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Michio Imawari

Researcher at University of Tokyo

Publications -  113
Citations -  2233

Michio Imawari is an academic researcher from University of Tokyo. The author has contributed to research in topics: Hepatitis C virus & Cytotoxic T cell. The author has an hindex of 26, co-authored 113 publications receiving 2121 citations. Previous affiliations of Michio Imawari include University of Tsukuba.

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Present status of autoimmune hepatitis in Japan - correlating the characteristics with international criteria in an area with a high rate of HCV infection

TL;DR: The International Diagnostic Scoring System for the diagnosis of autoimmune hepatitis worked well in these patients, except for HCV-infected individuals, that is, approximately 10% of the total of AIH patients.
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Cytotoxic T lymphocyte response and viral load in hepatitis C virus infection

TL;DR: The results suggest that the HLA B44‐restricted CTLs together with other HCV‐specific CTLS may inhibit the outgrowth of HCV and that high‐ titer infection with HCV may suppress the CTL responses.
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HLA B44–restricted cytotoxic T lymphocytes recognizing an epitope on hepatitis C virus nucleocapsid protein

TL;DR: The results demonstrate the presence of hepatitis C virus–specific cytotoxic T lymphocytes in the peripheral blood of patients with chronic hepatitis C and provide a strategy to study the role of cytot toxic T lymphocyte in the viral clearance and the pathogenesis of hepatitisC virus infection.
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Androgen and estrogen receptors in hepatocellular carcinoma and in the surrounding noncancerous liver tissue

TL;DR: The results suggest that the expression of androgen receptor may be augmented in association with malignant transformation of hepatocytes while theexpression of estrogen receptors may be rather suppressed and that some of hepatocellular carcinomas may be androgen‐dependent.
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Molecular differences between sporadic serrated and conventional colorectal adenomas.

TL;DR: In contrast, activation of the Ras/Raf/MEK/MAP kinase cascade by BRAF or KRAS mutation, independently of the genetic instability, may be associated with the progression of about half of SAs.