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  1. Article: [Immunotherapy for Inflammatory Myopathies].

    Honda, Masaya

    Brain and nerve = Shinkei kenkyu no shinpo

    2021  Volume 73, Issue 2, Page(s) 161–169

    Abstract: Inflammatory myopathies are heterogeneous disorders characterized by muscle inflammation. They are frequently accompanied by extra-muscular manifestations that affect the skin, lungs, heart, and joints. Owing to its low prevalence, wide phenotypic ... ...

    Abstract Inflammatory myopathies are heterogeneous disorders characterized by muscle inflammation. They are frequently accompanied by extra-muscular manifestations that affect the skin, lungs, heart, and joints. Owing to its low prevalence, wide phenotypic heterogeneity, and variable disease course, it is difficult to make clear recommendations for the treatment of inflammatory myopathies. Corticosteroids are administered as first-line treatment based on clinical experience rather than controlled trial findings. Empirically, addition of an immunosuppressive drug might offer a steroid-sparing effect or an additional benefit. Administration of intravenous immunoglobulins has been shown to be effective as second-line treatment. Recently, there has been a growing interest in assessing the potential of several biological agents in the treatment of inflammatory myopathies. There are multiple ongoing clinical trials that will lead to more treatment options for inflammatory myopathies.
    MeSH term(s) Adrenal Cortex Hormones ; Humans ; Immunoglobulins, Intravenous/therapeutic use ; Immunosuppressive Agents/therapeutic use ; Immunotherapy ; Myositis/drug therapy
    Chemical Substances Adrenal Cortex Hormones ; Immunoglobulins, Intravenous ; Immunosuppressive Agents
    Language Japanese
    Publishing date 2021-02-02
    Publishing country Japan
    Document type Journal Article
    ZDB-ID 390389-8
    ISSN 1344-8129 ; 1881-6096 ; 0006-8969
    ISSN (online) 1344-8129
    ISSN 1881-6096 ; 0006-8969
    DOI 10.11477/mf.1416201728
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: [Peripheral Neuropathy and Myopathy Associated with COVID-19].

    Honda, Masaya / Kanda, Takashi

    Brain and nerve = Shinkei kenkyu no shinpo

    2022  Volume 74, Issue 7, Page(s) 867–871

    Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its associated coronavirus disease (COVID-19) were reported to originate from Wuhan, China, in December 2019, spreading rapidly worldwide. With the emergence of this pandemic, an increasing ...

    Abstract Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its associated coronavirus disease (COVID-19) were reported to originate from Wuhan, China, in December 2019, spreading rapidly worldwide. With the emergence of this pandemic, an increasing number of cases of Guillain-Barré syndrome (GBS) have been reported following this infection. Most patients had a demyelinating subtype of GBS. The time interval between infectious and neuropathic symptoms, absence of cerebrospinal fluid pleocytosis, and negative polymerase chain reaction test result support a postinfectious mechanism. Skeletal muscle injury presents as muscle pain and elevated serum creatine kinase level in patients with COVID-19. Some patients developed several myopathic manifestations, including new-onset inflammatory myopathy. Muscle injury is caused by direct SARS-CoV-2 infection or through parainfectious mechanisms such as type I interferonopathy.
    MeSH term(s) COVID-19/complications ; Guillain-Barre Syndrome/diagnosis ; Guillain-Barre Syndrome/etiology ; Humans ; Myalgia/complications ; Pandemics ; SARS-CoV-2
    Language Japanese
    Publishing date 2022-07-20
    Publishing country Japan
    Document type Journal Article
    ZDB-ID 390389-8
    ISSN 1344-8129 ; 1881-6096 ; 0006-8969
    ISSN (online) 1344-8129
    ISSN 1881-6096 ; 0006-8969
    DOI 10.11477/mf.1416202140
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Contribution of Complement, Microangiopathy and Inflammation in Idiopathic Inflammatory Myopathies.

