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272 results on '"Maciewicz, Rose A."'

1. Selective IL-27 production by intestinal regulatory T cells permits gut-specific regulation of TH17 cell immunity

Author

Lin, Chia-Hao, Wu, Cheng-Jang, Cho, Sunglim, Patkar, Rasika, Huth, William J, Lin, Ling-Li, Chen, Mei-Chi, Israelsson, Elisabeth, Betts, Joanne, Niedzielska, Magdalena, Patel, Shefali A, Duong, Han G, Gerner, Romana R, Hsu, Chia-Yun, Catley, Matthew, Maciewicz, Rose A, Chu, Hiutung, Raffatellu, Manuela, Chang, John T, and Lu, Li-Fan

Subjects
Biomedical and Clinical Sciences, Immunology, Autoimmune Disease, Digestive Diseases, Inflammatory Bowel Disease, Aetiology, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Underpinning research, Inflammatory and immune system, Mice, Animals, T-Lymphocytes, Regulatory, Interleukin-27, T-Lymphocytes, Helper-Inducer, Immune Tolerance, Immunity, Cellular, Th17 Cells, Biochemistry and cell biology
Abstract

Regulatory T cells (Treg cells) are instrumental in establishing immunological tolerance. However, the precise effector mechanisms by which Treg cells control a specific type of immune response in a given tissue remains unresolved. By simultaneously studying Treg cells from different tissue origins under systemic autoimmunity, in the present study we show that interleukin (IL)-27 is specifically produced by intestinal Treg cells to regulate helper T17 cell (TH17 cell) immunity. Selectively increased intestinal TH17 cell responses in mice with Treg cell-specific IL-27 ablation led to exacerbated intestinal inflammation and colitis-associated cancer, but also helped protect against enteric bacterial infection. Furthermore, single-cell transcriptomic analysis has identified a CD83+CD62Llo Treg cell subset that is distinct from previously characterized intestinal Treg cell populations as the main IL-27 producers. Collectively, our study uncovers a new Treg cell suppression mechanism crucial for controlling a specific type of immune response in a particular tissue and provides further mechanistic insights into tissue-specific Treg cell-mediated immune regulation.

Published
2023

2. Novel Genetic Variants for Cartilage Thickness and Hip Osteoarthritis.

Author

Castaño-Betancourt, Martha C, Evans, Dan S, Ramos, Yolande FM, Boer, Cindy G, Metrustry, Sarah, Liu, Youfang, den Hollander, Wouter, van Rooij, Jeroen, Kraus, Virginia B, Yau, Michelle S, Mitchell, Braxton D, Muir, Kenneth, Hofman, Albert, Doherty, Michael, Doherty, Sally, Zhang, Weiya, Kraaij, Robert, Rivadeneira, Fernando, Barrett-Connor, Elizabeth, Maciewicz, Rose A, Arden, Nigel, Nelissen, Rob GHH, Kloppenburg, Margreet, Jordan, Joanne M, Nevitt, Michael C, Slagboom, Eline P, Hart, Deborah J, Lafeber, Floris, Styrkarsdottir, Unnur, Zeggini, Eleftheria, Evangelou, Evangelos, Spector, Tim D, Uitterlinden, Andre G, Lane, Nancy E, Meulenbelt, Ingrid, Valdes, Ana M, and van Meurs, Joyce BJ

Subjects
Cartilage, Hip Joint, Humans, Osteoarthritis, Hip, Genetic Predisposition to Disease, Trehalase, Transforming Growth Factor alpha, Regulatory Sequences, Nucleic Acid, Genetic Heterogeneity, Polymorphism, Single Nucleotide, Aged, Aged, 80 and over, Middle Aged, Female, Male, Receptor, Fibroblast Growth Factor, Type 3, Genome-Wide Association Study, Phosphatidylinositol 3-Kinases, Class Ia Phosphatidylinositol 3-Kinase, Osteoarthritis, Hip, Regulatory Sequences, Nucleic Acid, Polymorphism, Single Nucleotide, and over, Receptor, Fibroblast Growth Factor, Type 3, Genetics, Developmental Biology
Abstract

