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19 results on '"Riordan, Stephen"'

2. Multi-omics of the esophageal microenvironment identifies signatures associated with progression of Barrett’s esophagus

Author

Deshpande, Nandan P., primary, Riordan, Stephen M., additional, Gorman, Claire J., additional, Nielsen, Shaun, additional, Russell, Tonia L., additional, Correa-Ospina, Carolina, additional, Fernando, Bentotage S. M., additional, Waters, Shafagh A., additional, Castaño-Rodríguez, Natalia, additional, Man, Si Ming, additional, Tedla, Nicodemus, additional, Wilkins, Marc R., additional, and Kaakoush, Nadeem O., additional

Published
2021
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4. IFN-λ3, not IFN-λ4, likely mediates IFNL3–IFNL4 haplotype–dependent hepatic inflammation and fibrosis

Author

Eslam, Mohammed, McLeod, Duncan, Kelaeng, Kebitsaone Simon, Mangia, Alessandra, Berg, Thomas, Thabet, Khaled, Irving, William, Dore, Gregory J., Sheridan, David, Grønbæk, Henning, Abate, María Lorena, Hartmann, Rune, Bugianesi, Elisabetta, Spengler, Ulrich, Rojas Álvarez-Ossorio, M. Ángeles, Booth, David R., Weltman, Martin, Mollison, Lindsay, Cheng, Wendy, Riordan, Stephen, Mahajan, Hema, Fischer, Janett, Nattermann, Jacob, Douglas, Mark W., Liddle, Christopher, Powell, Elizabeth, Romero-Gómez, Manuel, George, Jacob, Metwally, Mayada, White, Rosa, Gallego-Durán, Rocío, Leung, Reynold, Mahajan, Neha, Bassendine, Margaret, Rahme, Antony, Rosso, Chiara, Mezzabotta, Lavinia, Malik, Barbara, Matthews, Gail, Asimakopoulos, Anastasia, Applegate, Tanya, Grebely, Jason, Fragomeli, Vicenzo, Jonsson, Julie R., Santoro, Rosanna, Sydney Medical Foundation, University of Sydney, and National Health and Medical Research Council (Australia)

Subjects
0301 basic medicine, LAMBDA 4, Genotype, health care facilities, manpower, and services, education, Inflammation, Hepacivirus, LIVER FIBROSIS, GENOME-WIDE-ASSOCIATION, Biology, Polymorphism, Single Nucleotide, Linkage Disequilibrium, INTERFERON-STIMULATED GENES, 03 medical and health sciences, Immune system, Gene Frequency, Fibrosis, INFECTION, Genetics, medicine, Humans, HCV CLEARANCE, SNP, C VIRUS, health care economics and organizations, Hepatitis, Reverse Transcriptase Polymerase Chain Reaction, Interleukins, Haplotype, medicine.disease, Hepatitis C, Phenotype, III INTERFERONS, Logistic Models, 030104 developmental biology, Haplotypes, Liver, Multivariate Analysis, Immunology, SOLID-ORGAN, Interferons, medicine.symptom, IL28B GENE
Abstract

The International Liver Disease Genetics Consortium (ILDGC)., Genetic variation in the IFNL3–IFNL4 (interferon-λ3–interferon-λ4) region is associated with hepatic inflammation and fibrosis1,2,3,4. Whether IFN-λ3 or IFN-λ4 protein drives this association is not known. We demonstrate that hepatic inflammation, fibrosis stage, fibrosis progression rate, hepatic infiltration of immune cells, IFN-λ3 expression, and serum sCD163 levels (a marker of activated macrophages) are greater in individuals with the IFNL3–IFNL4 risk haplotype that does not produce IFN-λ4, but produces IFN-λ3. No difference in these features was observed according to genotype at rs117648444, which encodes a substitution at position 70 of the IFN-λ4 protein and reduces IFN-λ4 activity, or between patients encoding functionally defective IFN-λ4 (IFN-λ4–Ser70) and those encoding fully active IFN-λ4–Pro70. The two proposed functional variants (rs368234815 and rs4803217)5,6 were not superior to the discovery SNP rs12979860 with respect to liver inflammation or fibrosis phenotype. IFN-λ3 rather than IFN-λ4 likely mediates IFNL3–IFNL4 haplotype–dependent hepatic inflammation and fibrosis., M.E., M.D., and J.G. are supported by the Robert W. Storr Bequest to the Sydney Medical Foundation, University of Sydney, and by a National Health and Medical Research Council of Australia (NHMRC) Program Grant (1053206) and NHMRC Project Grants (APP1107178 and APP1108422). G.D. is supported by an NHMRC Fellowship (1028432).

