num=26
en-affil=Membrane Protein and Ligand Analysis Center, Protosera Inc.,
kn-affil=
affil-num=27
en-affil=Membrane Protein and Ligand Analysis Center, Protosera Inc.,
kn-affil=
affil-num=28
en-affil=Membrane Protein and Ligand Analysis Center, Protosera Inc.,
kn-affil=
en-keyword=Alzheimer’s disease
kn-keyword=Alzheimer’s disease
en-keyword=biomarker
kn-keyword=biomarker
en-keyword=coagulation
kn-keyword=coagulation
en-keyword=complement
kn-keyword=complement
en-keyword=MALDI-TOF
kn-keyword=MALDI-TOF
en-keyword=mild cognitive impairment
kn-keyword=mild cognitive impairment
en-keyword=neuroinflammation
kn-keyword=neuroinflammation
en-keyword=peptidome
kn-keyword=peptidome
en-keyword=plasticity
kn-keyword=plasticity
END
start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=1
article-no=
start-page=17102
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20201013
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Therapeutic benefit of Muse cells in a mouse model of amyotrophic lateral sclerosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive motor neuron loss. Muse cells are endogenous reparative pluripotent-like stem cells distributed in various tissues. They can selectively home to damaged sites after intravenous injection by sensing sphingosine-1-phosphate produced by damaged cells, then exert pleiotropic effects, including tissue protection and spontaneous differentiation into tissue-constituent cells. In G93A-transgenic ALS mice, intravenous injection of 5.0x10(4) cells revealed successful homing of human-Muse cells to the lumbar spinal cords, mainly at the pia-mater and underneath white matter, and exhibited glia-like morphology and GFAP expression. In contrast, such homing or differentiation were not recognized in human mesenchymal stem cells but were instead distributed mainly in the lung. Relative to the vehicle groups, the Muse group significantly improved scores in the rotarod, hanging-wire and muscle strength of lower limbs, recovered the number of motor neurons, and alleviated denervation and myofiber atrophy in lower limb muscles. These results suggest that Muse cells homed in a lesion site-dependent manner and protected the spinal cord against motor neuron death. Muse cells might also be a promising cell source for the treatment of ALS patients.
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=KushidaYoshihiro
en-aut-sei=Kushida
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=WakaoShohei
en-aut-sei=Wakao
en-aut-mei=Shohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=TadokoroKoh
en-aut-sei=Tadokoro
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=NomuraEmi
en-aut-sei=Nomura
en-aut-mei=Emi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=OmoteYoshio
en-aut-sei=Omote
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=DezawaMari
en-aut-sei=Dezawa
en-aut-mei=Mari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
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 Stem Cell Biology and Histology, Tohoku University Graduate School of Medicine
kn-affil=
affil-num=3
en-affil=Department of Stem Cell Biology and Histology, Tohoku University Graduate School of Medicine
kn-affil=
affil-num=4
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=5
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=6
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=7
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=8
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=9
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=10
en-affil=Department of Stem Cell Biology and Histology, Tohoku University Graduate School of Medicine
kn-affil=
affil-num=11
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Mesenchymal stem cells
kn-keyword=Mesenchymal stem cells
en-keyword=Neurological disorders
kn-keyword=Neurological disorders
END
start-ver=1.4
cd-journal=joma
no-vol=20
cd-vols=
no-issue=1
article-no=
start-page=156
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200603
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Recovery from hypoxemia and Hypercapnia following noninvasive pressure support ventilation in a patient with statin-associated necrotizing myopathy: a case report
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Statin-associated necrotizing myopathy (SANM) is a rare autoimmune disorder caused by administration of statins. SANM is characterized by weakness due to necrosis and regeneration of myofibers. Here we report the first case of SANM with acute respiratory failure treated with noninvasive pressure support ventilation in addition to immunosuppressants.