Osteoarthritis is one of the most frequent and disabling diseases of the elderly. Only few genetic variants have been identified for osteoarthritis, which is partly due to large phenotype heterogeneity. To reduce heterogeneity, we here examined cartilage thickness, one of the structural components of joint health. We conducted a genome-wide association study of minimal joint space width (mJSW), a proxy for cartilage thickness, in a discovery set of 13,013 participants from five different cohorts and replication in 8,227 individuals from seven independent cohorts. We identified five genome-wide significant (GWS, P≤5·0×10-8) SNPs annotated to four distinct loci. In addition, we found two additional loci that were significantly replicated, but results of combined meta-analysis fell just below the genome wide significance threshold. The four novel associated genetic loci were located in/near TGFA (rs2862851), PIK3R1 (rs10471753), SLBP/FGFR3 (rs2236995), and TREH/DDX6 (rs496547), while the other two (DOT1L and SUPT3H/RUNX2) were previously identified. A systematic prioritization for underlying causal genes was performed using diverse lines of evidence. Exome sequencing data (n = 2,050 individuals) indicated that there were no rare exonic variants that could explain the identified associations. In addition, TGFA, FGFR3 and PIK3R1 were differentially expressed in OA cartilage lesions versus non-lesioned cartilage in the same individuals. In conclusion, we identified four novel loci (TGFA, PIK3R1, FGFR3 and TREH) and confirmed two loci known to be associated with cartilage thickness.The identified associations were not caused by rare exonic variants. This is the first report linking TGFA to human OA, which may serve as a new target for future therapies.

Published
2016

5. Selective IL-27 production by intestinal regulatory T cells permits gut-specific regulation of Th17 immunity

Author

Lin, Chia-Hao, primary, Wu, Cheng-Jang, additional, Cho, Sunglim, additional, Patkar, Rasika, additional, Lin, Ling-Li, additional, Chen, Mei-Chi, additional, Israelsson, Elisabeth, additional, Betts, Joanne, additional, Niedzielska, Magdalena, additional, Patel, Shefali A., additional, Duong, Han G., additional, Gerner, Romana R., additional, Hsu, Chia-Yun, additional, Catley, Matthew, additional, Maciewicz, Rose A., additional, Chu, Hiutung, additional, Raffatellu, Manuela, additional, Chang, John T., additional, and Lu, Li-Fan, additional

Published
2023
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7. Genome-wide association and functional studies identify the DOT1L gene to be involved in cartilage thickness and hip osteoarthritis

Author

Betancourt, Martha C. Castaño, Cailotto, Frederic, Kerkhof, Hanneke J., Cornelis, Frederique M. F., Doherty, Sally A., Hart, Deborah J., Hofman, Albert, Luyten, Frank P., Maciewicz, Rose A., Mangino, Massimo, Metrustry, Sarah, Muir, Kenneth, Peters, Marjolein J., Rivadeneira, Fernando, Wheeler, Maggie, Zhang, Weiya, Arden, Nigel, Spector, Tim D., Uitterlinden, Andre G., Doherty, Michael, Lories, Rik J. U., Valdes, Ana M., and van Meurs, Joyce B. J.

Published
2012

8. 688 - IDENTIFYING MOLECULAR PATHWAYS ASSOCIATED WITH RADIOGRAPHIC STAGE IN KNEE OSTEOARTHRITIS THROUGH LARGE-SCALE PROTEOMICS OF SYNOVIAL FLUID: DATA FROM THE STEPUP OA CONSORTIUM

Author

Perry, Thomas A., Deng, Yun, Hulley, Philippa, Maciewicz, Rose A., Mitchelmore, Joanna, Gogain, Joe, Larsson, Staffan, Brachat, Sophie, Struglics, André, Appleton, C. Thomas, Kluzek, Stefan, Arden, Nigel, Felson, David, Bondi, Laura, Kapoor, Mohit, Lohmander, Stefan, Welting, Tim, Walsh, David A., Valdes, Ana, Watt, Fiona E., Tom, Brian, Jostins-Dean, Luke, and Vincent, Tonia

