Analysis of neuropeptide S receptor gene (NPSR1) polymorphism in rheumatoid arthritis
Polymorphism in the neuropeptide S receptor gene NPSR1 is associated with asthma and inflammatory bowel disease. NPSR1 is expressed in the brain, where it modulates anxiety and responses to stress, but also in other tissues and cell types including lymphocytes, the lungs, and the intestine, where it...
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| creator | D'Amato, Mauro Zucchelli, Marco Seddighzadeh, Maria Anedda, Francesca Lindblad, Staffan Kere, Juha Alfredsson, Lars Klareskog, Lars Padyukov, Leonid |
| description | Polymorphism in the neuropeptide S receptor gene NPSR1 is associated with asthma and inflammatory bowel disease. NPSR1 is expressed in the brain, where it modulates anxiety and responses to stress, but also in other tissues and cell types including lymphocytes, the lungs, and the intestine, where it appears to be up-regulated in inflammation. We sought to determine whether genetic variability at the NPSR1 locus influences the susceptibility and clinical manifestation of rheumatoid arthritis (RA).
From the Epidemiological Investigation of Rheumatoid Arthritis (EIRA) case-control study, 1,888 rheumatoid arthritis patients and 888 controls were genotyped for 19 single-nucleotide polymorphisms (SNPs) spanning the entire NPSR1 gene and 220 KB of DNA on chromosome 7p14. The association between individual genetic markers and their haplotypic combinations, respectively, and diagnosis of RA, presence of autoantibodies to citrullinated proteins (ACPA), and disease activity score based on 28 joints (DAS28) was tested. There was no association between diagnosis of RA and NPSR1 variants. However, several associations of nominal significance were detected concerning susceptibility to ACPA-negative RA and disease activity measures (DAS28). Among these, the association of SNP rs324987 with ACPA-negative RA [(p=0.004, OR=0.674 (95% CI 0.512-0.888)] and that of SNP rs10263447 with DAS28 [p=0.0002, OR=0.380 (95% CI 0.227-0.635)] remained significant after correction for multiple comparisons.
NPSR1 polymorphism may be relevant to RA susceptibility and its clinical manifestation. Specific alleles at the NPSR1 locus may represent common risk factors for chronic inflammatory diseases, including RA. |
| doi_str_mv | 10.1371/journal.pone.0009315 |
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From the Epidemiological Investigation of Rheumatoid Arthritis (EIRA) case-control study, 1,888 rheumatoid arthritis patients and 888 controls were genotyped for 19 single-nucleotide polymorphisms (SNPs) spanning the entire NPSR1 gene and 220 KB of DNA on chromosome 7p14. The association between individual genetic markers and their haplotypic combinations, respectively, and diagnosis of RA, presence of autoantibodies to citrullinated proteins (ACPA), and disease activity score based on 28 joints (DAS28) was tested. There was no association between diagnosis of RA and NPSR1 variants. However, several associations of nominal significance were detected concerning susceptibility to ACPA-negative RA and disease activity measures (DAS28). Among these, the association of SNP rs324987 with ACPA-negative RA [(p=0.004, OR=0.674 (95% CI 0.512-0.888)] and that of SNP rs10263447 with DAS28 [p=0.0002, OR=0.380 (95% CI 0.227-0.635)] remained significant after correction for multiple comparisons.