Published
2017
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5. OPCML is hypermethylated in a subset of patients with metaplastic changes in their esophagus

Author

Castaño-Rodríguez, Natalia, primary, Popple, Georgia L., additional, Porras-Hurtado, Gloria Liliana, additional, Cardona-Deazza, José Luis, additional, Montoya-Martinez, Juan José, additional, Cadavid-Velez, Antonio Javier, additional, Toro-Hidalgo, Héctor William, additional, Cobo-Alvarado, Alba Ruth, additional, del Socorro Hincapié-Rincón, Ofelia, additional, Riordan, Stephen M., additional, and Kaakoush, Nadeem O., additional

Published
2018
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14. Acute-on-chronic liver failure: consensus recommendations of the Asian Pacific Association for the study of the liver (APASL)

Author

Sarin, Shiv Kumar, primary, Kumar, Ashish, additional, Almeida, John A., additional, Chawla, Yogesh Kumar, additional, Fan, Sheung Tat, additional, Garg, Hitendra, additional, de Silva, H. Janaka, additional, Hamid, Saeed Sadiq, additional, Jalan, Rajiv, additional, Komolmit, Piyawat, additional, Lau, George K., additional, Liu, Qing, additional, Madan, Kaushal, additional, Mohamed, Rosmawati, additional, Ning, Qin, additional, Rahman, Salimur, additional, Rastogi, Archana, additional, Riordan, Stephen M., additional, Sakhuja, Puja, additional, Samuel, Didier, additional, Shah, Samir, additional, Sharma, Barjesh Chander, additional, Sharma, Praveen, additional, Takikawa, Yasuhiro, additional, Thapa, Babu Ram, additional, Wai, Chun-Tao, additional, and Yuen, Man-Fung, additional

Published
2008
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19. IL28B is associated with response to chronic hepatitis C interferon-α and ribavirin therapy

Author

Vijayaprakash Suppiah, Tobias Müller, Max Moldovan, Maria Lorena Abate, Margaret F. Bassendine, David Sheridan, Martin Weltman, Ulrich Spengler, Jacob George, Melanie Bahlo, Thomas Berg, Vincenzo Fragomeli, Gregory J. Dore, Antonina Smedile, Elizabeth E. Powell, Stephen M. Riordan, Graeme J. Stewart, David R. Booth, Golo Ahlenstiel, Suppiah, Vijayaprakash, Moldovan, Max, Ahlenstiel, Golo, Berg, Thomas, Weltman, Martin, Abate, Maria Lorena, Bassendine, Margaret, Spengler, Ulrich, Dore, Gregory J, Powell, Elizabeth, Riordan, Stephen, Sheridan, David, Smedile, Antonina, Fragomeli, Vincenzo, Muller, Tobias, Bahlo, Melanie, Stewart, Graeme J, Booth, David R, and George, Jacob

Subjects
ribavirin, Hepatitis C virus, Population, drug response, Alpha interferon, Biology, PEGylated interferon-alpha, medicine.disease_cause, chemistry.chemical_compound, Interferon, Genetics, medicine, Interleukin 28, education, education.field_of_study, Ribavirin, virus diseases, Hepatitis C, medicine.disease, Virology, digestive system diseases, Interleukin 28B, chemistry, Immunology, gene expression, antiviral activity, hepatitis C, medicine.drug
Abstract

Hepatitis C virus (HCV) infects 3% of the world's population. Treatment of chronic HCV consists of a combination of PEGylated interferon-alpha (PEG-IFN-alpha) and ribavirin (RBV). To identify genetic variants associated with HCV treatment response, we conducted a genome-wide association study of sustained virological response (SVR) to PEG-IFN-alpha/RBV combination therapy in 293 Australian individuals with genotype 1 chronic hepatitis C, with validation in an independent replication cohort consisting of 555 individuals. We report an association to SVR within the gene region encoding interleukin 28B (IL28B, also called IFNlambda3; rs8099917 combined P = 9.25 x 10(-9), OR = 1.98, 95% CI = 1.57-2.52). IL28B contributes to viral resistance and is known to be upregulated by interferons and by RNA virus infection. These data suggest that host genetics may be useful for the prediction of drug response, and they also support the investigation of the role of IL28B in the treatment of HCV and in other diseases treated with IFN-alpha.

Published
2009
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