Published
2024
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9. 074 - SYNOVIAL FLUID BASED MOLECULAR ENDOTYPES IN KNEE OSTEOARTHRITIS: FULL PRIMARY ANALYSIS FROM THE STEPUp OA CONSORTIUM

Author

Deng, Yun, Perry, Thomas A., Hulley, Philippa, Maciewicz, Rose A., Mitchelmore, Joanna, Gogain, Joe, Larsson, Staffan, Brachat, Sophie, Struglics, André, Appleton, C. Thomas, Kluzek, Stefan, Arden, Nigel, Felson, David, Bondi, Laura, Kapoor, Mohit, Lohmander, Stefan, Welting, Tim, Walsh, David A., Valdes, Ana, Tom, Brian, Vincent, Tonia, Watt, Fiona E., and Jostins-Dean, Luke

Published
2024
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13. Intestinal-derived ILCs migrating in lymph increase IFNγ production in response to Salmonella Typhimurium infection

Author

Kästele, Verena, primary, Mayer, Johannes, additional, Lee, Edward S., additional, Papazian, Natalie, additional, Cole, John J., additional, Cerovic, Vuk, additional, Belz, Gabrielle, additional, Tomura, Michio, additional, Eberl, Gerard, additional, Goodyear, Carl, additional, Maciewicz, Rose A., additional, Wall, Daniel, additional, Cupedo, Tom, additional, Withers, David R., additional, and Milling, Simon, additional

Published
2021
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14. Large-scale plasma proteomics can reveal distinct endotypes in chronic obstructive pulmonary disease and severe asthma

Author

1000010374290, Suzuki, Masaru, Cole, John J., 1000020399835, Konno, Satoshi, 1000070533537, Makita, Hironi, 1000060773314, Kimura, Hiroki, 1000000208224, Nishimura, Masaharu, Maciewicz, Rose A., 1000010374290, Suzuki, Masaru, Cole, John J., 1000020399835, Konno, Satoshi, 1000070533537, Makita, Hironi, 1000060773314, Kimura, Hiroki, 1000000208224, Nishimura, Masaharu, and Maciewicz, Rose A.

Abstract

Background Chronic airway diseases including chronic obstructive pulmonary disease (COPD) and asthma are heterogenous in nature and endotypes within are underpinned by complex biology. This study aimed to investigate the utility of proteomic profiling of plasma combined with bioinformatic mining, and to define molecular endotypes and expand our knowledge of the underlying biology in chronic respiratory diseases. Methods The plasma proteome was evaluated using an aptamer-based affinity proteomics platform (SOMAscan (R)), representing 1238 proteins in 34 subjects with stable COPD and 51 subjects with stable but severe asthma. For each disease, we evaluated a range of clinical/demographic characteristics including bronchodilator reversibility, blood eosinophilia levels, and smoking history. We applied modified bioinformatic approaches used in the evaluation of RNA transcriptomics. Results Subjects with COPD and severe asthma were distinguished from each other by 365 different protein abundancies, with differential pathway networks and upstream modulators. Furthermore, molecular endotypes within each disease could be defined. The protein groups that defined these endotypes had both known and novel biology including groups significantly enriched in exosomal markers derived from immune/inflammatory cells. Finally, we observed associations to clinical characteristics that previously have been under-explored. Conclusion This investigational study evaluating the plasma proteome in clinically-phenotyped subjects with chronic airway diseases provides support that such a method can be used to define molecular endotypes and pathobiological mechanisms that underpins these endotypes. It provided new concepts about the complexity of molecular pathways that define these diseases. In the longer term, such information will help to refine treatment options for defined groups.

Published
2021

15. Large-scale plasma proteomics can reveal distinct endotypes in chronic obstructive pulmonary disease and severe asthma

Author

Suzuki, Masaru, Cole, John J., Konno, Satoshi, Makita, Hironi, Kimura, Hiroki, Nishimura, Masaharu, Maciewicz, Rose A., Suzuki, Masaru, Cole, John J., Konno, Satoshi, Makita, Hironi, Kimura, Hiroki, Nishimura, Masaharu, and Maciewicz, Rose A.

