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和田, 泰三 ; Wada, Taizo
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Wada, Taizo ; Toma, Tomoko ; Miyazawa, Hanae ; Koizumi, Eiko ; Shirahashi, Tetsujiro ; Matsuda, Yusuke ; Yachie, Akihiro ; 和田, 泰三 ; 東馬, 智子 ; 白橋, 徹志郎 ; 谷内江, 昭宏
概要:
金沢大学附属病院小児科<br />Epstein-Barr virus (EBV)-associated T- or natural killer (NK)-cell lymphoproliferative disease (LPD) is
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a heterogeneous group of disorders characterized by chronic proliferation of EBV-infected lymphocytes. Patients may present with severe skin manifestations, including hypersensitivity to mosquito bites (HMB) and hydroa vacciniforme (HV)-like eruption, which are characterized by blister formation and necrotic ulceration. Skin biopsy specimens show inflammatory reactions comprising EBV-infected lymphocytes. However, blister fluids have not been fully assessed in patients with this disease. Blister fluids were collected from three patients with EBV-associated LPD: two with HMB and one with HV. Immunophenotyping of blister lymphocytes and measurement of tumor necrosis factor (TNF)-α in blister fluids were performed. The patients with HMB and HV exhibited markedly increased percentages of NK and γδ T cells, respectively, in both peripheral blood and blister fluids. These NK and γδ T cells strongly expressed the activation marker human leukocyte antigen-DR and were considered to be cellular targets of EBV infections. TNF-α was highly elevated in all blister fluids. Severe local skin reactions of EBV-associated LPD may be associated with infiltrating EBV-infected lymphocytes and a high TNF-α concentration in blister fluids. © 2018 Japanese Dermatological Association.<br />Embargo Period 12 months
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Wada, Taizo ; Toma, Tomoko ; Matsuda, Yusuke ; Yachie, Akihiro ; Itami, Saori ; Taguchi, Y-h ; Murakami, Yoshiki
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Objectives: Familial Mediterranean fever (FMF) is an autoinflammatory disease caused by mutations in MEFV. Mutations in
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exon 10 are associated with typical FMF phenotypes, whereas the pathogenic role of variants in exons 2 and 3 remains uncertain. Recent evidence suggests that circulating microRNAs (miRNAs) are potentially useful biomarkers in several diseases. Therefore, their expression was assessed in FMF. Methods: The subjects were 24 patients with FMF who were between attacks: eight with exon 10 mutations (group A), eight with exon 3 mutations (group B), and eight without exon 3 or 10 mutations (group C). We also investigated eight cases of PFAPA as disease controls. Exosome-rich fractionated RNA was subjected to miRNA profiling by microarray. Results: Using the expression patterns of 26 miRNAs, we classified FMF (groups A, B, and C) and PFAPA with 78.1% accuracy. In FMF patients, groups A and B, A and C, and B and C were distinguished with 93.8, 87.5, and 100% accuracy using 24, 30, and 25 miRNA expression patterns, respectively. Conclusions: These findings suggest that expression patterns of circulating miRNAs differ among FMF subgroups based on MEFV mutations between FMF episodes. These patterns may serve as a useful biomarker for detecting subgroups of FMF. © 2017 Japan College of Rheumatology<br />Embargo Period 12 months
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Wada, Taizo ; Toma, Tomoko ; Miyazawa, Hanae ; Koizumi, Eiko ; Shirahashi, Tetsujiro ; Matsuda, Yusuke ; Yachie, Akihiro ; 和田, 泰三 ; 東馬, 智子 ; 小泉, 瑛子 ; 松田, 裕介 ; 谷内江, 昭宏
概要:
金沢大学附属病院小児科<br />Background: Familial Mediterranean fever (FMF) is an autoinflammatory disease caused by mutations in th
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e MEFV gene. Mutations in exon 10 are associated with typical FMF phenotypes, and patients with exon 10 mutations have higher serum levels of interleukin (IL)-18 both during attacks and afebrile phases, compared to those without exon 10 mutations. However, longitudinal changes of serum IL-18 in FMF have not been fully characterized. Methods: We serially evaluated serum levels of pro-inflammatory cytokines, including IL-18, in 12 patients with FMF carrying exon 10 mutations, all of whom showed typical FMF attacks. Results: Markedly high concentrations of IL-18 were observed in all patients at diagnosis (5099. ±. 6084. pg/mL). Serum IL-18 levels declined progressively after colchicine treatment in 7 patients (group A), whereas 5 patients showed continued elevation of circulating IL-18, despite declines in IL-6 and neopterin (group B). The mean follow-up times in the two groups were 4.7. ±. 3.2 and 4.8. ±. 1.5 years, respectively. The mean serum IL-18 level at the last hospital visit in group B was 4190. ±. 2610[U+202F]pg/mL. There were no differences in onset age, initial IL-18 levels, and colchicine doses between the groups. FMF attacks almost disappeared in both groups, but there were trends towards more frequent subtle symptoms such as abdominal discomfort in group B. Conclusions: Sustained elevation of serum IL-18 may suggest the presence of persistent subclinical inflammation. Therefore, longitudinal examination of serum IL-18 may contribute to better follow-up of FMF patients with exon 10 mutations. © 2017 Elsevier Ltd.<br />Embargo Period 12 moths
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Yachie, Akihiro ; Niida, Yo ; Wada, Taizo ; Igarashi, Noboru ; Kaneda, Hisashi ; Toma, Tomoko ; Ohta, Kazuhide ; Kasahara, Yoshihito ; Koizumi, Shoichi
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金沢大学医薬保健研究域医学系<br />The first known human case of heme oxygenase-1 (HO-1) deficiency is presented in this report. The pa
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tient is a six-year-old boy with severe growth retardation. He has been suffering from persistent hemolytic anemia characterized by marked erythrocyte fragmentation and intravascular hemolysis, with paradoxical increase of serum haptoglobin and low bilirubin. An abnormal coagulation/fibrinolysis system, associated with elevated thrombomodulin and von Willebrand factor, indicated the presence of severe, persistent endothelial damage. Electron microscopy of renal glomeruli revealed detachment of endothelium, with subendothelial deposition of an unidentified material. Iron deposition was noted in renal and hepatic tissue. Immunohistochemistry of hepatic tissue and immunoblotting of a cadmium- stimulated Epstein-Barr virus-transformed lymphoblastoid cell line (LCL) revealed complete absence of HO-1 production. An LCL derived from the patient was extremely sensitive to hemin-induced cell injury. Sequence analysis of the patient's HO-1 gene revealed complete loss of exon-2 of the maternal allele and a two-nucleotide deletion within exon3 of the paternal allele. Growth retardation, anemia, iron deposition, and vulnerability to stressful injury are all characteristics observed in recently described HO-1 targeted mice. This study presents not only the first human case of HO-1 deficiency but may also provide clues to the key roles played by this important enzyme in vivo.