    Honda, Masaya / Shimizu, Fumitaka / Sato, Ryota / Nakamori, Masayuki

    Journal of neuromuscular diseases

    2023  Volume 11, Issue 1, Page(s) 5–16

    Abstract: Purpose of review: Idiopathic inflammatory myopathies (IIMs) are a heterogeneous group characterized by muscle weakness and skin symptoms and are categorized into six subtypes: dermatomyositis (DM), polymyositis (PM), anti-synthetase syndrome (ASS), ... ...

    Abstract Purpose of review: Idiopathic inflammatory myopathies (IIMs) are a heterogeneous group characterized by muscle weakness and skin symptoms and are categorized into six subtypes: dermatomyositis (DM), polymyositis (PM), anti-synthetase syndrome (ASS), immune-mediated myopathy (IMNM), inclusion body myopathy (IBM), and overlap myositis. Myositis-specific autoantibodies were detected for the diagnosis and classification of IIM. This review highlights the pathogenic contributions of the complement system, microangiopathy, and inflammation in IIM.
    Recent findings: Deposition of complement around capillaries and/or the sarcolemma was observed in muscle biopsy specimens from patients with DM, ASS, and IMNM, suggesting the pathomechanism of complement-dependent muscle and endothelial cell injury. A recent study using human muscle microvascular endothelial cells showed that Jo-1 antibodies from ASS induce complement-dependent cellular cytotoxicity in vitro. Based on both clinical and pathological observations, antibody- and complement-mediated microangiopathy may contribute to the development of DM and anti-Jo-1 ASS. Juvenile DM is characterized by the loss of capillaries, perivascular inflammation, and small-vessel angiopathies, which may be related to microinfarction and perifascicular atrophy. Several serum biomarkers that reflect the IFN1 signature and microangiopathy are elevated in patients with DM. The pathological observation of myxovirus resistance protein A (MxA), which suggests a type 1 interferon (IFN1) signature in DM, supports the diagnosis and further understanding of the pathomechanism of IIM. A recent report showed that an increase in triggering receptor expressed on myeloid cells (TREM-1) around perimysial blood vessels and muscles in patients with IIM plays a role in triggering inflammation and promoting the migration of inflammatory cells by secreting proinflammatory cytokines, such as tumor necrosis factor α.
    Summary: The deposition of complement in muscles and capillaries is a characteristic feature of DM, ASS, and IMNM. Microangiopathy plays a pathogenic role in DM, possibly resulting in perifascicular atrophy. Further understanding of the detailed pathomechanism regarding complement, microangiopathy, and inflammation may lead to novel therapeutic approaches for IIM.
    MeSH term(s) Humans ; Capillaries/pathology ; Endothelial Cells/pathology ; Myositis/diagnosis ; Muscle, Skeletal/pathology ; Muscular Diseases/pathology ; Inflammation/pathology ; Atrophy/pathology
    Language English
    Publishing date 2023-12-16
    Publishing country Netherlands
    Document type Journal Article ; Review
    ISSN 2214-3602
    ISSN (online) 2214-3602
    DOI 10.3233/JND-230168
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Total synthesis of the cyclic pentapeptides PF1171B, D, E, and avellanins A, B, C with inhibitory activity against apolipoprotein B production

    Honda, Masaya / Inagaki, Minoru / Masuda, Yuichi

    Tetrahedron letters. 2021 Sept. 28, v. 81

    2021  

    Abstract: The total synthesis of PF1171B, D, and E, and avellanins A, B, and C, which are cyclic pentapeptides containing non-proteinogenic amino acid residues, was achieved by solid-phase peptide elongation and solution-phase macrolactamization. PF1171B and D and ...

