2026/04/10 更新

写真a

イシバザワ エミ
石羽澤 映美
ISHIBAZAWA Emi
所属
病院 診療科 小児科
外部リンク

論文

  • The usefulness of parametric mapping in a patient with juvenile systemic sclerosis

    Hideharu Oka, Masayuki Sato, Keita Ito, Emi Ishibazawa, Tsunehisa Nagamori, Kouichi Nakau, Satoru Takahashi

    Pediatrics International   66 ( 1 )   2024年1月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:Wiley  

    DOI: 10.1111/ped.15825

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  • A novel scoring system for the prediction of disease severity in STEC‐HUS 査読

    Emi Ishibazawa, Tsunehisa Nagamori, Mio June Kurisawa, Masayuki Sato, Yoichiro Yoshida, Hironori Takahashi, Hiromi Manabe, Toru Ishioka, Yurika Miura, Hiroki Kajino, Yasuto Suzuki, Soichiro Wada, Shigetoshi Ogiwara, Yuji Tomii, Hayato Aoyagi, Kazushige Nagai, Hiroyuki Naito, Satoru Takahashi

    Pediatrics International   66 ( 1 )   2024年1月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Wiley  

    Abstract

    Background

    Shiga toxin‐producing Escherichia coli ‐associated hemolytic uremic syndrome (STEC‐HUS) is a life‐threatening condition complicated by acute kidney injury, acute respiratory distress syndrome, and central nervous system disorders. The early identification of high‐risk patients is required to facilitate timely and appropriate treatment.

    Methods

    The medical records of patients with STEC‐HUS treated at 11 hospitals in Hokkaido, Japan, were reviewed retrospectively. A multi‐institutional retrospective analysis was performed in which patients were divided into two groups according to the presence or absence of severe complications requiring blood purification therapy or encephalopathy. We compared the laboratory values at diagnosis between the severe and mild groups. To identify patients at high risk of developing severe complications, a scoring system, referred to as the “STEC‐HUS severity (STEC‐HUSS) score,” was constructed based on the parameters showing significant differences.

    Results

    Of the 41 patients with STEC‐HUS, 11 were classified into the severe group and 30 into the mild group. Significant differences were observed between the groups in terms of white blood cell count, activated partial thromboplastin time, fibrinogen, D ‐dimer, total protein, aspartate transaminase, alanine transaminase, lactate dehydrogenase, creatinine, and C‐reactive protein levels. The STEC‐HUSS score was calculated on a scale of 0–10 by summing the number of test items that demonstrated abnormal values. The STEC‐HUSS score, when the cut‐off value was 4, showed a sensitivity of 100% and a specificity of 91% in the severe group.

    Conclusion

    We developed a novel scoring system to identify patients at high risk of severe STEC‐HUS.

    DOI: 10.1111/ped.15833

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  • Demonstration of equivocal anti-glomerular basement membrane antibody positivity as a non-specific reaction through multiple immunologic assays in a case of pediatric asymptomatic hematuria

    Masayuki Sato, Yuka Nishibata, Sakiko Masuda, Tsunehisa Nagamori, Emi Ishibazawa, Yoichiro Yoshida, Hironori Takahashi, Akihiro Ishizu, Satoru Takahashi

    Clinical Biochemistry   120   110650 - 110650   2023年10月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:Elsevier BV  

    DOI: 10.1016/j.clinbiochem.2023.110650

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  • A Continuous Increase in CXC-Motif Chemokine Ligand 10 in a Case of Anti-Nuclear Matrix Protein-2-Positive Juvenile Dermatomyositis

    Tsunehisa Nagamori, Emi Ishibazawa, Yoichiro Yoshida, Kengo Izumi, Masayuki Sato, Yuki Ichimura, Naoko Okiyama, Ichizo Nishino, Hiroshi Azuma

    Journal of Medical Cases   13 ( 6 )   290 - 296   2022年6月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:Elmer Press, Inc.  