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Wada, Taizo ; Nishimura, Kashiku ; Kuroda, Mondo ; Asai, Erika ; Vu, Quang Van ; Toma, Tomoko ; Niida, Yo ; Yachie, Akihiro
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We report on a 9-year-old boy who presented with acute encephalopathy and hemophagocytic lymphohistiocytosis (HLH). The
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patient was referred to our hospital because of fever, seizures, and decreased consciousness. He showed moderately elevated levels of proinflammatory cytokines in the cerebrospinal fluid and plasma, and clonal expansion of highly activated CD8 + T cells in the peripheral blood. These CD8 + T cells were found to be larger cells that stained positive for T-cell receptor Vβ13.6, and decreased shortly after steroid therapy. Our findings suggest that his acute encephalopathy was likely a clinical manifestation of HLH, and that immunophenotypic analysis may be helpful for early recognition of HLH in such rare encephalopathy. © 2011 The Japanese Society of Child Neurology.
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Inoue, Mika ; Kasahara, Yoshihito ; Okajima, Michiko ; Wada, Taizo ; Toma, Tomoko ; Shimizu, Masaki ; Koizumi, Shoichi ; Yachie, Akihiro
概要:
金沢大学医薬保健研究域保健学系<br />[Originals][原著]平成22年10月28日受付, 平成22年12月3日受理.
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Wada, Taizo ; Yokoyama, Tadafumi ; Nakagawa, Hiroyasu ; Asai, Erika ; Taga, Akiko ; Sakakibara, Yasuhisa ; Shibata, Fumie ; Tone, Yumi ; Shimizu, Masaki ; Toma, Tomoko ; Yachie, Akihiro
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金沢大学医薬保健研究域医学系<br />In chronic active Epstein-Barr virus (EBV) infection (CAEBV), ectopic EBV infection has been describ
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ed in T or natural killer (NK) cells. NK cell-type infection (NK-CAEBV) is characterized by large granular lymphocytosis, high IgE levels and unusual reactions to mosquito bites, including severe local skin reactions, fever and liver dysfunction. However, the mechanisms underlying these reactions remain undetermined. Herein, we describe a patient with NK-CAEBV whose blister fluid after mosquito bites was analyzed. The patient exhibited significant increases in the percentage of CD56+ NK cells in the fluid compared with a simple mosquito allergy, in which the majority of infiltrated cells were CD203c+ cells, indicating basophils and/or mast cells. His fluid also contained CD203c+ cells, and his circulating basophils were activated by mosquito extracts in vitro. These results suggest that CD203c+ cells as well as NK cells may play pathogenic roles in the severe skin reactions to mosquito bites in NK-CAEBV. © 2009 The Japanese Society of Hematology.<br />出版者に照会中.2010年12月より全文公開予定.
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| 9.
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Shimizu, Masaki ; Tone, Yumi ; Toga, Akiko ; Yokoyama, Tadafumi ; Wada, Taizo ; Toma, Tomoko ; Yachie, Akihiro
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金沢大学医薬保健研究域医学系
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Wada, Taizo ; Konno, Akihiro ; Schurman, Shepherd H. ; Garabedian, Elizabeth K. ; Anderson, Stacie M. ; Kirby, Martha ; Nelson, David L. ; Candotti, Fabio
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金沢大学附属病院小児科<br />Revertant mosaicism due to true back mutations or second-site mutations has been identified in several
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inherited disorders. The occurrence of revertants is considered rare, and the underlying genetic mechanisms remain mostly unknown. Here we describe somatic mosaicism in two brothers affected with Wiskott-Aldrich syndrome (WAS). The original mutation causing disease in this family is a single base insertion (1305insG) in the WAS protein (WASP) gene, which results in frameshift and abrogates protein expression. Both patients, however, showed expression of WASP in a fraction of their T cells that were demonstrated to carry a second-site mutation causing the deletion of 19 nucleotides from nucleotide 1299 to 1316. This deletion abrogated the effects of the original mutation and restored the WASP reading frame. In vitro expression studies indicated that mutant protein encoded by the second-site mutation was expressed and functional, since it was able to bind to cellular partners and mediate T cell receptor/CD3 downregulation. These observations were consistent with evidence of in vivo selective advantage of WASP-expressing lymphocytes. Molecular analysis revealed that the sequence surrounding the deletion contained two 4-bp direct repeats and that a hairpin structure could be formed by five GC pairs within the deleted fragment. These findings strongly suggest that slipped mispairing was the cause of this second-site mutation and that selective accumulation of WASP-expressing T lymphocytes led to revertant mosaicism in these patients.
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