    Abstract The total synthesis of PF1171B, D, and E, and avellanins A, B, and C, which are cyclic pentapeptides containing non-proteinogenic amino acid residues, was achieved by solid-phase peptide elongation and solution-phase macrolactamization. PF1171B and D and avellanins A and C were found to inhibit apolipoprotein B production in Hep G2 cells without exhibiting cytotoxicity. PF1171B had the most potent inhibitory activity against apolipoprotein B production. The synthesis and bioactivity evaluation of the enantiomer and a linear analog of PF1171B suggested its essential structural features.
    Keywords amino acids ; apolipoprotein B ; cytotoxicity ; enantiomers ; peptides
    Language English
    Dates of publication 2021-0928
    Publishing place Elsevier Ltd
    Document type Article
    ZDB-ID 204287-3
    ISSN 1873-3581 ; 0040-4039
    ISSN (online) 1873-3581
    ISSN 0040-4039
    DOI 10.1016/j.tetlet.2021.153340
    Database NAL-Catalogue (AGRICOLA)

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  5. Article: [A Patient Developing Guillain-Barré Syndrome After Receiving the BNT162b2 COVID-19 mRNA Vaccine].

    Oshibe, Namiko / Honda, Masaya / Koga, Michiaki / Sato, Ryota / Oishi, Mariko / Kanda, Takashi

    Brain and nerve = Shinkei kenkyu no shinpo

    2022  Volume 74, Issue 8, Page(s) 1025–1030

    Abstract: We report a 71-year-old woman who presented with paresthesia, progressive weakness, difficulty walking, diarrhea, and bladder dysfunction one week after she received the BNT162b2 COVID-19 vaccine. Her neurological signs and symptoms gradually worsened up ...

    Abstract We report a 71-year-old woman who presented with paresthesia, progressive weakness, difficulty walking, diarrhea, and bladder dysfunction one week after she received the BNT162b2 COVID-19 vaccine. Her neurological signs and symptoms gradually worsened up to 27 days after onset, after which her weakness slowly improved without immunotherapy. Analysis of serial cerebrospinal fluid specimens showed gradually increasing protein levels. Results of a nerve conduction study suggested functional axonal disturbance. The clinical findings together with the monophasic clinical course were consistent with Guillain-Barré syndrome. Her previous history was negative for symptomatic infection. Serological and bacterial tests, including the presence of anti-glycolipid antibodies, were negative for prior infection. Few cases have been reported on the development of Guillain-Barré syndrome after the BNT162b2 vaccine. Our patient's syndrome was characterized by atypical proximal weakness of the dominant lower limb. (Received January 28, 2022; Accepted April 4, 2022; Published August 1, 2022).
    MeSH term(s) Aged ; BNT162 Vaccine ; COVID-19/prevention & control ; COVID-19 Vaccines/adverse effects ; Female ; Guillain-Barre Syndrome/diagnosis ; Guillain-Barre Syndrome/etiology ; Humans ; RNA, Messenger ; Vaccines, Synthetic ; mRNA Vaccines
    Chemical Substances COVID-19 Vaccines ; RNA, Messenger ; Vaccines, Synthetic ; mRNA Vaccines ; BNT162 Vaccine (N38TVC63NU)
    Language Japanese
    Publishing date 2022-07-30
    Publishing country Japan
    Document type Case Reports ; Journal Article
    ZDB-ID 390389-8
    ISSN 1344-8129 ; 1881-6096 ; 0006-8969
    ISSN (online) 1344-8129
    ISSN 1881-6096 ; 0006-8969
    DOI 10.11477/mf.1416202173
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: [Intravenous immunoglobulin-induced eczematous eruption in autoimmune neuromuscular diseases].

    Hatake, Seira / Shimizu, Fumitaka / Honda, Masaya / Takahashi, Shiori / Koga, Michiaki / Kimura, Kazumi / Kanda, Takashi

    Rinsho shinkeigaku = Clinical neurology

    2022  Volume 62, Issue 4, Page(s) 267–271

    Abstract: Background: Intravenous immunoglobulin (IVIg) have been administrated for the long time in patients with several autoimmune neuromuscular diseases. Eczematous eruption has been described as IVIg-induced adverse effect.: Objective: The purpose of this ...