    DOI: 10.14740/jmc3940

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  • Variations in the pathophysiology of respiratory syncytial virus infection depend on the age at onset

    Tsunehisa Nagamori, Youichiro Yoshida, Emi Ishibazawa, Hideharu Oka, Hironori Takahashi, Hiromi Manabe, Genya Taketazu, Masaru Shirai, Hiroshi Sakata, Junichi Oki, Hiroshi Azuma

    Pediatrics International   64 ( 1 )   2022年1月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:Wiley  

    Abstract

    Background

    Lower respiratory tract infections due to respiratory syncytial virus are associated with morbidity and mortality in infants and children. Thus precise elucidation of respiratory syncytial virus lower respiratory tract infection pathophysiology is important.

    Methods

    Medical records of hospitalized patients were reviewed. Patients were divided into three groups. Group I: patients who improved without oxygen supply. Group II: patients who received oxygen supply, but not nasal high‐flow cannula therapy. Group III: patients who received nasal high‐flow cannula. Patients were also divided by age group into the <6 months and ≥6 months groups. Parameters for differentiating the severity among groups were then evaluated. Further, serum concentration of high‐mobility group box‐1 and several cytokines (Inerleukin‐6, soluble tumor necrosis factor receptor‐1/2, Interleukin‐18, Interferon‐gamma responsive protein‐100) were evaluated.

    Results

    One hundred eighty‐nine were enrolled. An analysis of variance for those <6 months showed overall differences including younger age, lower pH, and increased partial pressure of carbon dioxide (pCO2), bicarbonate (HCO3‐), and base excess at the time of admission. On the other hand, analysis of variance for ≥6 months revealed that, in addition to a lower pH and increased pCO2, patients showed differences including decreased serum total protein and albumin, and increased aspartate aminotransferase (AST), alanin aminotransferase (ALT), lactate dehydrogenase (LDH), Ferritin and C‐reactive protein (CRP) levels. Further, evaluation of serum cytokines showed that IL‐6, s tumor necrotizing factor receptor‐1/2, and high‐mobility group box‐1 were higher in Group II/III among the ≥6 months age group, but not for those in the <6 months group.

    Conclusions

    The pathophysiology of severe respiratory syncytial virus lower respiratory tract infection varies according to the age at onset. In late infancy and childhood, a certain proportion of patients show a hyperinflammatory status.

    DOI: 10.1111/ped.14720

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    その他リンク: https://onlinelibrary.wiley.com/doi/full-xml/10.1111/ped.14720

  • A novel <i>STAT3</i> mutation associated with hyper immunoglobulin E syndrome with a paucity of connective tissue signs

    Yoichiro Yoshida, Tsunehisa Nagamori, Hironori Takahashi, Emi Ishibazawa, Sorachi Shimada, Toshinao Kawai, Hiroshi Azuma

    Pediatrics International   63 ( 5 )   510 - 515   2021年3月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:Wiley  

    Abstract

    Background

    A heterozygous mutation of STAT3 causes autosomal dominant hyper immunoglobulin E (IgE) syndrome; however, there are still many unclear points regarding the clinical spectrum of this syndrome.

    Methods

    In addition to a clinical description of patients in terms of pedigree, a genetic analysis, quantitation of peripheral blood Th17 and ex vivo IL‐17 production were carried out.

    Results

    The proband, a 2‐year‐old boy (Patient 1) with early onset atopic dermatitis‐like eczema and recurrent bacterial infections, was suspected of autosomal dominant hyper immunoglobulin E syndrome on the basis of his symptoms and family history. His mother (Patient 2) also had skin eczema and recurrent bacterial infections, and his sister (Patient 3) had skin eczema. A novel STAT3 mutation (p.S476F) was detected in all three patients, but not in the father, who had no such symptoms. A significant decrease in peripheral blood Th17 subsets and IL‐17 production was found in all the patients. Curiously, all three patients carrying the p.S476F mutation in STAT3 lacked connective tissue signs such as distinctive facial features, retention of primary teeth, and joint hyperextensibility.

    Conclusions

    Autosomal dominant hyper IgE syndrome should, perhaps, be considered even if patients lack connective tissue signs, as long as hypersensitivity to infection and skin manifestations with hyper IgE are present.

