Browsing by Autor "Juan Eiki Nishizawa"

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    21-Hydroxylase gene mutant allele CYP21A2∗15 strongly linked to the resistant HLA haplotype B∗14:02-DRB1∗01:02 in chronic Chagas disease
    (Elsevier BV, 2013) Florencia del Puerto; Mihoko Kikuchi; Juan Eiki Nishizawa; Yelin Roca; Cinthia Avila; Alberto Gianella; Javier Lora; Freddy Udalrico Gutierrez Velarde; Kenji Hirayama
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    Follow up study during and after two month regimen of Benznidazole in pediatric chronic Chagas patients in Bolivia
    (Japanese Pharmacological Society, 2018) Clara Vásquez Velásquez; Emilio E. Espínola; Zunilda Sánchez; Kota Mochizuki; Jimmy Revollo; Angelica Guzman; Benjamín Quiroga; Juan Eiki Nishizawa; Graciela Russomando; Kenji Hirayama
    Introduction: Chagas disease is a parasitic infection endemic in Latin America caused by Trypanosoma cruzi. In Bolivia, vector control activity by the National Program for Chagas has greatly decreased the number of natural infections since 2006. The program began a treatment regimen of Benznidazole (BNZ) (5mg/kg/day) for 2 months in seropositive children aged 4-15 years living in certified vector controlled areas.
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    Lineage Analysis of Circulating Trypanosoma cruzi Parasites and Their Association with Clinical Forms of Chagas Disease in Bolivia
    (Public Library of Science, 2010) Florencia del Puerto; Juan Eiki Nishizawa; Mihoko Kikuchi; Naomi Iihoshi; Yelin Roca; Cinthia Avilas; Alberto Gianella; Javier Lora; Freddy Udalrico Gutierrez Velarde; Luis Alberto Renjel
    None of the identified lineages or sublineages was significantly associated with any particular clinical manifestations in the chronic Chagas patients in Bolivia.
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    Protective Human Leucocyte Antigen Haplotype, HLA-DRB1*01-B*14, against Chronic Chagas Disease in Bolivia
    (Public Library of Science, 2012) Florencia del Puerto; Juan Eiki Nishizawa; Mihoko Kikuchi; Yelin Roca; Cinthia Avilas; Alberto Gianella; Javier Lora; Freddy Udalrico Gutierrez Velarde; Sachio Miura; Norihiro Komiya
    This is the first report of HLA haplotype association with resistance to chronic Chagas disease.
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    Proteomic profile of circulating immune complexes in chronic Chagas disease
    (Wiley, 2016) Kaname Ohyama; Nguyen Tien Huy; Hiroki Yoshimi; Naoya Kishikawa; Juan Eiki Nishizawa; Yelin Roca; R. J. Revollo Guzmán; Freddy Udalrico Gutierrez Velarde; Naotaka Kuroda; Kenji Hirayama
    Immune complexes (ICs) are the direct and real-time products of humoral immune responses. The identification of constituent foreign or autoantigens within ICs might bring new insights into the pathology of infectious diseases. We applied immune complexome analysis of plasma to the study of Chagas disease caused by Trypanosoma cruzi. Twenty seropositive plasma samples including cardiac and/or megacolon determinate patients (n = 11) and indeterminate (n = 9) were analysed along with 10 seronegative individuals to characterize the antigens bound to circulating ICs. We identified 39 T. cruzi antigens and 114 human autoantigens specific to patients with Chagas. Among those antigens, two T. cruzi antigens (surface protease GP63, glucose-6-isomerase) and six human autoantigens (CD180 antigen, ceruloplasmin, fibrinogen beta chain, fibrinogen beta chain isoform 2 preprotein, isoform gamma-A of fibrinogen γ-chain, serum paraoxonase) were detected in more than 50% of the patients tested. Human isoform short of complement factor H-related protein 2 and trans-sialidase of T. cruzi were more frequently found in the indeterminate (5/9 for both) compared with in the determinate Chagas (0/11, P = 0·046 for human, 1/11, P = 0·0498 for T. cruzi). The immune complexome could illustrate the difference of immune status between clinical forms of chronic Chagas disease.