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1. Full Text In recognition of Anthony J. Culyer
by Chalkley, Martin and Cutler, David and Frank, Richard G and Lleras-Muney, Adriana and Rice, Nigel and Siciliani, Luigi and Street, Andrew D
Journal of health economics, ISSN 0167-6296, 12/2013, Volume 32, Issue 6, pp. A1 - A1
Economics | Social Sciences | Life Sciences & Biomedicine | Health Care Sciences & Services | Business & Economics | Health Policy & Services | Science & Technology
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2. Marx's 'Capital' and capitalism today
by Cutler, Anthony
1977, Routledge library editions. Political science, ISBN 0710087462, Volume 52, 2 v.
Marx, Karl, 1818-1883. Kapital | Capitalism | Marxian economics | Anarchism | Marxism & Communism | Politics & International Relations | Socialism | Marx, Karl | 1818-1883 | Kapital
Book
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3. Full Text Genetic Variants Predisposing Most Strongly to Type 1 Diabetes Diagnosed Under Age 7 Years Lie Near Candidate Genes That Function in the Immune System and in Pancreatic beta-Cells
by Inshaw, Jamie R. J and Cutler, Antony J and Crouch, Daniel J. M and Wicker, Linda S and Todd, John A
Diabetes care, ISSN 0149-5992, 01/2020, Volume 43, Issue 1, pp. 169 - 177
Life Sciences & Biomedicine | Endocrinology & Metabolism | Science & Technology | Diabetes Mellitus, Type 1 - epidemiology | Haplotypes | Humans | Middle Aged | Child, Preschool | Infant | Male | Case-Control Studies | Young Adult | Insulin-Secreting Cells - metabolism | Islets of Langerhans - metabolism | Adult | Female | Diabetes Mellitus, Type 1 - immunology | Child | Infant, Newborn | Genetic Predisposition to Disease | Diabetes Mellitus, Type 1 - genetics | Islets of Langerhans - immunology | Genotype | Insulin-Secreting Cells - immunology | Polymorphism, Genetic | Diabetes Mellitus, Type 1 - diagnosis | Autoantibodies - immunology | Immune System - metabolism | Adolescent | Age of Onset | Alleles | Insulin-Secreting Cells - pathology | Autoantibodies - genetics | Pancreatic beta cells | Genetic aspects | Type 1 diabetes | Risk factors | Interleukin 2 receptors | Genes | Diabetes mellitus | Lymphocytes T | Diabetes mellitus (insulin dependent) | Regression analysis | Loci | Beta cells | Genetic variance | Regression models | Etiology | Lymphocytes | Interleukin 10 | Interleukin 1 | Histocompatibility antigen HLA | Research design | Diabetes | Children | Pancreas | Age | Genotypes | Immune system | Index Medicus | Pathophysiology | Complications
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4. Full Text A type I Interferon transcriptional signature precedes autoimmunity in children genetically at risk for type 1 diabetes
by Ferreira, Ricardo C and Guo, Hui and Coulson, Richard M. R and Smyth, Deborah J and Pekalski, Marcin L and Burren, Oliver S and Cutler, Antony J and Doecke, James D and Flint, Shaun and McKinney, Eoin F and Lyons, Paul A and Smith, Kenneth G. C and Achenbach, Peter and Beyerlein, Andreas and Dunger, David B and Clayton, David G and Wicker, Linda S and Todd, John A and Bonifacio, Ezio and Wallace, Chris and Ziegler, Anette-G
Diabetes (New York, N.Y.), ISSN 0012-1797, 2014, Volume 63, Issue 7, pp. 2538 - 2550
Life Sciences & Biomedicine | Endocrinology & Metabolism | Science & Technology | Biological and medical sciences | Endocrinopathies | Etiopathogenesis. Screening. Investigations. Target tissue resistance | Diabetes. Impaired glucose tolerance | Medical sciences | Endocrine pancreas. Apud cells (diseases) | Genetic Predisposition to Disease | Humans | Middle Aged | Autoimmunity - genetics | Diabetes Mellitus, Type 1 - genetics | Male | Risk | Transcriptome - drug effects | Transcriptome - immunology | Interferon Type I - immunology | Gene Expression Regulation - drug effects | Young Adult | Interferon Type I - pharmacology | Adolescent | Adult | Female | Diabetes Mellitus, Type 1 - immunology | Child | Cohort Studies | Type 1 diabetes | Analysis | Islands of Langerhans | Influence | Interferon | Diagnosis | Research | Gene expression | Risk factors | Diabetes | Epidemiology | Children & youth | Index Medicus | Abridged Index Medicus | Metabolomics | Genetics | Genomes | Proteomics
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5. Full Text Umbilical cord-derived mesenchymal stromal cells modulate monocyte function to suppress T cell proliferation
by Cutler, Antony J and Limbani, Vasanti and Girdlestone, John and Navarrete, Cristina V
The Journal of immunology (1950), ISSN 0022-1767, 12/2010, Volume 185, Issue 11, pp. 6617 - 6623
Life Sciences & Biomedicine | Immunology | Science & Technology | T-Lymphocyte Subsets - immunology | Cell Communication - immunology | Dinoprostone - physiology | Cell Proliferation | T-Lymphocyte Subsets - cytology | Dinoprostone - biosynthesis | Monocytes - cytology | Coculture Techniques | Humans | Umbilical Cord - cytology | Monocytes - metabolism | Monocytes - immunology | Lymphocyte Culture Test, Mixed | Mesenchymal Stromal Cells - immunology | Mesenchymal Stromal Cells - cytology | Umbilical Cord - metabolism | Receptors, Antigen, T-Cell - immunology | Fetal Blood - immunology | Receptors, Antigen, T-Cell - metabolism | Stromal Cells - metabolism | Cells, Cultured | Umbilical Cord - immunology | Mesenchymal Stromal Cells - metabolism | Stromal Cells - immunology | Fetal Blood - cytology | Fetal Blood - metabolism | Cross-Linking Reagents - metabolism | Down-Regulation - immunology | Stromal Cells - cytology | Index Medicus | Abridged Index Medicus