    DOI: 10.1111/ped.14463

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    その他リンク: https://onlinelibrary.wiley.com/doi/full-xml/10.1111/ped.14463

  • Contribution of long-chain fatty acid to induction of myeloid-derived suppressor cell (MDSC)-like cells – induction of MDSC by lipid vesicles (liposome)

    Yoichiro Yoshida, Tsunehisa Nagamori, Emi Ishibazawa, Hiroya Kobayashi, Tomoko Kure, Hiromi Sakai, Daisuke Takahashi, Mitsuhiro Fujihara, Hiroshi Azuma

    Immunopharmacology and Immunotoxicology   42 ( 6 )   614 - 624   2020年11月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:Informa UK Limited  

    DOI: 10.1080/08923973.2020.1837866

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  • Liposomal microparticle injection can induce myeloid-derived suppressor cells (MDSC)-like cells<i>in vivo</i>

    Hiroshi Azuma, Yoichiro Yoshida, Hironori Takahashi, Emi Ishibazawa, Hiroya Kobayashi, Hiromi Sakai, Daisuke Takahashi, Mitsuhiro Fujihara

    Immunopharmacology and Immunotoxicology   39 ( 3 )   140 - 147   2017年4月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:Informa UK Limited  

    DOI: 10.1080/08923973.2017.1306867

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▼全件表示

共同研究・競争的資金等の研究課題

  • iPS細胞を用いたSIFDの病態解明と治療法開発のための基盤研究

    研究課題/領域番号:24K11037  2024年4月 - 2027年3月

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    長森 恒久, 佐藤 雅之, 甲賀 大輔, 石羽澤 映美, 林 洋平

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    配分額:4,680,000円 ( 直接経費:3,600,000円 、 間接経費:1,080,000円 )

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  • リポソームを捕捉したマクロファージのMDSC様細胞への変容に関わる分子基盤の解明

    研究課題/領域番号:23K07243  2023年4月 - 2026年3月

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    吉田 陽一郎, 東 寛, 佐藤 雅之, 甲賀 大輔, 長森 恒久, 青山 藍子, 酒井 宏水, 石羽澤 映美

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    配分額:4,160,000円 ( 直接経費:3,200,000円 、 間接経費:960,000円 )

    A)リポソーム捕捉マクロファージの表現型解析
    RAW264.3細胞にリポソームを添加した際に、まず細胞内シグナル伝達に関して、添加後1時間後からIkBaの減少、リン酸化ERK、p38MAPK、JNKの増加を見た。サイトカイン分泌に関してはリポソームを添加した際にIL-6,TNFなどの向炎症性サイトカインのごく少量の増加を見た。また、iNOSと、免疫チェックポイント分子の発現量をフローサイトで解析し、リポソーム添加後12時間以降にiNOS、及びPD-L1の発現増加を確認した。
    これらは先行するラットでのex vivo研究と共通するもので、リポソーム捕捉マクロファージのMDSC様変容と合致する所見であった。

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  • SIFD病態解明のためのTRNT1機能解析

    研究課題/領域番号:21K07836  2021年4月 - 2024年3月

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    長森 恒久, 吉田 陽一郎, 石羽澤 映美

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    配分額:4,290,000円 ( 直接経費:3,300,000円 、 間接経費:990,000円 )

    研究期間全体では①患者細胞ではTRNT1蛋白は健常と同じサイズで発現低下する事、これは不安定性によりプロテアソームで恒常的分解を受けている為とわかった。②患者線維芽細胞では、健常に比して薬剤誘導小胞体ストレスの亢進をみた。③不死化線維芽細胞におけるTRNT1siRNAノックダウンでは、同様に小胞体ストレス亢進を認め、またケミカルシャペロンである4-フェニル酪酸により解除を受ける事を見た。④マウスマクロファージ系のRaw細胞でTRNT1ノックダウンするとTNF産生の亢進とNF-kBシグナルの亢進を見た。
    上記から、SIFDでは小胞体ストレス反応亢進が起こり、これが病状に関わる可能性が高まった。

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