    Abstract Background: Intravenous immunoglobulin (IVIg) have been administrated for the long time in patients with several autoimmune neuromuscular diseases. Eczematous eruption has been described as IVIg-induced adverse effect.
    Objective: The purpose of this study is to clarify the incidence and characteristic of IVIg-induced eczematous eruption in autoimmune neuromuscular disease.
    Methods: We retrospectively collected the data from 92 patients with autoimmune neuromuscular diseases, including 35 patients with chronic inflammatory demyelinating polyneuropathy (CIDP), 8 patients with multifocal motor neuropathy (MMN), 25 patients with myositis, 15 patients with Guillain-Barré syndrome (GBS), and 9 patients with myasthenia gravis (MG), who have administrated IVIg in Yamaguchi University Hospital.
    Results: There are 10 patients (6 CIDP/4 MMN), who had an eczematous skin reaction after IVIg infusion. The frequencies of IVIg-induced eczematous eruption were significantly higher in patients with multifocal acquired demyelinating sensory and motor (MADSAM) and MMN than in patients with GBS, myositis, and MG. In addition, corticosteroids or immunosuppressive drugs had been administrated before IVIg treatment more frequently in patients with myositis and MG than in those with MADSAM and MMN.
    Conclusion: MADSAM or MMN patients had more frequently IVIg-induced eczematous eruption than other autoimmune neuromuscular diseases. Pathophysiology of MADAM and MMN is considered to be cell-mediated immunity against the peripheral nerve and the accumulation of IgG in both epidermis and dermis of the hand after IVIg may induce the infiltration of inflammatory cells around the vessels in the skin, causing eczematous eruption in MADSAM and MMN.
    MeSH term(s) Autoimmune Diseases/drug therapy ; Exanthema/drug therapy ; Guillain-Barre Syndrome/drug therapy ; Humans ; Immunoglobulins, Intravenous/adverse effects ; Myositis/drug therapy ; Neuromuscular Diseases/drug therapy ; Polyneuropathies/drug therapy ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/therapy ; Retrospective Studies
    Chemical Substances Immunoglobulins, Intravenous
    Language Japanese
    Publishing date 2022-03-29
    Publishing country Japan
    Document type Journal Article
    ZDB-ID 604200-4
    ISSN 1882-0654 ; 0009-918X
    ISSN (online) 1882-0654
    ISSN 0009-918X
    DOI 10.5692/clinicalneurol.cn-001681
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Jo-1 Antibodies From Myositis Induce Complement-Dependent Cytotoxicity and TREM-1 Upregulation in Muscle Endothelial Cells.

    Honda, Masaya / Shimizu, Fumitaka / Sato, Ryota / Mizukami, Yoichi / Watanabe, Kenji / Takeshita, Yukio / Maeda, Toshihiko / Koga, Michiaki / Kanda, Takashi

    Neurology(R) neuroimmunology & neuroinflammation

    2023  Volume 10, Issue 4

    Abstract: Background and objectives: Muscle microangiopathy due to dysfunction of endothelial cells because of inflammation is a critical hallmark of dermatomyositis (DM); however, its pathomechanism remains unclear. The aim of this study was to evaluate the ... ...