NPSR1 polymorphism may be relevant to RA susceptibility and its clinical manifestation. Specific alleles at the NPSR1 locus may represent common risk factors for chronic inflammatory diseases, including RA.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0009315</identifier><identifier>PMID: 20179762</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adolescent ; Adult ; Aged ; Analysis ; Anxiety ; Arthritis ; Arthritis, Rheumatoid - epidemiology ; Arthritis, Rheumatoid - genetics ; Arthritis, Rheumatoid - pathology ; Asthma ; Autoantibodies ; Autoimmunity ; Brain ; Case-Control Studies ; Chromosome 7 ; Citrulline ; Deoxyribonucleic acid ; Diagnosis ; DNA ; Epidemiology ; Ethics ; Female ; Gene Frequency ; Gene polymorphism ; Genes ; Genetic aspects ; Genetic markers ; Genetic Predisposition to Disease ; Genetic variability ; Genetics ; Genetics and Genomics/Complex Traits ; Genetics and Genomics/Genetics of Disease ; Genetics and Genomics/Genetics of the Immune System ; Genetics and Genomics/Medical Genetics ; Genotype ; Haplotypes ; Health risks ; Humans ; Incidence ; Inflammatory bowel disease ; Inflammatory bowel diseases ; Inflammatory diseases ; Intestine ; Joint diseases ; Linkage Disequilibrium ; Loci ; Lungs ; Lymphocytes ; Male ; Medical research ; Medicine ; Middle Aged ; Mutation ; Neuropeptides ; Nutrition ; Odds Ratio ; Physiology ; Polymorphism ; Polymorphism, Single Nucleotide ; Population ; Principal components analysis ; Proteins ; Receptors, G-Protein-Coupled - genetics ; Rheumatoid arthritis ; Rheumatoid factor ; Rheumatology ; Rheumatology/Rheumatoid Arthritis ; Risk analysis ; Risk Factors ; Single nucleotide polymorphisms ; Single-nucleotide polymorphism ; Studies ; Sweden - epidemiology ; Tissues ; Young Adult</subject><ispartof>PloS one, 2010-02, Vol.5 (2), p.e9315-e9315</ispartof><rights>COPYRIGHT 2010 Public Library of Science</rights><rights>2010 D'Amato et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>D'Amato et al. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c630t-4c68b8d56e15200d0ba53db0067814194705c2e0fdee5db2f1d54ce06b8551c03</citedby><cites>FETCH-LOGICAL-c630t-4c68b8d56e15200d0ba53db0067814194705c2e0fdee5db2f1d54ce06b8551c03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2825264/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2825264/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,550,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20179762$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:120094076$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>D'Amato, Mauro</creatorcontrib><creatorcontrib>Zucchelli, Marco</creatorcontrib><creatorcontrib>Seddighzadeh, Maria</creatorcontrib><creatorcontrib>Anedda, Francesca</creatorcontrib><creatorcontrib>Lindblad, Staffan</creatorcontrib><creatorcontrib>Kere, Juha</creatorcontrib><creatorcontrib>Alfredsson, Lars</creatorcontrib><creatorcontrib>Klareskog, Lars</creatorcontrib><creatorcontrib>Padyukov, Leonid</creatorcontrib><title>Analysis of neuropeptide S receptor gene (NPSR1) polymorphism in rheumatoid arthritis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Polymorphism in the neuropeptide S receptor gene NPSR1 is associated with asthma and inflammatory bowel disease. NPSR1 is expressed in the brain, where it modulates anxiety and responses to stress, but also in other tissues and cell types including lymphocytes, the lungs, and the intestine, where it appears to be up-regulated in inflammation. We sought to determine whether genetic variability at the NPSR1 locus influences the susceptibility and clinical manifestation of rheumatoid arthritis (RA).
From the Epidemiological Investigation of Rheumatoid Arthritis (EIRA) case-control study, 1,888 rheumatoid arthritis patients and 888 controls were genotyped for 19 single-nucleotide polymorphisms (SNPs) spanning the entire NPSR1 gene and 220 KB of DNA on chromosome 7p14. The association between individual genetic markers and their haplotypic combinations, respectively, and diagnosis of RA, presence of autoantibodies to citrullinated proteins (ACPA), and disease activity score based on 28 joints (DAS28) was tested. There was no association between diagnosis of RA and NPSR1 variants. However, several associations of nominal significance were detected concerning susceptibility to ACPA-negative RA and disease activity measures (DAS28). Among these, the association of SNP rs324987 with ACPA-negative RA [(p=0.004, OR=0.674 (95% CI 0.512-0.888)] and that of SNP rs10263447 with DAS28 [p=0.0002, OR=0.380 (95% CI 0.227-0.635)] remained significant after correction for multiple comparisons.