Case presentation: A 59-year-old woman who had been treated with 2.5 mg/day of rosuvastatin calcium for 5 years stopped taking the drug 4 months before admission to our hospital due to elevation of creatine kinase (CK). Withdrawal of rosuvastatin for 1 month did not decrease the level of CK, and she was admitted to our hospital due to the development of muscle weakness of her neck and bilateral upper extremities. Anti-3-hydroxy-3-methylglutaryl coenzyme A reductase antibodies were positive. Magnetic resonance imaging showed myositis, and muscle biopsy from the right biceps brachii muscle showed muscle fiber necrosis and regeneration without inflammatory cell infiltration, suggesting SANM. After the diagnosis, she received methylprednisolone pulse therapy (mPSL, 1 g/day × 3 days, twice) and subsequent oral prednisolone therapy (PSL, 30 mg/day for 1 month, 25 mg/day for 1 month and 22.5 mg/day for 1 month), leading to improvement of her muscle weakness. One month after the PSL tapering to 20 mg/day, her muscle weakness deteriorated with oxygen desaturation (SpO2: 93% at room air) due to hypoventilation caused by weakness of respiratory muscles. BIPAP was used for the management of acute respiratory failure in combination with IVIG (20 g/day × 5 days) followed by mPSL pulse therapy (1 g/day × 3 days), oral PSL (30 mg/day × 3 weeks, then tapered to 25 mg/day) and tacrolimus (3 mg/day). Twenty-seven days after the start of BIPAP, she was weaned from BIPAP with improvement of muscle weakness, hypoxemia and hypercapnia. After she achieved remission with improvement of muscle weakness and reduction of serum CK level to a normal level, the dose of oral prednisolone was gradually tapered to 12.5 mg/day without relapse for 3 months.
Conclusions: Our report provides new insights into the role of immunosuppressants and biphasic positive airway pressure for induction of remission in patients with SANM.
en-copyright=
kn-copyright=
en-aut-name=YamamuraYuriko
en-aut-sei=Yamamura
en-aut-mei=Yuriko
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=TadokoroKoh
en-aut-sei=Tadokoro
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=
en-aut-name=YamamuraMasahiro
en-aut-sei=Yamamura
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=SadaKen-Ei
en-aut-sei=Sada
en-aut-mei=Ken-Ei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical 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 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=Center for Rheumatology, Okayama Saiseikai General Hospital
kn-affil=
affil-num=8
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=9
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=10
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Noninvasive pressure support ventilation
kn-keyword=Noninvasive pressure support ventilation
en-keyword=Statin-associated necrotizing myopathy
kn-keyword=Statin-associated necrotizing myopathy
en-keyword=BIPAP
kn-keyword=BIPAP
END
start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=5
article-no=
start-page=288
end-page=290
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190629
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Late presented congenital myasthenic syndrome with novel compound heterozygous CHRNE mutations mimicking seronegative myasthenia gravis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= We found a late presented congenital myasthenic syndrome (CMS) patient with novel CHRNE gene mutations. Although our patient has shown blepharoptosis since youth, fatigable muscle weakness began at age 71. Genetic analysis revealed novel compound heterozygous CHRNE mutations (c.1032+2T>G, c.1306_1307 delGA). His myasthenic symptoms were well managed by oral anti‐cholinesterase drug until he died at 82‐year‐old. The present case showed mild myasthenic symptoms with very late presentation and slow progression. Late presented CMS is often underdiagnosed; therefore, genetic testing is important to distinguish it from other myasthenic disease.
en-copyright=
kn-copyright=
en-aut-name=NakanoYumiko
en-aut-sei=Nakano
en-aut-mei=Yumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
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=3
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=4
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=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=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
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=10
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=11
ORCID=
affil-num=1
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=2
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=3
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=4
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=5
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=6
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=7
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=8
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=9
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=10
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=11
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=anti-cholinesterase drug
kn-keyword=anti-cholinesterase drug
en-keyword=the CHRNE gene
kn-keyword=the CHRNE gene
en-keyword=congenital myasthenic syndrome
kn-keyword=congenital myasthenic syndrome
en-keyword=late presentation
kn-keyword=late presentation
en-keyword=mimicking seronegative myasthenia gravis
kn-keyword=mimicking seronegative myasthenia gravis
END
start-ver=1.4
cd-journal=joma
no-vol=97
cd-vols=
no-issue=5
article-no=
start-page=607
end-page=609
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2018
dt-pub=20181219
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Enhanced oxidative stress and the treatment by edaravone in mice model of amyotrophic lateral sclerosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Oxidative stress is associated with the degeneration of both motor neurons and skeletal muscles in amyotrophic lateral sclerosis (ALS). A free radical scavenger edaravone has been proven as a therapeutic drug for ALS patients, but the neuroprotective mechanism for the oxidative stress of ALS has not been fully investigated. In this study, we investigated oxidative stress in ALS model mice bearing both oxidative stress sensor nuclear erythroid 2-related factor 2 (Nrf2) and G93A-human Cu/Zn superoxide dismutase (Nrf2/G93A) treated by edaravone. In vivo Nrf2 imaging analysis showed the accelerated oxidative stress both in spinal motor neurons and lower limb muscles of Nrf2/G93A mice according to disease progression in addition to the enhancement of serum oxidative stress marker dROMS. These were significantly alleviated by edaravone treatment accompanied by clinical improvements (rotarod test). The present study suggests that in vivo optical imaging of Nrf2 is useful for detecting oxidative stress in ALS, and edaravone alleviates the degeneration of both motor neurons and muscles related to oxidative stress in ALS patients.