    Abstract Background and objectives: Muscle microangiopathy due to dysfunction of endothelial cells because of inflammation is a critical hallmark of dermatomyositis (DM); however, its pathomechanism remains unclear. The aim of this study was to evaluate the effect of immunogloblin G (IgG) from patients with idiopathic inflammatory myopathies (IIM) on muscle endothelial cells in vitro.
    Methods: Using a high-content imaging system, we analyzed whether IgG purified from sera from patients with IIM (n = 15), disease controls (DCs: n = 7), and healthy controls (HCs: n = 7) can bind to muscle endothelial cells and induce complement-dependent cellular cytotoxicity.
    Results: IgGs from Jo-1 antibody myositis could bind to muscle endothelial cells and caused complement-dependent cell cytotoxicity. RNA-seq demonstrated the upregulation of genes associated with tumor necrosis factor (TNF)-α, triggering receptor expressed on myeloid cells-1 (TREM-1), CD25, and mitochondria pathways after exposure to IgG from the Jo-1, signal recognition particle (SRP), and polymyositis (PM) groups. The high-content imaging system showed that TREM-1 expression in the Jo-1, SRP, and PM groups was increased in comparison with DCs and HCs and that the TNF-α expression in the Jo-1 group was higher in comparison with the SRP, PM, DC, and HC groups. The expression of TREM-1 was observed in biopsied capillaries and the muscle membrane from patients with Jo-1 and in biopsied muscle fiber and capillaries from patients with DM and SRP. The depletion of Jo-1 antibodies by IgG of patients with Jo-1 antibody myositis reduced the Jo-1 antibody-induced complement-dependent cellular cytotoxicity in muscle endothelial cells.
    Discussion: Jo-1 antibodies from Jo-1 antibody myositis show complement-dependent cellular cytotoxicity in muscle endothelial cells. IgGs from patients with Jo-1, SRP, and DM increase the TREM-1 expression in endothelial cells and muscles.
    MeSH term(s) Humans ; Triggering Receptor Expressed on Myeloid Cells-1 ; Endothelial Cells ; Up-Regulation ; Myositis ; Polymyositis ; Muscles/pathology ; Immunoglobulin G
    Chemical Substances Jo-1 antibody ; Triggering Receptor Expressed on Myeloid Cells-1 ; Immunoglobulin G
    Language English
    Publishing date 2023-05-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2767740-0
    ISSN 2332-7812 ; 2332-7812
    ISSN (online) 2332-7812
    ISSN 2332-7812
    DOI 10.1212/NXI.0000000000200116
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: [Neuropathy presenting conduction block in ANCA-negative eosinophilic granulomatosis with polyangiitis].

    Honda, Masaya / Takeshita, Yukio / Koga, Michiaki / Sato, Ryota / Omoto, Masatoshi / Kanda, Takashi

    Rinsho shinkeigaku = Clinical neurology

    2021  Volume 61, Issue 9, Page(s) 613–617

    Abstract: A 74-year-old woman with a history of asthma and allergic rhinitis rapidly developed multiple mononeuropathy. Although anti-neutrophil cytoplasmic antibodies were negative, the presence of eosinophilia and eosinophilic infiltrations in the sural nerve ... ...

    Abstract A 74-year-old woman with a history of asthma and allergic rhinitis rapidly developed multiple mononeuropathy. Although anti-neutrophil cytoplasmic antibodies were negative, the presence of eosinophilia and eosinophilic infiltrations in the sural nerve led to a diagnosis of eosinophilic granulomatosis with polyangiitis. A motor nerve conduction study on admission revealed conduction block, which promptly disappeared after initiating immunotherapy without findings suggestive for remyelination or axonal degeneration. This electrophysiological change distinct from that of Wallerian degeneration. A biopsy of the sural nerve showed many eosinophil infiltrations and degranulation of eosinophilic cationic protein within nerve fascicles, whereas findings of necrotizing vasculitis were absent. These findings suggest that a direct effect of eosinophilic cationic protein, rather than ischemic damage due to vasculitis, was the main mechanism of transient nerve conduction failure in this patient.
    MeSH term(s) Aged ; Antibodies, Antineutrophil Cytoplasmic ; Churg-Strauss Syndrome/complications ; Churg-Strauss Syndrome/diagnosis ; Granulomatosis with Polyangiitis/complications ; Granulomatosis with Polyangiitis/diagnosis ; Humans
    Chemical Substances Antibodies, Antineutrophil Cytoplasmic
    Language Japanese
    Publishing date 2021-08-26
    Publishing country Japan
    Document type Case Reports ; Journal Article
    ZDB-ID 604200-4
    ISSN 1882-0654 ; 0009-918X
    ISSN (online) 1882-0654
    ISSN 0009-918X
    DOI 10.5692/clinicalneurol.cn-001564
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: [A case of Hashimoto's encephalopathy successfully treated with cyclophosphamide pulse therapy].

