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Masashi Mizokami

Researcher at Nagoya City University

Publications -  684
Citations -  37168

Masashi Mizokami is an academic researcher from Nagoya City University. The author has contributed to research in topics: Hepatitis B virus & Hepatitis C virus. The author has an hindex of 85, co-authored 650 publications receiving 34868 citations. Previous affiliations of Masashi Mizokami include National Institute of Advanced Industrial Science and Technology & University of Florida.

Papers
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Journal ArticleDOI

Analysis of Conserved Ambisense Sequences within GB Virus C

TL;DR: Results indicated that a novel protein associated with GBV-C might be expressed from the ambisense of this virus.
Journal ArticleDOI

Outcome of nucleos(t)ide analog intervention in patients with preventive or on‐demand therapy for hepatitis B virus reactivation

TL;DR: HBsAg predicted HBV relapse after the cessation of NA therapy in HBsAg‐positive patients, and anti‐HBs could be a predictive marker for NA therapy cessation in patients with resolved HBV.
Journal ArticleDOI

Nucleotide sequence of the core region of hepatitis C virus in Pakistan and Bangladesh and the geographic characterisation of hepatitis C virus in south Asia.

TL;DR: Detailed determination and evaluation of partial sequences in the core region of HCV obtained from patients with chronic hepatitis in Pakistan and Bangladesh suggest that clones might be classified into the same genotype as HCV‐TR, and further analysis using molecular evolutionary methods strongly supported the classification of these sequences.
Book ChapterDOI

Transmission of Hepatitis C Virus Through Needlestick Accidents in Health Care Workers

TL;DR: Though this transmission rate is not necessarily high, needlestick accident is an apparent HCV transmission route, and appropriate precautions in hospital employees and careful follow-up of such accidents are needed.
Journal ArticleDOI

Orchestration of Intracellular Circuits by G Protein-Coupled Receptor 39 for Hepatitis B Virus Proliferation

TL;DR: GPR39 and the regulated signaling networks would serve as antiviral targets, and strategies with selective inhibitors of GPR39 functions can develop host-targeted antiviral therapies preventing HCC.