en-copyright=
kn-copyright=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=NomuraEmi
en-aut-sei=Nomura
en-aut-mei=Emi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=ShangJingwei
en-aut-sei=Shang
en-aut-mei=Jingwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=FengTian
en-aut-sei=Feng
en-aut-mei=Tian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=HuangYong
en-aut-sei=Huang
en-aut-mei=Yong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=LiuXia
en-aut-sei=Liu
en-aut-mei=Xia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=ShiXiaowen
en-aut-sei=Shi
en-aut-mei=Xiaowen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
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=12
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=13
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=
en-keyword=ALS
kn-keyword=ALS
en-keyword=SOD1
kn-keyword=SOD1
en-keyword=edaravone
kn-keyword=edaravone
en-keyword=in vivo imaging
kn-keyword=in vivo imaging
en-keyword=nrf2
kn-keyword=nrf2
en-keyword=oxidative stress
kn-keyword=oxidative stress
END
start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=3
article-no=
start-page=146
end-page=149
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190219
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Very rare solitary primary peripheral nerve onset cytotoxic molecule-positive peripheral T-cell lymphoma (PTCL)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Here we present the first report of solitary primary peripheral nerve onset cytotoxic molecule (CM)-positive peripheral T-cell lymphoma (PTCL) diagnosed after nerve biopsy. An 84-year-old female with rheumatoid arthritis (RA) complained of asymmetric severe tenderness in her upper limbs. The biopsy pathology revealed a direct invasion of CM-positive PTCL. When RA patients complain of numbness, tenderness, or weakness, lymphomatic peripheral nerve invasion should be considered.
en-copyright=
kn-copyright=
en-aut-name=MatsumotoNamiko
en-aut-sei=Matsumoto
en-aut-mei=Namiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=TakahashiYoshiaki
en-aut-sei=Takahashi
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=KawaharaYuko
en-aut-sei=Kawahara
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=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=ShangJingwei
en-aut-sei=Shang
en-aut-mei=Jingwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
ORCID=
en-aut-name=SakamotoMaiko
en-aut-sei=Sakamoto
en-aut-mei=Maiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=KondouEisei
en-aut-sei=Kondou
en-aut-mei=Eisei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=ShibataRei
en-aut-sei=Shibata
en-aut-mei=Rei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
en-aut-name=YoshinoTadashi
en-aut-sei=Yoshino
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
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=15
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=16
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 Hematology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=12
en-affil=Department of Hematology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=13
en-affil=Department of Pathology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=14
en-affil=Department of Pathology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=15
en-affil=Department of Orthopedic Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=16
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=neurolymphomatosis
kn-keyword=neurolymphomatosis
en-keyword= neuro-oncology
kn-keyword= neuro-oncology
en-keyword=peripheral neuropathy
kn-keyword=peripheral neuropathy
en-keyword=peripheral nerve
kn-keyword=peripheral nerve
en-keyword=rheumatoid arthritis
kn-keyword=rheumatoid arthritis
en-keyword= T-cell lymphoma
kn-keyword= T-cell lymphoma
END
start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=1
article-no=
start-page=10956
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190729
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=In vivo direct reprogramming of glial linage to mature neurons after cerebral ischemia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= The therapeutic effect of in vivo direct reprogramming on ischemic stroke has not been evaluated. In the present study, a retroviral solution (1.5-2.0?×?107 /ul) of mock pMX-GFP (n?=?13) or pMX-Ascl1/Sox2/NeuroD1 (ASN) (n?=?14) was directly injected into the ipsilateral striatum and cortex 3 days after 30?min of transient cerebral ischemia. The reprogrammed cells first expressed neuronal progenitor marker Dcx 7 and 21 days after viral injection, then expressed mature neuronal marker NeuN. This was accompanied by morphological changes, including long processes and synapse-like structures, 49 days after viral injection. Meanwhile, therapeutic improvement was not detected both in clinical scores or infarct volume. The present study provides a future novel self-repair strategy for ischemic stroke with beneficial modifications of the inducer-suppressor balance.