Abstract

Background Chronic airway diseases including chronic obstructive pulmonary disease (COPD) and asthma are heterogenous in nature and endotypes within are underpinned by complex biology. This study aimed to investigate the utility of proteomic profiling of plasma combined with bioinformatic mining, and to define molecular endotypes and expand our knowledge of the underlying biology in chronic respiratory diseases. Methods The plasma proteome was evaluated using an aptamer-based affinity proteomics platform (SOMAscan (R)), representing 1238 proteins in 34 subjects with stable COPD and 51 subjects with stable but severe asthma. For each disease, we evaluated a range of clinical/demographic characteristics including bronchodilator reversibility, blood eosinophilia levels, and smoking history. We applied modified bioinformatic approaches used in the evaluation of RNA transcriptomics. Results Subjects with COPD and severe asthma were distinguished from each other by 365 different protein abundancies, with differential pathway networks and upstream modulators. Furthermore, molecular endotypes within each disease could be defined. The protein groups that defined these endotypes had both known and novel biology including groups significantly enriched in exosomal markers derived from immune/inflammatory cells. Finally, we observed associations to clinical characteristics that previously have been under-explored. Conclusion This investigational study evaluating the plasma proteome in clinically-phenotyped subjects with chronic airway diseases provides support that such a method can be used to define molecular endotypes and pathobiological mechanisms that underpins these endotypes. It provided new concepts about the complexity of molecular pathways that define these diseases. In the longer term, such information will help to refine treatment options for defined groups.

Published
2021

19. A role for PACE4 in osteoarthritis pain: evidence from human genetic association and null mutant phenotype

Author

Malfait, Anne-Marie, Seymour, Albert B, Gao, Feng, Tortorella, Micky D, Le Graverand-Gastineau, Marie-Pierre Hellio, Wood, Linda S, Doherty, Michael, Doherty, Sally, Zhang, Weiya, Arden, Nigel K, Vaughn, Frances L, Leaverton, Paul E, Spector, Tim D, Hart, Deborah J, Maciewicz, Rose A, Muir, Kenneth R, Das, Rosalina, Sorge, Robert E, Sotocinal, Susanna G, Schorscher-Petcu, Ara, Valdes, Ana M, and Mogil, Jeffrey S

Published
2012
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20. The Ile585Val TRPV1 variant is involved in risk of painful knee osteoarthritis

Author

Valdes, Ana M, De Wilde, Gert, Doherty, Sally A, Lories, Rik J, Vaughn, Frances L, Laslett, Laura L, Maciewicz, Rose A, Soni, Anushka, Hart, Deborah J, Zhang, Weiya, Muir, Kenneth R, Dennison, Elaine M, Wheeler, Margaret, Leaverton, Paul, Cooper, Cyrus, Spector, Tim D, Cicuttini, Flavia M, Chapman, Victoria, Jones, Graeme, Arden, Nigel K, and Doherty, Michael

Published
2011
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22. The GDF5 rs143383 polymorphism is associated with osteoarthritis of the knee with genome-wide statistical significance

Author

Valdes, Ana M, Evangelou, Evangelos, Kerkhof, Hanneke J M, Tamm, Agu, Doherty, Sally A, Kisand, Kalle, Tamm, Ann, Kerna, Irina, Uitterlinden, Andre, Hofman, Albert, Rivadeneira, Fernando, Cooper, Cyrus, Dennison, Elaine M, Zhang, Weiya, Muir, Kenneth R, Ioannidis, John P A, Wheeler, Margaret, Maciewicz, Rose A, van Meurs, Joyce B, Arden, Nigel K, Spector, Tim D, and Doherty, Michael

Published
2011
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31. Additional file 1: of MEK inhibition drives anti-viral defence in RV but not RSV challenged human airway epithelial cells through AKT/p70S6K/4E-BP1 signalling