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6. Full Text Author Correction: Approaches and advances in the genetic causes of autoimmune disease and their implications
by Inshaw, Jamie R J and Cutler, Antony J and Burren, Oliver S and Stefana, M Irina and Todd, John A
Nature immunology, ISSN 1529-2908, 06/2020, Volume 21, Issue 6, pp. 695 - 695
Autoimmune diseases | Index Medicus
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7. Full Text Approaches and advances in the genetic causes of autoimmune disease and their implications
by Inshaw, Jamie R. J and Cutler, Antony J and Burren, Oliver S and Stefana, M. Irina and Todd, John A
Nature immunology, ISSN 1529-2908, 07/2018, Volume 19, Issue 7, pp. 674 - 684
Life Sciences & Biomedicine | Immunology | Science & Technology | Autoimmune Diseases - genetics | Genetic Variation | Genome-Wide Association Study | Microbiota | Sample Size | Infections - complications | Humans | Autoimmune Diseases - microbiology | Chromosome Mapping | Random Allocation | Biological effects | Pathways | Therapeutic applications | Phenotyping | Health risks | Genomes | Environmental factors | Gene expression | Autoimmune diseases | Index Medicus
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8. Full Text Publisher Correction: Approaches and advances in the genetic causes of autoimmune disease and their implications
by Inshaw, Jamie R J and Cutler, Antony J and Burren, Oliver S and Stefana, M Irina and Todd, John A
Nature immunology, ISSN 1529-2908, 02/2019, Volume 20, Issue 3, pp. 375 - 375
Interleukin 2 receptors | Rheumatoid arthritis | Symbols | Genetics | Arthritis | Autoimmune diseases | PTEN protein | Genotypes
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9. Full Text Chromosome contacts in activated T cells identify autoimmune disease candidate genes
by Burren, Oliver S and Rubio García, Arcadio and Javierre, Biola-Maria and Rainbow, Daniel B and Cairns, Jonathan and Cooper, Nicholas J and Lambourne, John J and Schofield, Ellen and Castro Dopico, Xaquin and Ferreira, Ricardo C and Coulson, Richard and Burden, Frances and Rowlston, Sophia P and Downes, Kate and Wingett, Steven W and Frontini, Mattia and Ouwehand, Willem H and Fraser, Peter and Spivakov, Mikhail and Todd, John A and Wicker, Linda S and Cutler, Antony J and Wallace, Chris
Genome Biology, ISSN 1474-7596, 09/2017, Volume 18, Issue 1, pp. 165 - 165
CD4 | Genome-wide association studies | T cell activation | Chromatin conformation | Genomics | Autoimmune disease | Genetics | T cells | Genetics & Heredity | Life Sciences & Biomedicine | Biotechnology & Applied Microbiology | Science & Technology | Interleukin 2 receptors | Disease | Transcription | Lymphocytes T | Genomes | Regulatory sequences | Gene expression | Ribonucleic acid--RNA | CD4 antigen | Cell activation | Lymphocytes | Rheumatoid arthritis | Transcription activation | DNA methylation | Autoimmune diseases | Bioinformatics | Chromosomes | Index Medicus | CD4+ T cell activation | Research | CD4+ T cells
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10. Full Text Lineage-Specific Genome Architecture Links Enhancers and Non-coding Disease Variants to Target Gene Promoters
by Javierre, Biola M and Burren, Oliver S and Wilder, Steven P and Kreuzhuber, Roman and Hill, Steven M and Sewitz, Sven and Cairns, Jonathan and Wingett, Steven W and Várnai, Csilla and Thiecke, Michiel J and Burden, Frances and Farrow, Samantha and Cutler, Antony J and Rehnström, Karola and Downes, Kate and Grassi, Luigi and Kostadima, Myrto and Freire-Pritchett, Paula and Wang, Fan and Martens, Joost H and Kim, Bowon and Sharifi, Nilofar and Janssen-Megens, Eva M and Yaspo, Marie-Laure and Linser, Matthias and Kovacsovics, Alexander and Clarke, Laura and Richardson, David and Datta, Avik and Flicek, Paul and Stunnenberg, Hendrik G and Todd, John A and Zerbino, Daniel R and Stegle, Oliver and Ouwehand, Willem H and Frontini, Mattia and Wallace, Chris and Spivakov, Mikhail and Fraser, Peter and The BLUEPRINT Consortium and BLUEPRINT Consortium
Cell (Cambridge), ISSN 0092-8674, 11/2016, Volume 167, Issue 5, pp. 1369 - 1384.e19
promoter capture Hi-C | non-coding genetic variation | disease gene prioritization | gene regulation | chromosome conformation | Biochemistry & Molecular Biology | Life Sciences & Biomedicine | Science & Technology | Cell Biology | Promoter Regions, Genetic | Chromatin | Genetic Predisposition to Disease | Genome-Wide Association Study | Epigenomics | Disease - genetics | Cell Separation | Humans | Cell Lineage | Blood Cells - cytology | Enhancer Elements, Genetic | Hematopoiesis | Polymorphism, Single Nucleotide | Quantitative Trait Loci | Genes | Genomics | Genetic aspects | Medical research | Medical genetics | Medicine, Experimental | Index Medicus | Resource
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