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=ShangJingwei
en-aut-sei=Shang
en-aut-mei=Jingwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
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=4
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=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=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
affil-num=1
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=2
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=3
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=4
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=5
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=6
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=7
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=8
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=9
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END
start-ver=1.4
cd-journal=joma
no-vol=68
cd-vols=
no-issue=4
article-no=
start-page=1667
end-page=1675
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190423
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Acute Anti-Inflammatory Markers ITIH4 and AHSG in Mice Brain of a Novel Alzheimer's Disease Model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Alzheimer's disease (AD) is the most common dementia and a progressive neurodegenerative disorder aggravated by chronic hypoperfusion (HP). Since numerous evidence suggests that inflammation is related with AD pathology, we investigated the expression change of two anti-inflammatory markers, inter-alpha-trypsin inhibitor heavy chain H4 (ITIH4) and alpha-2-HS-glycoprotein (AHSG), in a novel AD model (APP23) with HP at 12 month of age. As compared with wild type (WT, n?=?10), immunohistochemical analysis showed a higher ITIH4 and a lower AHSG expressions in the cerebral cortex, hippocampus, and thalamus of the APP23?+?HP group (n?=?12) than the simple APP23 (n?=?10) group (*p?0.05 and **p?0.01 versus WT; #p?0.05 and # #p?0.01 versus APP23). The present study provides an upregulation of anti-inflammatory ITIH4 and a downregulation of pro-inflammatory TNFα-dependent AHSG in a novel AD plus HP mice model.
en-copyright=
kn-copyright=
en-aut-name=ShiXiaowen
en-aut-sei=Shi
en-aut-mei=Xiaowen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=LiuXia
en-aut-sei=Liu
en-aut-mei=Xia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=ShangJingwei
en-aut-sei=Shang
en-aut-mei=Jingwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=5
ORCID=
en-aut-name=FengTian
en-aut-sei=Feng
en-aut-mei=Tian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=HuangYong
en-aut-sei=Huang
en-aut-mei=Yong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=山下徹
kn-aut-sei=山下
kn-aut-mei=徹
aut-affil-num=11
ORCID=
en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
affil-num=1
en-affil=Department of Neurology, 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=
en-keyword=AHSG
kn-keyword=AHSG
en-keyword=APP23 mice
kn-keyword=APP23 mice
en-keyword=ITIH4
kn-keyword=ITIH4
en-keyword=alzheimer’s disease
kn-keyword=alzheimer’s disease
en-keyword=hypoperfusion
kn-keyword=hypoperfusion
en-keyword=inflammation
kn-keyword=inflammation
END
start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=3
article-no=
start-page=132
end-page=135
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2018
dt-pub=20181228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Multi‐modal combination therapy rescued a frequent ischemic stroke patient due to giant cell arteritis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ischemic stroke (IS) due to giant cell arteritis (GCA) is rare, but highly mortal. Here, we report a 72-year-old man who showed frequent IS with GCA. Initial therapy with prednisolone increased the frequency of IS, which disappeared after continuous multi-modal combination therapy with corticosteroids, immunosuppressive agents, antiplatelets, and statin. The present case was discharged with independent walk, suggesting that a multi-modal combination therapy rescued the GCA patient from frequent IS.