Author

Baturcam, Engin, Vollmer, Stefan, Schlüter, Holger, Maciewicz, Rose, Kurian, Nisha, Vaarala, Outi, Ludwig, Stephan, and Danen Cunoosamy

Abstract

Figure S1. MEK inhibitor works to reduce pERK1/2 and enhances IFN-β release. Figure S2. Challenge with poly(I:C) is similar but not identical to challenge with RV2. Figure S3. PI3Ki does not cause cytotoxicity. Figure S4. Enhanced IFN-β response due to MEKi is not associated with increased IRF7 protein expression. Figure S5. Challenge with poly(I:C) is similar but not identical to challenge with RV2 or RSVA2. Figure S6. Induction of ISG15 mRNA by poly(I:C) is similar to that of RV2. Figure S7. MEKi reduces phosphorylation of STAT3 at S727. Table S1. NHBE donors. Table S2. Structure of small molecules and PROTACs. Table S3. List of antibodies used for immunoblotting. Table S4. Target sequence of short interfering RNA (siRNA). Table S5. List of Taqman primer/probe. (DOCX 1110 kb)

Published
2019
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35. Sensing of apoptotic cells through Axl causes lung basal cell proliferation in inflammatory diseases

Author

Fujino, Naoya, primary, Brand, Oliver J., additional, Morgan, David J., additional, Fujimori, Toshifumi, additional, Grabiec, Aleksander M., additional, Jagger, Christopher P., additional, Maciewicz, Rose A., additional, Yamada, Mitsuhiro, additional, Itakura, Koji, additional, Sugiura, Hisatoshi, additional, Ichinose, Masakazu, additional, and Hussell, Tracy, additional

Published
2019
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36. Upper Airway Cell Transcriptomics Identify a Major New Immunological Phenotype with Strong Clinical Correlates in Young Children with Acute Wheezing

Author

Khoo, Siew-Kim, primary, Read, James, additional, Franks, Kimberley, additional, Zhang, Guicheng, additional, Bizzintino, Joelene, additional, Coleman, Laura, additional, McCrae, Christopher, additional, Öberg, Lisa, additional, Troy, Niamh M., additional, Prastanti, Franciska, additional, Everard, Janet, additional, Oo, Stephen, additional, Borland, Meredith L., additional, Maciewicz, Rose A., additional, Le Souëf, Peter N., additional, Laing, Ingrid A., additional, and Bosco, Anthony, additional

Published
2019
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43. Intestinal-derived ILCs migrating in lymph increase IFNγ production in response to SalmonellaTyphimurium infection

Author

Kästele, Verena, Mayer, Johannes, Lee, Edward S., Papazian, Natalie, Cole, John J., Cerovic, Vuk, Belz, Gabrielle, Tomura, Michio, Eberl, Gerard, Goodyear, Carl, Maciewicz, Rose A., Wall, Daniel, Cupedo, Tom, Withers, David R., and Milling, Simon

Abstract

Innate lymphoid cells (ILCs) are enriched in mucosae and have been described as tissue-resident. Interestingly, ILCs are also present within lymph nodes (LNs), in the interfollicular regions, the destination for lymph-migratory cells. We have previously shown that LN ILCs are supplemented by peripheral tissue-derived ILCs. Using thoracic duct cannulations, we here enumerate the intestinal lymph ILCs that traffic from the intestine to the mesenteric LNs (MLNs). We provide, for the first time, a detailed characterisation of these lymph-migratory ILCs. We show that all ILC subsets migrate in lymph, and while global transcriptional analysis reveals a shared signature with tissue-resident ILCs, lymph ILCs express migration-associated genes including S1PRs, SELL(CD62L) and CCR7. Interestingly, we discovered that while SalmonellaTyphimurium infections do not increase the numbers of migrating ILCs, infection changes their composition and cytokine profile. Infection increases the proportions of RORyt+T-bet+ILCs, levels of IFNγ, and IFNγ/GM-CSF co-expression. Infection-induced changes in migratory ILCs are reflected in colon-draining MLN ILCs, where RORyt+T-bet+ILCs accumulate and display corresponding increased cytokine expression. Thus, we reveal that ILCs respond rapidly to intestinal infection and can migrate to the MLN where they produce cytokines.

