J
Julie R. Jonsson
Researcher at University of Queensland
Publications - 64
Citations - 5400
Julie R. Jonsson is an academic researcher from University of Queensland. The author has contributed to research in topics: Fibrosis & Steatosis. The author has an hindex of 34, co-authored 64 publications receiving 5178 citations. Previous affiliations of Julie R. Jonsson include QIMR Berghofer Medical Research Institute & Princess Alexandra Hospital.
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Journal ArticleDOI
Relationship Between Steatosis, Inflammation, and Fibrosis in Chronic Hepatitis C: A Meta-Analysis of Individual Patient Data
Gioacchino Leandro,Alessandra Mangia,Jason M. Hui,Paolo Fabris,Laura Rubbia Brandt,Guido Colloredo,Luigi Elio Adinolfi,Tarik Asselah,Julie R. Jonsson,Antonina Smedile,Norah A. Terrault,Valerio Pazienza,Maria Teresa Giordani,Emiliano Giostra,Aurelio Sonzogni,Giuseppe Ruggiero,Patrick Marcellin,Elizabeth E. Powell,Jacob George,Francesco Negro +19 more
TL;DR: In this large and geographically different group of CHC patients, steatosis is confirmed as significantly and independently associated with fibrosis in CHC.
Journal ArticleDOI
Progressive Fibrosis in Nonalcoholic Steatohepatitis: Association With Altered Regeneration and a Ductular Reaction
Michelle M. Richardson,Julie R. Jonsson,Elizabeth E. Powell,Elizabeth M. Brunt,Brent A. Neuschwander-Tetri,Prithi S. Bhathal,John Dixon,Martin Weltman,Herbert Tilg,Alexander R. Moschen,D. M. Purdie,Anthony J. Demetris,Andrew D. Clouston +12 more
TL;DR: It is proposed that activation of this pathway, with increased cell injury in NASH, also induces a periportal ductular reaction (DR) that could produce a profibrogenic stimulus that in turn may provoke progressive perip Mortal fibrogenesis.
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Interleukin-10 promoter polymorphism predicts initial response of chronic hepatitis C to interferon alfa.
Catherine Edwards-Smith,Julie R. Jonsson,David M. Purdie,Amolak S. Bansal,Claudia Shorthouse,Elizabeth E. Powell,Elizabeth E. Powell +6 more
TL;DR: Heterogeneity in the promoter region of the IL‐10 gene has a role in determining the initial response of chronic hepatitis C to IFN‐α therapy and patients who are genetically predisposed to high IL-10 production have a poor response to IFn‐α and may benefit from additional treatment strategies designed to enhance a T‐helper type 1 (Th1) response.
Journal ArticleDOI
Steatosis: Co-factor in other liver diseases
TL;DR: In conclusion, active management of obesity and a reduction in steatosis may improve liver injury and decrease the progression of fibrosis.
Journal ArticleDOI
Fibrosis correlates with a ductular reaction in hepatitis C: Roles of impaired replication, progenitor cells and steatosis
Andrew D. Clouston,Elizabeth E. Powell,Elizabeth E. Powell,M. J. Walsh,Michelle M. Richardson,A. Jake Demetris,Julie R. Jonsson +6 more
TL;DR: The strong correlation between portal fibrosis and a periportal ductular reaction with HPC expansion, the exacerbation by steatosis, and the associations with impaired hepatocyte replication suggest that an altered regeneration pathway drives theductular reaction.