en-copyright=
kn-copyright=
en-aut-name=TakahashiYoshiaki
en-aut-sei=Takahashi
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=MatsumotoNamiko
en-aut-sei=Matsumoto
en-aut-mei=Namiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=KawaharaYuko
en-aut-sei=Kawahara
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=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=ShangJingwei
en-aut-sei=Shang
en-aut-mei=Jingwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
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=11
ORCID=
affil-num=1
en-affil=Departments of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=2
en-affil=Departments of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=3
en-affil=Departments of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=4
en-affil=Departments of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=5
en-affil=Departments of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=6
en-affil=Departments of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=7
en-affil=Departments of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=8
en-affil=Departments of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=9
en-affil=Departments of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=10
en-affil=Departments of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
affil-num=11
en-affil=Departments of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
en-keyword=combination therapy
kn-keyword=combination therapy
en-keyword=contrast-enhanced magnetic resonance imaging
kn-keyword=contrast-enhanced magnetic resonance imaging
en-keyword=frequent ischemic stroke
kn-keyword=frequent ischemic stroke
en-keyword=giant cell arteritis
kn-keyword=giant cell arteritis
en-keyword=temporal artery biopsy
kn-keyword=temporal artery biopsy
END
start-ver=1.4
cd-journal=joma
no-vol=28
cd-vols=
no-issue=10
article-no=
start-page=104310
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20191031
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Twendee X Ameliorates Phosphorylated Tau, α-Synuclein and Neurovascular Dysfunction in Alzheimer's Disease Transgenic Mice With Chronic Cerebral Hypoperfusion
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=BACKGROUND:
The pathological impact of chronic cerebral hypoperfusion (CCH) on Alzheimer's disease (AD) is still poorly understood. In the present study, we investigated the role of CCH on an AD mouse model in phosphorylated tau and α-synuclein pathology, neurovascular unit, cerebrovascular remodeling, and neurovascular trophic coupling. Moreover, examined protective effect of a new antioxidant Twendee X (TwX).
METHODS:
APP23 mice were implanted to bilateral common carotid arteries stenosis with ameroid constrictors to gradually decrease the cerebral blood flow. The effects of the administration of TwX were evaluated by immunohistochemical analysis and Immunofluorescent histochemistry.
RESULTS:
The present study revealed that the expressions of phospho-tau and phospho-α-synuclein were significantly increased in the APP23?+?CCH mice group as compared with wild type and APP23 mice groups (*P < .05 and ??P < .01 versus WT; #P < .05 and ##P < .01 versus APP23). In addition, CCH significantly exacerbated MMP-9 activation relating to blood-brain barrier destruction (??P < .01 versus WT; #P < .05, and ##P < .01 versus APP23), enhanced neurovascular remodeling, and impaired a neurovascular trophic coupling in the vascular endothelial BDNF expression of the APP23?+?CCH group. TwX treatment (20 mg/kg/day, from 4.5 to 12 months) significantly reduced tau and α-synuclein pathologies, ameliorated neurovascular dysfunction compared with APP23?+?CCH group.
CONCLUSIONS:
Our findings indicate that administration of a new antioxidative mixture TwX substantially reduced the above neuropathologic abnormalities, suggesting a potential therapeutic benefit of TwX for AD with CCH.
en-copyright=
kn-copyright=
en-aut-name=LiuXia
en-aut-sei=Liu
en-aut-mei=Xia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=
en-aut-name=ShangJingwei
en-aut-sei=Shang
en-aut-mei=Jingwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=ShiXiaowen
en-aut-sei=Shi
en-aut-mei=Xiaowen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=
en-aut-name=HuangYong
en-aut-sei=Huang
en-aut-mei=Yong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
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=
en-keyword=APP23 mice
kn-keyword=APP23 mice
en-keyword=Alzheimer's disease
kn-keyword=Alzheimer's disease
en-keyword=chronic cerebral hypoperfusion
kn-keyword=chronic cerebral hypoperfusion
en-keyword=neurovascular dysfunction
kn-keyword=neurovascular dysfunction
en-keyword=phosphorylated tau
kn-keyword=phosphorylated tau
en-keyword=α-synuclein
kn-keyword=α-synuclein
END
start-ver=1.4
cd-journal=joma
no-vol=28
cd-vols=
no-issue=7
article-no=
start-page=1993
end-page=2002
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190731
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical and Pathological Benefit of Twendee X in Alzheimer's Disease Transgenic Mice with Chronic Cerebral Hypoperfusion
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=BACKGROUND:
Multiple pathogeneses are involved in Alzheimer's disease (AD), such as amyloid-β accumulation, neuroinflammation, and oxidative stress. The pathological impact of chronic cerebral hypoperfusion on Alzheimer's disease is still poorly understood.