Published
2021
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44. Airway IRF7hiversus IRF7lomolecular response patterns determine clinical phenotypes in children with acute wheezing

Author

Khoo, Siew-Kim, primary, Read, James, additional, Franks, Kimberley, additional, Zhang, Guicheng, additional, Bizzintino, Joelene, additional, Coleman, Laura, additional, McCrae, Christopher, additional, Öberg, Lisa, additional, Troy, Niamh, additional, Prastanti, Franciska, additional, Everard, Janet, additional, Oo, Stephen, additional, Borland, Meredith L, additional, Maciewicz, Rose A, additional, Le Souëf, Peter N, additional, Laing, Ingrid A, additional, and Bosco, Anthony, additional

Published
2017
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45. Beta-blocker use associates with lower prevalence of joint pain and lower opioid requirement in people with osteoarthritis

Author

Valdes, Ana M., Abhishek, Abhishek, Muir, Kenneth, Zhang, Weiya, Maciewicz, Rose A., and Doherty, Michael

Subjects
musculoskeletal diseases
Abstract

Objective: Recent findings suggest that β-adrenergic blockers have anti-nociceptive properties. The aim of this study was to compare levels of large joint pain between those on adrenergic blockers and those on other antihypertensive medications. Methods: Data from the GOAL study, a secondary care cohort of osteoarthritis (OA), were used. Joint pain was assessed using the Western Ontario and McMaster Universities Arthritis (WOMAC) pain score in 873 individuals who had symptomatic hip and/or knee OA and hypertension, and who were on ≥1 prescription antihypertensive medications. The association between adrenergic blocker prescription and a) at least moderate joint pain (WOMAC

Published
2016

46. Phosphoinositide-3-kinase gamma/delta isoform signalling defines a mixed T cell severe asthmatic endotype

Author

Thomas, Matt, primary, Bjorhall, Karin, additional, Israelsson, Elisabeth, additional, LammBergstrom, Eva, additional, Horvat, Jay, additional, Kim, Richard, additional, Maciewicz, Rose, additional, Muthas, Daniel, additional, Nordberg, Maria, additional, RodrigoBlomqvist, Sandra, additional, Saarne, Tiiu, additional, Winkler, Carla, additional, Karabelas, Kostas, additional, Adcock, Ian, additional, Chung, Fan, additional, Hansbro, Philip, additional, Malmgren, Anna, additional, and Perry, Matthew, additional

Published
2017
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47. Central role for phosphoinositide-3-kinase gamma/delta dependent signalling in eosinophilic pulmonary inflammation driven by innate lymphoid cells

Author

Thomas, Matt, primary, Bjorhall, Karin, additional, Collins, Mia, additional, Israelsson, Elisabeth, additional, Krutrok, Nina, additional, LammBergstrom, Eva, additional, Maciewicz, Rose, additional, Muthas, Daniel, additional, Nordberg, Maria, additional, Perry, Matthew, additional, RodrigoBlomqvist, Sandra, additional, Saarne, Tiiu, additional, Winkler, Carla, additional, Karabelas, Kostas, additional, Malmgren, Anna, additional, Adcock, Ian, additional, Chung, Fan, additional, and Wymann, Matthias, additional

Published
2017
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49. Novel Genetic Variants for Cartilage Thickness and Hip Osteoarthritis

