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Paul J. Clark

Researcher at Mater Health Services

Publications -  93
Citations -  1870

Paul J. Clark is an academic researcher from Mater Health Services. The author has contributed to research in topics: Hepatitis C & Medicine. The author has an hindex of 22, co-authored 80 publications receiving 1474 citations. Previous affiliations of Paul J. Clark include University of New South Wales & James Cook University.

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Projections of primary liver cancer to 2030 in 30 countries worldwide

TL;DR: In this article, the authors predicted the future burden of primary liver cancer (PLC) in 30 countries around 2030 using age-period-cohort models (NORDPRED software).
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Global Trends in Incidence Rates of Primary Adult Liver Cancers: A Systematic Review and Meta-Analysis

TL;DR: Incidence is increasing for adult liver cancers and HCC in Western countries, whereas trends are decreasing in the Asian region, although still remaining high, and highlights the importance of viral hepatitis control and lifestyle interventions to reduce global liver cancer burden.
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IL28B Genomic-Based Treatment Paradigms for Patients With Chronic Hepatitis C Infection: The Future of Personalized HCV Therapies

TL;DR: Future studies will investigate the possibility of individualizing treatment duration and novel regimens according to IL28B type, and the biological mechanisms responsible for these genetic associations remain unknown and are the focus of ongoing research.
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Beneficial IL28B genotype associated with lower frequency of hepatic steatosis in patients with chronic hepatitis C

TL;DR: IL28B CC genotype is associated with less pronounced disturbances of lipid metabolism, as reflected both in serum lipoprotein levels and hepatic steatosis, in HCV infection.
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Hepatitis C virus selectively perturbs the distal cholesterol synthesis pathway in a genotype-specific manner

TL;DR: Hepatitis C virus G3, but not G2, selectively interferes with the late cholesterol synthesis pathway, evidenced by lower distal sterol metabolites and preserved lanosterol levels, which may explain why hypocholesterolemia persists in chronic HCV infection, and is not overcome by host cholesterol compensatory mechanisms.