METHODS:
APP23 mice were implanted to bilateral common carotid arteries stenosis with ameroid constrictors for slowly progressive chronic cerebral hypoperfusion (CCH). The effects of the administration of Twendee X (TwX) were evaluated by behavioral analysis, immunohistochemical analysis, and immunofluorescent histochemistry.
RESULTS:
In the present study, chronic cerebral hypoperfusion, which is commonly found in aged Alzheimer's disease, significantly exacerbated motor dysfunction of APP23 mice from 5 months and cognitive deficit from 8 months of age, as well as neuronal loss, extracellular amyloid-β plaque and intracellular oligomer formations, and amyloid angiopathy at 12 months. Severe upregulations of oxidative markers and inflammatory markers were found in the cerebral cortex, hippocampus, and thalamus at 12 months. Twendee X treatment (20 mg/kg/d, from 4.5 to 12 months) substantially rescued the cognitive deficit and reduced the above amyloid-β pathology and neuronal loss, alleviated neuroinflammation and oxidative stress.
CONCLUSIONS:
The present findings suggested a potential therapeutic benefit of Twendee X for Alzheimer's disease with chronic cerebral hypoperfusion.
en-copyright=
kn-copyright=
en-aut-name=LiuXia
en-aut-sei=Liu
en-aut-mei=Xia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=
en-aut-name=ShangJingwei
en-aut-sei=Shang
en-aut-mei=Jingwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=ShiXiaowen
en-aut-sei=Shi
en-aut-mei=Xiaowen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=
en-aut-name=HuangYong
en-aut-sei=Huang
en-aut-mei=Yong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
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, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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=
en-keyword=APP23 mice
kn-keyword=APP23 mice
en-keyword=Alzheimer's disease
kn-keyword=Alzheimer's disease
en-keyword=anti-inflammatory
kn-keyword=anti-inflammatory
en-keyword=antioxidative
kn-keyword=antioxidative
en-keyword=chronic cerebral hypoperfusion
kn-keyword=chronic cerebral hypoperfusion
END
start-ver=1.4
cd-journal=joma
no-vol=400
cd-vols=
no-issue=
article-no=
start-page=145
end-page=147
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190515
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A unique Japanese CPEO family with a novel homozygous m.14819?T?>?G (p. S25A) substitution
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=
en-aut-name=NomuraEmi
en-aut-sei=Nomura
en-aut-mei=Emi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=TadokoroKoh
en-aut-sei=Tadokoro
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=SasakiRyo
en-aut-sei=Sasaki
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=TakahashiYoshiaki
en-aut-sei=Takahashi
en-aut-mei=Yoshiaki
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=TakemotoMami
en-aut-sei=Takemoto
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=GotoYu-ichi
en-aut-sei=Goto
en-aut-mei=Yu-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
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=Medical Genome Center (MGC), Department of Mental Retardation and Birth Defect Research, National Institute of Neuroscience (NIN), National Center of Neurology and Psychiatry
kn-affil=
affil-num=11
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=CPEO
kn-keyword=CPEO
en-keyword=Homozygous
kn-keyword=Homozygous
en-keyword=Mitochondrial DNA
kn-keyword=Mitochondrial DNA
END
start-ver=1.4
cd-journal=joma
no-vol=92
cd-vols=
no-issue=1
article-no=
start-page=46
end-page=53
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=201401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Reducing Hemorrhagic Complication by Dabigatran Via Neurovascular Protection After Recanalization With Tissue Plasminogen Activator in Ischemic Stroke of Rat
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This study assesses the risks and benefits of tissue plasminogen activator (tPA) treatment under oral anticoagulation with dabigatran compared with warfarin or vehicle control in transient middle cerebral artery occlusion (tMCAO). After pretreatment with warfarin (0.2 mg/kg/day), dabigatran (20 mg/kg/day), or vehicle (0.5% carboxymethyl cellulose sodium salt) for 7 days, tMCAO was induced for 120 min, followed by reperfusion and tPA (10 mg/kg/10 ml). Clinical parameters, including cerebral infarction volume, hemorrhagic volume, and blood coagulation, were examined. At 24 hr after reperfusion, markers for the neurovascular unit at the peri-ischemic lesion were immunohistochemically examined in brain sections, and MMP-9 activity was measured by zymography. Paraparesis and intracerebral hemorrhage volume were significantly improved in the dabigatran-pretreated group compared with the warfarin-pretreated group. A marked dissociation between astrocyte foot processes and the basal lamina or pericyte was observed in the warfarin-pretreated group, which was greatly improved in the dabigatran-pretreated group. Furthermore, a remarkable activation of MMP-9 in the ipsilateral warfarin-pretreated rat brain was greatly reduced in dabigatran-pretreated rats. The present study reveals that the mechanism of intracerebral hemorrhage with warfarin-pretreatment plus tPA in ischemic stroke rats is the dissociation of the neurovascular unit, including the pericyte. Neurovascular protection by dabigatran, which was first shown in this study, could partially explain the reduction in hemorrhagic complication by dabigatran reported from clinical study.
