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Institution

University of Western Australia

EducationPerth, Western Australia, Australia
About: University of Western Australia is a education organization based out in Perth, Western Australia, Australia. It is known for research contribution in the topics: Population & Poison control. The organization has 29613 authors who have published 87405 publications receiving 3064466 citations. The organization is also known as: UWA & University of WA.


Papers
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01 Jan 1998
TL;DR: In this article, the authors found that the risk of developing hepatocellular carcinoma is significantly increased in patients with genetic hemochromatosis, alcoholic liver disease, or chronic hepatitis C infection.
Abstract: The risk of developing hepatocellular carcinoma is significantly increased in patients with genetic hemochromatosis, alcoholic liver disease, or chronic hepatitis C infection. The precise mechanisms underlying the development of hepatocellular carcinoma in these conditions are not well understood. Stem cells within the liver, termed oval cells, are involved in the pathogenesis of hepatocellular carcinoma in animal models and may be important in the development of hepatocellular carcinoma in human chronic liver diseases. The aims of this study were to determine whether oval cells could be detected in the liver of patients with genetic hemochromatosis, alcoholic liver disease, or chronic hepatitis C, and whether there is a relationship between the severity of the liver disease and the number of oval cells. Oval cells were detected using histology and immunohistochemistry in liver biopsies from patients with genetic hemochromatosis, alcoholic liver disease, or chronic hepatitis C. Oval cells were not observed in normal liver controls. Oval cell numbers increased significantly with the progression of disease severity from mild to severe in each of the diseases studied. We conclude that oval cells are frequently found in subjects with genetic hemochromatosis, alcoholic liver disease, or chronic hepatitis C. There is an association between severity of liver disease and increase in the number of oval cells consistent with the hypothesis that oval cell proliferation is associated with increased risk for development of hepatocellular carcinoma in chronic liver disease.

416 citations

Journal ArticleDOI
Sean Walkowiak1, Sean Walkowiak2, Liangliang Gao3, Cécile Monat4, Georg Haberer, Mulualem T. Kassa5, Jemima Brinton6, Ricardo H. Ramirez-Gonzalez6, Markus C. Kolodziej7, Emily Delorean3, Dinushika Thambugala8, Valentyna Klymiuk2, Brook Byrns2, Heidrun Gundlach, Venkat Bandi2, Jorge Nunez Siri2, Kirby T. Nilsen2, Catharine Aquino, Axel Himmelbach4, Dario Copetti9, Dario Copetti7, Tomohiro Ban10, Luca Venturini11, Michael W. Bevan6, Bernardo J. Clavijo6, Dal-Hoe Koo3, Jennifer Ens2, Krystalee Wiebe2, Amidou N’Diaye2, Allen K. Fritz3, Carl Gutwin2, Anne Fiebig4, Christine Fosker6, Bin Xiao Fu1, Gonzalo Garcia Accinelli6, Keith A. Gardner, Nick Fradgley, Juan J. Gutierrez-Gonzalez12, Gwyneth Halstead-Nussloch7, Masaomi Hatakeyama7, Chu Shin Koh2, Jasline Deek13, Alejandro C. Costamagna14, Pierre R. Fobert5, Darren Heavens6, Hiroyuki Kanamori, Kanako Kawaura10, Fuminori Kobayashi, Ksenia V. Krasileva6, Tony Kuo15, Tony Kuo16, Neil McKenzie6, Kazuki Murata17, Yusuke Nabeka17, Timothy Paape7, Sudharsan Padmarasu4, Lawrence Percival-Alwyn, Sateesh Kagale5, Uwe Scholz4, Jun Sese15, Philomin Juliana18, Ravi P. Singh18, Rie Shimizu-Inatsugi7, David Swarbreck6, James Cockram, Hikmet Budak, Toshiaki Tameshige10, Tsuyoshi Tanaka, Hiroyuki Tsuji10, Jonathan M. Wright6, Jianzhong Wu, Burkhard Steuernagel6, Ian Small19, Sylvie Cloutier8, Gabriel Keeble-Gagnère, Gary J. Muehlbauer12, Josquin Tibbets, Shuhei Nasuda17, Joanna Melonek19, Pierre Hucl2, Andrew G. Sharpe2, Matthew D. Clark11, Erik Legg20, Arvind K. Bharti20, Peter Langridge21, Anthony Hall6, Cristobal Uauy6, Martin Mascher4, Simon G. Krattinger7, Simon G. Krattinger22, Hirokazu Handa23, Kentaro Shimizu7, Kentaro Shimizu10, Assaf Distelfeld24, Kenneth J. Chalmers21, Beat Keller7, Klaus F. X. Mayer25, Jesse Poland3, Nils Stein4, Nils Stein26, Curt A. McCartney8, Manuel Spannagl, Thomas Wicker7, Curtis J. Pozniak2 
25 Nov 2020-Nature
TL;DR: Comparative analysis of multiple genome assemblies from wheat reveals extensive diversity that results from the complex breeding history of wheat and provides a basis for further potential improvements to this important food crop.
Abstract: Advances in genomics have expedited the improvement of several agriculturally important crops but similar efforts in wheat (Triticum spp.) have been more challenging. This is largely owing to the size and complexity of the wheat genome1, and the lack of genome-assembly data for multiple wheat lines2,3. Here we generated ten chromosome pseudomolecule and five scaffold assemblies of hexaploid wheat to explore the genomic diversity among wheat lines from global breeding programs. Comparative analysis revealed extensive structural rearrangements, introgressions from wild relatives and differences in gene content resulting from complex breeding histories aimed at improving adaptation to diverse environments, grain yield and quality, and resistance to stresses4,5. We provide examples outlining the utility of these genomes, including a detailed multi-genome-derived nucleotide-binding leucine-rich repeat protein repertoire involved in disease resistance and the characterization of Sm16, a gene associated with insect resistance. These genome assemblies will provide a basis for functional gene discovery and breeding to deliver the next generation of modern wheat cultivars.