NPSR1 polymorphism may be relevant to RA susceptibility and its clinical manifestation. Specific alleles at the NPSR1 locus may represent common risk factors for chronic inflammatory diseases, including RA.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Analysis</subject><subject>Anxiety</subject><subject>Arthritis</subject><subject>Arthritis, Rheumatoid - epidemiology</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Arthritis, Rheumatoid - pathology</subject><subject>Asthma</subject><subject>Autoantibodies</subject><subject>Autoimmunity</subject><subject>Brain</subject><subject>Case-Control Studies</subject><subject>Chromosome 7</subject><subject>Citrulline</subject><subject>Deoxyribonucleic acid</subject><subject>Diagnosis</subject><subject>DNA</subject><subject>Epidemiology</subject><subject>Ethics</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Gene polymorphism</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic markers</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic variability</subject><subject>Genetics</subject><subject>Genetics and Genomics/Complex Traits</subject><subject>Genetics and Genomics/Genetics of Disease</subject><subject>Genetics and Genomics/Genetics of the Immune System</subject><subject>Genetics and Genomics/Medical Genetics</subject><subject>Genotype</subject><subject>Haplotypes</subject><subject>Health risks</subject><subject>Humans</subject><subject>Incidence</subject><subject>Inflammatory bowel disease</subject><subject>Inflammatory bowel diseases</subject><subject>Inflammatory diseases</subject><subject>Intestine</subject><subject>Joint diseases</subject><subject>Linkage Disequilibrium</subject><subject>Loci</subject><subject>Lungs</subject><subject>Lymphocytes</subject><subject>Male</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Neuropeptides</subject><subject>Nutrition</subject><subject>Odds Ratio</subject><subject>Physiology</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Population</subject><subject>Principal components analysis</subject><subject>Proteins</subject><subject>Receptors, G-Protein-Coupled - genetics</subject><subject>Rheumatoid arthritis</subject><subject>Rheumatoid factor</subject><subject>Rheumatology</subject><subject>Rheumatology/Rheumatoid Arthritis</subject><subject>Risk analysis</subject><subject>Risk Factors</subject><subject>Single nucleotide polymorphisms</subject><subject>Single-nucleotide polymorphism</subject><subject>Studies</subject><subject>Sweden - epidemiology</subject><subject>Tissues</subject><subject>Young Adult</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>D8T</sourceid><sourceid>DOA</sourceid><recordid>eNptkltv1DAQhSMEoqXwDxBE4gF42GV8TfKCtKq4VKoAUfpsOfZk10sSBzsB7b_Hy6ZVF1V5yGj8nePx6GTZcwJLwgrybuun0Ot2OfgelwBQMSIeZKekYnQhKbCHd-qT7EmMWwDBSikfZycUSFEVkp5m16vksYsu5r7Je5yCH3AYncX8Kg9oUu1DvsYe8zdfvl19J2_zwbe7zodh42KXuz4PG5w6PXpncx3GTXCji0-zR41uIz6b_2fZ9ccPP84_Ly6_fro4X10ujGQwLriRZV1aIZEICmCh1oLZGkAWJeGk4gUIQxEaiyhsTRtiBTcIsi6FIAbYWfby4Du0Pqp5I1ERWlZUVEJWibg4ENbrrRqC63TYKa-d-tfwYa3S1M60qBqowNQNagOak4LrutQVsZTTEpBKnrwWB6_4B4epPnKbWz9ThUoIBrDn38_TTXWH1mA_Bt0eyY5PerdRa_9b0ZKKw4WvZ4Pgf00YR9W5aLBtdY9-iqpgTBaUl2UiX_1H3r-MmVrr9F7XNz5da_aeasULVhHOK5qo5T1U-ix2zqS0NS71jwT8IDDBxxiwuX0iAbXP6s0wap9VNWc1yV7cXc-t6Cac7C8wo-aG</recordid><startdate>20100222</startdate><enddate>20100222</enddate><creator>D'Amato, Mauro</creator><creator>Zucchelli, Marco</creator><creator>Seddighzadeh, Maria</creator><creator>Anedda, Francesca</creator><creator>Lindblad, Staffan</creator><creator>Kere, Juha</creator><creator>Alfredsson, Lars</creator><creator>Klareskog, Lars</creator><creator>Padyukov, Leonid</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope><scope>DOA</scope></search><sort><creationdate>20100222</creationdate><title>Analysis of neuropeptide S receptor gene (NPSR1) polymorphism in rheumatoid arthritis</title><author>D'Amato, Mauro ; Zucchelli, Marco ; Seddighzadeh, Maria ; Anedda, Francesca ; Lindblad, Staffan ; Kere, Juha ; Alfredsson, Lars ; Klareskog, Lars ; Padyukov, Leonid</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c630t-4c68b8d56e15200d0ba53db0067814194705c2e0fdee5db2f1d54ce06b8551c03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Analysis</topic><topic>Anxiety</topic><topic>Arthritis</topic><topic>Arthritis, Rheumatoid - epidemiology</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>Arthritis, Rheumatoid - pathology</topic><topic>Asthma</topic><topic>Autoantibodies</topic><topic>Autoimmunity</topic><topic>Brain</topic><topic>Case-Control Studies</topic><topic>Chromosome 7</topic><topic>Citrulline</topic><topic>Deoxyribonucleic acid</topic><topic>Diagnosis</topic><topic>DNA</topic><topic>Epidemiology</topic><topic>Ethics</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Gene polymorphism</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic markers</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetic variability</topic><topic>Genetics</topic><topic>Genetics and Genomics/Complex Traits</topic><topic>Genetics and Genomics/Genetics of Disease</topic><topic>Genetics