en-copyright=
kn-copyright=
en-aut-name=KonoSyoichiro
en-aut-sei=Kono
en-aut-mei=Syoichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=
en-aut-name=OmoteYoshio
en-aut-sei=Omote
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=5
ORCID=
en-aut-name=KurataTomoko
en-aut-sei=Kurata
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
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=8
ORCID=
affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol
affil-num=2
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol
affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol
affil-num=4
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol
affil-num=5
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol
affil-num=6
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol
affil-num=7
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol
affil-num=8
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol
en-keyword=dabigatran
kn-keyword=dabigatran
en-keyword=hemorrhagic complication
kn-keyword=hemorrhagic complication
en-keyword=neurovascular unit
kn-keyword=neurovascular unit
en-keyword=pericyte
kn-keyword=pericyte
en-keyword=thrombolysis
kn-keyword=thrombolysis
en-keyword=tPA
kn-keyword=tPA
END
start-ver=1.4
cd-journal=joma
no-vol=43
cd-vols=
no-issue=6
article-no=
start-page=1639
end-page=1646
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=201206
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical and Pathological Improvement in Stroke-Prone Spontaneous Hypertensive Rats Related to the Pleiotropic Effect of Cilostazol
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background and Purpose-Cerebral infarction is a major cause of death or decreasing activities of daily living. This study aimed to investigate the efficacy of commonly used antiplatelet drugs on stroke and motor and cognitive functions in relation to oxidative stress markers and insulin-like growth factor 1 receptor (IGF-1R).
Methods-Stroke-prone spontaneously hypertensive rats were treated with vehicle, aspirin, clopidogrel, and cilostazol from 8 to 10 weeks of age. Physiological parameters, regional cerebral blood flow, and serum lipids were examined. Motor and cognitive functions were evaluated weekly by the Rotorod and water maze task. Spontaneous infarct volume, oxidative stress markers for lipid, protein, and DNA at the ischemic boundary zone of spontaneous infarction, and the IGF-1R-positive cell ratio in the hippocampus were immunohistochemically examined in brain sections. IGF-1R beta expression in the hippocampus was assessed by Western blotting.
Results-The antiplatelet drugs, cilostazol and clopidogrel, reduced the spontaneous infarct volume more than aspirin. Only cilostazol improved motor and cognitive functions with a significant increase (P<0.05) in the memory-related IGF-1R-positive ratio and IGF-1R beta expression in the hippocampus. Cilostazol reduced the 4 oxidative stress markers in affected neurons in stroke-prone spontaneously hypertensive rats regardless of blood pressure, regional cerebral blood flow, or serum lipid levels.
Conclusions-The present results suggest that a possible pleiotropic effect of cilostazol resulted in the reduction of spontaneous infarct volume and preservation of motor and spatial cognitive functions. The increase of IGF-1R-positive cells in the hippocampal CA1 region could partly explain the preservation of spatial cognitive function in stroke-prone spontaneously hypertensive rats.