416 citations

Journal ArticleDOI
TL;DR: The authors used the approach in the under/over education literature to analyze the extent of matching of educational level to occupational attainment among adult native born and foreign born men in the US, using the 2000 Census.

416 citations

Journal ArticleDOI
TL;DR: The pH at the root surface will often differ from the pH a few millimeters away by 1-2 units as mentioned in this paper, and the pH buffering capacity, moisture content, initial pH and pCO2 of the soil.
Abstract: Plants that absorb nitrogen as NO3 − tend to raise the pH in the rhizosphere. Those absorbing nitrogen as NH4 + or N2 lower the pH. The change in pH near the root surface may be calculated approximately from the H+ or HCO3 − efflux and radius of the root; and the pH buffering capacity, moisture content, initial pH and pCO 2 of the soil. An accurate equation, solved numerically, also takes account of root hairs, mass flow and slow acid-base reaction in the soil. The pH at the root surface will often differ from the pH a few mm away by 1–2 units.

415 citations

Journal ArticleDOI
TL;DR: This approach should reduce the severity of DMD by allowing a dystrophic gene transcript to be modified, such that it can be translated into a Becker-dystrophin-like protein.
Abstract: Duchenne muscular dystrophy (DMD) is a severe muscle wasting disease arising from defects in the dystrophin gene, typically nonsense or frameshift mutations, that preclude the synthesis of a functional protein. A milder, allelic version of the disease, Becker muscular dystrophy, generally arises from in-frame deletions that allow synthesis of a shorter but still semifunctional protein. Therapies to introduce functional dystrophin into dystrophic tissue through either cell or gene replacement have not been successful to date. We report an alternative approach where 2′-O-methyl antisense oligoribonucleotides have been used to modify processing of the dystrophin pre-mRNA in the mdx mouse model of DMD. By targeting 2′-O-methyl antisense oligoribonucleotides to block motifs involved in normal dystrophin pre-mRNA splicing, we induced excision of exon 23, and the mdx nonsense mutation, without disrupting the reading frame. Exon 23 skipping was first optimized in vitro in transfected H-2Kb-tsA58 mdx myoblasts and then induced in vivo. Immunohistochemical staining demonstrated the synthesis and correct subsarcolemmal localization of dystrophin and γ-sarcoglycan in the mdx mouse after intramuscular delivery of antisense oligoribonucleotide:liposome complexes. This approach should reduce the severity of DMD by allowing a dystrophic gene transcript to be modified, such that it can be translated into a Becker-dystrophin-like protein.

414 citations


Authors

Showing all 29972 results

NameH-indexPapersCitations
Nicholas G. Martin1921770161952
Cornelia M. van Duijn1831030146009
Kay-Tee Khaw1741389138782
Steven N. Blair165879132929
David W. Bates1591239116698
Mark E. Cooper1581463124887
David Cameron1541586126067
Stephen T. Holgate14287082345
Jeremy K. Nicholson14177380275
Xin Chen1391008113088
Graeme J. Hankey137844143373
David Stuart1361665103759
Joachim Heinrich136130976887
Carlos M. Duarte132117386672
David Smith1292184100917
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023138
2022656
20215,967
20205,589
20195,452
20184,923