and Genomics/Genetics of the Immune System</topic><topic>Genetics and Genomics/Medical Genetics</topic><topic>Genotype</topic><topic>Haplotypes</topic><topic>Health risks</topic><topic>Humans</topic><topic>Incidence</topic><topic>Inflammatory bowel disease</topic><topic>Inflammatory bowel diseases</topic><topic>Inflammatory diseases</topic><topic>Intestine</topic><topic>Joint diseases</topic><topic>Linkage Disequilibrium</topic><topic>Loci</topic><topic>Lungs</topic><topic>Lymphocytes</topic><topic>Male</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Neuropeptides</topic><topic>Nutrition</topic><topic>Odds Ratio</topic><topic>Physiology</topic><topic>Polymorphism</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Population</topic><topic>Principal components analysis</topic><topic>Proteins</topic><topic>Receptors, G-Protein-Coupled - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SwePub Articles full text</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>D'Amato, Mauro</au><au>Zucchelli, Marco</au><au>Seddighzadeh, Maria</au><au>Anedda, Francesca</au><au>Lindblad, Staffan</au><au>Kere, Juha</au><au>Alfredsson, Lars</au><au>Klareskog, Lars</au><au>Padyukov, Leonid</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Analysis of neuropeptide S receptor gene (NPSR1) polymorphism in rheumatoid arthritis</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2010-02-22</date><risdate>2010</risdate><volume>5</volume><issue>2</issue><spage>e9315</spage><epage>e9315</epage><pages>e9315-e9315</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Polymorphism in the neuropeptide S receptor gene NPSR1 is associated with asthma and inflammatory bowel disease. NPSR1 is expressed in the brain, where it modulates anxiety and responses to stress, but also in other tissues and cell types including lymphocytes, the lungs, and the intestine, where it appears to be up-regulated in inflammation. We sought to determine whether genetic variability at the NPSR1 locus influences the susceptibility and clinical manifestation of rheumatoid arthritis (RA).
From the Epidemiological Investigation of Rheumatoid Arthritis (EIRA) case-control study, 1,888 rheumatoid arthritis patients and 888 controls were genotyped for 19 single-nucleotide polymorphisms (SNPs) spanning the entire NPSR1 gene and 220 KB of DNA on chromosome 7p14. The association between individual genetic markers and their haplotypic combinations, respectively, and diagnosis of RA, presence of autoantibodies to citrullinated proteins (ACPA), and disease activity score based on 28 joints (DAS28) was tested. There was no association between diagnosis of RA and NPSR1 variants. However, several associations of nominal significance were detected concerning susceptibility to ACPA-negative RA and disease activity measures (DAS28). Among these, the association of SNP rs324987 with ACPA-negative RA [(p=0.004, OR=0.674 (95% CI 0.512-0.888)] and that of SNP rs10263447 with DAS28 [p=0.0002, OR=0.380 (95% CI 0.227-0.635)] remained significant after correction for multiple comparisons.
NPSR1 polymorphism may be relevant to RA susceptibility and its clinical manifestation. Specific alleles at the NPSR1 locus may represent common risk factors for chronic inflammatory diseases, including RA.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>20179762</pmid><doi>10.1371/journal.pone.0009315</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2010-02, Vol.5 (2), p.e9315-e9315 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1289259569 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; SWEPUB Freely available online; Free Full-Text Journals in Chemistry |
| subjects | Adolescent Adult Aged Analysis Anxiety Arthritis Arthritis, Rheumatoid - epidemiology Arthritis, Rheumatoid - genetics Arthritis, Rheumatoid - pathology Asthma Autoantibodies Autoimmunity Brain Case-Control Studies Chromosome 7 Citrulline Deoxyribonucleic acid Diagnosis DNA Epidemiology Ethics Female Gene Frequency Gene polymorphism Genes Genetic aspects Genetic markers Genetic Predisposition to Disease Genetic variability Genetics Genetics and Genomics/Complex Traits Genetics and Genomics/Genetics of Disease Genetics and Genomics/Genetics of the Immune System Genetics and Genomics/Medical Genetics Genotype Haplotypes Health risks Humans Incidence Inflammatory bowel disease Inflammatory bowel diseases Inflammatory diseases Intestine Joint diseases Linkage Disequilibrium Loci Lungs Lymphocytes Male Medical research Medicine Middle Aged Mutation Neuropeptides Nutrition Odds Ratio Physiology Polymorphism Polymorphism, Single Nucleotide Population Principal components analysis Proteins Receptors, G-Protein-Coupled - genetics Rheumatoid arthritis Rheumatoid factor Rheumatology Rheumatology/Rheumatoid Arthritis Risk analysis Risk Factors Single nucleotide polymorphisms Single-nucleotide polymorphism Studies Sweden - epidemiology Tissues Young Adult |
| title | Analysis of neuropeptide S receptor gene (NPSR1) polymorphism in rheumatoid arthritis |
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