Author

Castaño-Betancourt, Martha C., Evans, Dan S., Ramos, Yolande F M, Boer, Cindy G., Metrustry, Sarah, Liu, Youfang, den Hollander, Wouter, van Rooij, Jeroen, Kraus, Virginia B., Yau, Michelle S., Mitchell, Braxton D., Muir, Kenneth, Hofman, Albert, Doherty, Michael, Doherty, Sally, Zhang, Weiya, Kraaij, Robert, Rivadeneira, Fernando, Barrett-Connor, Elizabeth, Maciewicz, Rose A., Arden, Nigel, Nelissen, Rob G H H, Kloppenburg, Margreet, Jordan, Joanne M., Nevitt, Michael C., Slagboom, Eline P., Hart, Deborah J., Lafeber, Floris, Styrkarsdottir, Unnur, Zeggini, Eleftheria, Evangelou, Evangelos, Spector, Tim D., Uitterlinden, Andre G., Lane, Nancy E., Meulenbelt, Ingrid, Valdes, Ana M., van Meurs, Joyce B J, Castaño-Betancourt, Martha C., Evans, Dan S., Ramos, Yolande F M, Boer, Cindy G., Metrustry, Sarah, Liu, Youfang, den Hollander, Wouter, van Rooij, Jeroen, Kraus, Virginia B., Yau, Michelle S., Mitchell, Braxton D., Muir, Kenneth, Hofman, Albert, Doherty, Michael, Doherty, Sally, Zhang, Weiya, Kraaij, Robert, Rivadeneira, Fernando, Barrett-Connor, Elizabeth, Maciewicz, Rose A., Arden, Nigel, Nelissen, Rob G H H, Kloppenburg, Margreet, Jordan, Joanne M., Nevitt, Michael C., Slagboom, Eline P., Hart, Deborah J., Lafeber, Floris, Styrkarsdottir, Unnur, Zeggini, Eleftheria, Evangelou, Evangelos, Spector, Tim D., Uitterlinden, Andre G., Lane, Nancy E., Meulenbelt, Ingrid, Valdes, Ana M., and van Meurs, Joyce B J

Published
2016

50. Novel Genetic Variants for Cartilage Thickness and Hip Osteoarthritis

Author

Lab Reumatologie/Klinische Immunologie, Regenerative Medicine and Stem Cells, Infection & Immunity, dLAB Biobank, Castaño-Betancourt, Martha C., Evans, Dan S., Ramos, Yolande F M, Boer, Cindy G., Metrustry, Sarah, Liu, Youfang, den Hollander, Wouter, van Rooij, Jeroen, Kraus, Virginia B., Yau, Michelle S., Mitchell, Braxton D., Muir, Kenneth, Hofman, Albert, Doherty, Michael, Doherty, Sally, Zhang, Weiya, Kraaij, Robert, Rivadeneira, Fernando, Barrett-Connor, Elizabeth, Maciewicz, Rose A., Arden, Nigel, Nelissen, Rob G H H, Kloppenburg, Margreet, Jordan, Joanne M., Nevitt, Michael C., Slagboom, Eline P., Hart, Deborah J., Lafeber, Floris, Styrkarsdottir, Unnur, Zeggini, Eleftheria, Evangelou, Evangelos, Spector, Tim D., Uitterlinden, Andre G., Lane, Nancy E., Meulenbelt, Ingrid, Valdes, Ana M., van Meurs, Joyce B J, Lab Reumatologie/Klinische Immunologie, Regenerative Medicine and Stem Cells, Infection & Immunity, dLAB Biobank, Castaño-Betancourt, Martha C., Evans, Dan S., Ramos, Yolande F M, Boer, Cindy G., Metrustry, Sarah, Liu, Youfang, den Hollander, Wouter, van Rooij, Jeroen, Kraus, Virginia B., Yau, Michelle S., Mitchell, Braxton D., Muir, Kenneth, Hofman, Albert, Doherty, Michael, Doherty, Sally, Zhang, Weiya, Kraaij, Robert, Rivadeneira, Fernando, Barrett-Connor, Elizabeth, Maciewicz, Rose A., Arden, Nigel, Nelissen, Rob G H H, Kloppenburg, Margreet, Jordan, Joanne M., Nevitt, Michael C., Slagboom, Eline P., Hart, Deborah J., Lafeber, Floris, Styrkarsdottir, Unnur, Zeggini, Eleftheria, Evangelou, Evangelos, Spector, Tim D., Uitterlinden, Andre G., Lane, Nancy E., Meulenbelt, Ingrid, Valdes, Ana M., and van Meurs, Joyce B J

Published
2016

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