    Matsuo, Kinya / Koga, Michiaki / Honda, Masaya / Kanda, Takashi

    Rinsho shinkeigaku = Clinical neurology

    2018  Volume 58, Issue 6, Page(s) 390–394

    Abstract: Hashimoto's encephalopathy has been described as an autoimmune disorder which demonstrates favorable response to corticosteroid therapy. However, steroid-resistant cases which require additional treatment are frequently reported, and there is no ... ...

    Abstract Hashimoto's encephalopathy has been described as an autoimmune disorder which demonstrates favorable response to corticosteroid therapy. However, steroid-resistant cases which require additional treatment are frequently reported, and there is no consensus how such cases should be treated. We present a 69 years-old man, who progressed cognitive dysfunction in the past three months. Anti-thyroid and anti-NH
    MeSH term(s) Aged ; Autoantibodies/blood ; Biomarkers/blood ; Cyclophosphamide/administration & dosage ; Drug Resistance ; Drug Therapy, Combination ; Encephalitis/diagnosis ; Encephalitis/drug therapy ; Hashimoto Disease/diagnosis ; Hashimoto Disease/drug therapy ; Humans ; Male ; Methylprednisolone/administration & dosage ; Prednisolone/administration & dosage ; Pulse Therapy, Drug ; Treatment Outcome ; Ubiquitin-Activating Enzymes/immunology
    Chemical Substances Autoantibodies ; Biomarkers ; Cyclophosphamide (8N3DW7272P) ; Prednisolone (9PHQ9Y1OLM) ; Ubiquitin-Activating Enzymes (EC 6.2.1.45) ; NAE protein, human (EC 6.3.2.-) ; Methylprednisolone (X4W7ZR7023)
    Language Japanese
    Publishing date 2018-06-01
    Publishing country Japan
    Document type Case Reports ; Journal Article
    ZDB-ID 604200-4
    ISSN 1882-0654 ; 0009-918X
    ISSN (online) 1882-0654
    ISSN 0009-918X
    DOI 10.5692/clinicalneurol.cn-001169
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: A Japanese Patient with Hereditary Myopathy with Early Respiratory Failure Due to the p.P31732L Mutation of Titin.

    Sano, Yasuteru / Ota, Satoko / Oishi, Mariko / Honda, Masaya / Omoto, Masatoshi / Kawai, Motoharu / Okubo, Mariko / Nishino, Ichizo / Kanda, Takashi

    Internal medicine (Tokyo, Japan)

    2021  Volume 61, Issue 10, Page(s) 1587–1592

    Abstract: Hereditary myopathy with early respiratory failure (HMERF) is caused by titin A-band mutations in exon 344 and is considered quite rare. Respiratory insufficiency can be the sole symptom in the disease course. We herein report the first Japanese HMERF ... ...

    Abstract Hereditary myopathy with early respiratory failure (HMERF) is caused by titin A-band mutations in exon 344 and is considered quite rare. Respiratory insufficiency can be the sole symptom in the disease course. We herein report the first Japanese HMERF patient with a p.P31732L mutation in titin. The patient manifested respiratory failure and mild weakness of the neck flexor muscle at 69 years old and showed fatty replacement of the bilateral semitendinosus muscles on muscle imaging. Our case indicates that HMERF with a heterozygous p.P31732L mutation should be included in the differential diagnosis of muscular diseases presenting with early respiratory failure.
    MeSH term(s) Aged ; Connectin/genetics ; Genetic Diseases, Inborn ; Humans ; Japan ; Muscle, Skeletal ; Muscular Diseases/complications ; Muscular Diseases/diagnostic imaging ; Muscular Diseases/genetics ; Mutation/genetics ; Respiratory Insufficiency/diagnosis ; Respiratory Insufficiency/genetics
    Chemical Substances Connectin ; TTN protein, human
    Language English
    Publishing date 2021-10-19
    Publishing country Japan
    Document type Journal Article
    ZDB-ID 32371-8
    ISSN 1349-7235 ; 0021-5120 ; 0918-2918
    ISSN (online) 1349-7235
    ISSN 0021-5120 ; 0918-2918
    DOI 10.2169/internalmedicine.7733-21
    Database MEDical Literature Analysis and Retrieval System OnLINE

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