en-copyright=
kn-copyright=
en-aut-name=OmoteYoshio
en-aut-sei=Omote
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=
en-aut-name=TianFengFeng
en-aut-sei=Tian
en-aut-mei=FengFeng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=KawaiHiromi
en-aut-sei=Kawai
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=KurataTomoko
en-aut-sei=Kurata
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=
en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=
affil-num=1
en-affil=
kn-affil=Okayama Univ, Dept Neurol, Grad Sch Med Dent & Pharmaceut Sci
affil-num=2
en-affil=
kn-affil=Okayama Univ, Dept Neurol, Grad Sch Med Dent & Pharmaceut Sci
affil-num=3
en-affil=
kn-affil=Okayama Univ, Dept Neurol, Grad Sch Med Dent & Pharmaceut Sci
affil-num=4
en-affil=
kn-affil=Okayama Univ, Dept Neurol, Grad Sch Med Dent & Pharmaceut Sci
affil-num=5
en-affil=
kn-affil=Okayama Univ, Dept Neurol, Grad Sch Med Dent & Pharmaceut Sci
affil-num=6
en-affil=
kn-affil=Okayama Univ, Dept Neurol, Grad Sch Med Dent & Pharmaceut Sci
affil-num=7
en-affil=
kn-affil=Okayama Univ, Dept Neurol, Grad Sch Med Dent & Pharmaceut Sci
affil-num=8
en-affil=
kn-affil=Okayama Univ, Dept Neurol, Grad Sch Med Dent & Pharmaceut Sci
en-keyword=cerebral infarction
kn-keyword=cerebral infarction
en-keyword=cilostazol
kn-keyword=cilostazol
en-keyword=IGF-1R
kn-keyword=IGF-1R
en-keyword=oxidative stress
kn-keyword=oxidative stress
en-keyword=SHR-SP
kn-keyword=SHR-SP
END
start-ver=1.4
cd-journal=joma
no-vol=221
cd-vols=
no-issue=
article-no=
start-page=47
end-page=55
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20120927
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Strong neuroprotection with a novel platinum nanoparticle against ischemic stroke- andtissue plasminogen activator-related brain damages in mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Reactive oxygen species (ROS) are major exacerbation factor in acute ischemic stroke, and thrombolytic agent tissue plasminogen activator (tPA) may worsen motor function and cerebral infarcts. The platinum nanoparticle (nPt) is a novel ROS scavenger, and thus we examined the clinical and neuroprotective effects of nPt in ischemic mouse brains. Mice were subjected to transient middle cerebral artery occlusion (tMCAO) for 60 min and divided into the following four groups by intravenous administration upon reperfusion, vehicle, tPA, tPA + nPt, and nPt. At 48 h after tMCAO, motor function, infarct volume, immunohistochemical analyses of neurovascular unit (NVU), in vivo imaging of matrix metalloproteinase (MMP), and zymography for MMP-9 activity were examined. Superoxide anion generation at 2 h after tMCAO was also examined with hydroethidine (HEt). As a result, administration of tPA deteriorated the motor function and infarct volume as compared to vehicle. In vivo optical imaging of MMP showed strong fluorescent signals in affected regions of tMCAO groups. Immunohistochemical analyses revealed that tMCAO resulted in a minimal decrease of NAGO and occludin, but a great decrease of collagen IV and a remarkable increase of MMP-9. HEt stain showed increased ROS generation by tMCAO. All these results became pronounced with tPA administration, and were greatly reduced by nPt. The present study demonstrates that nPt treatment ameliorates neurological function and brain damage in acute cerebral infarction with neuroprotective effect on NVU and inactivation of MMP-9. The strong reduction of ROS production by nPt could account for these remarkable neurological and neuroprotective effects against ischemic stroke.
en-copyright=
kn-copyright=
en-aut-name=TakamiyaM.
en-aut-sei=Takamiya
en-aut-mei=M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=MiyamotoY.
en-aut-sei=Miyamoto
en-aut-mei=Y.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=YamashitaT.
en-aut-sei=Yamashita
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=DeguchiK.
en-aut-sei=Deguchi
en-aut-mei=K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=OhtaY.
en-aut-sei=Ohta
en-aut-mei=Y.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=AbeK.
en-aut-sei=Abe
en-aut-mei=K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol
affil-num=2
en-affil=
kn-affil=Univ Tokyo, Grad Sch Frontier Sci, Dept Integrated Biosci
affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol
affil-num=4
en-affil=
kn-affil=
affil-num=5
en-affil=
kn-affil=
affil-num=6
en-affil=
kn-affil=
en-keyword=platinum nanoparticle
kn-keyword=platinum nanoparticle
en-keyword=cerebral ischemia
kn-keyword=cerebral ischemia
en-keyword=free radical scavenger
kn-keyword=free radical scavenger
en-keyword=neuroprotection
kn-keyword=neuroprotection
en-keyword=matrix metalloproteinase-9
kn-keyword=matrix metalloproteinase-9
en-keyword=tissue plasminogen activator
kn-keyword=tissue plasminogen activator
END