Plasminogen activator inhibitor-1 C/G polymorphism in relation to plasma levels in rheumatoid arthritis
Plasminogen activator inhibitor type 1 (PAI-1) is an inhibitor of plasmin production. Plasmin can directly or indirectly to degrade cartilage and bone matrix. The PAI-1 Hin dIII polymorphism has been associated with high PAI-1 plasma levels in myocardial infarction patients and control populations....
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creator | Torres-Carrillo, Norma Torres-Carrillo, Nora Magdalena Martínez-Bonilla, Gloria Esther Vázquez-Del Mercado, Mónica Palafox-Sánchez, Claudia Azucena Oregón-Romero, Edith Bernard-Medina, Ana Guilaisne Rangel-Villalobos, Héctor Muñoz-Valle, José Francisco |
description | Plasminogen activator inhibitor type 1 (PAI-1) is an inhibitor of plasmin production. Plasmin can directly or indirectly to degrade cartilage and bone matrix. The
PAI-1
Hin
dIII polymorphism has been associated with high PAI-1 plasma levels in myocardial infarction patients and control populations. Furthermore, it has been associated with the angiographic extent of coronary artery disease, but their involvement in other diseases is still uncertain. Here, we assessed the relationship between
PAI-1
Hin
dIII polymorphism and PAI-1 plasma levels in rheumatoid arthritis (RA). One hundred and twenty-five RA patients and 132 control subjects (CS) were included. Genotypes were identified by the polymerase chain reaction-restriction fragment length polymorphism technique and PAI-1 plasma levels were quantified using an ELISA kit. Not significant differences in genotype and allele frequencies between both studied groups were observed (
P
> 0.05). RA patients showed lower PAI-1 plasma levels (18.92 ± 12.94 ng/ml) than CS (23.68 ± 23.38 ng/ml), without significant difference (
P
= 0.299). However, in RA patients the C/G genotype carriers showed higher PAI-1 plasma levels (23.00 ± 13.81 ng/ml) with respect to C/C (16.77 ± 11.97 ng/ml) and G/G (10.47 ± 7.07 ng/ml) genotype carriers (
P
= 0.036). The
PAI-1
Hin
dIII polymorphism was not associated with RA susceptibility. However, the C/G genotype is associated with high PAI-1 plasma levels in RA patients. |
doi_str_mv | 10.1007/s10238-009-0038-0 |
format | Article |
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PAI-1
Hin
dIII polymorphism has been associated with high PAI-1 plasma levels in myocardial infarction patients and control populations. Furthermore, it has been associated with the angiographic extent of coronary artery disease, but their involvement in other diseases is still uncertain. Here, we assessed the relationship between
PAI-1
Hin
dIII polymorphism and PAI-1 plasma levels in rheumatoid arthritis (RA). One hundred and twenty-five RA patients and 132 control subjects (CS) were included. Genotypes were identified by the polymerase chain reaction-restriction fragment length polymorphism technique and PAI-1 plasma levels were quantified using an ELISA kit. Not significant differences in genotype and allele frequencies between both studied groups were observed (
P
> 0.05). RA patients showed lower PAI-1 plasma levels (18.92 ± 12.94 ng/ml) than CS (23.68 ± 23.38 ng/ml), without significant difference (
P
= 0.299). However, in RA patients the C/G genotype carriers showed higher PAI-1 plasma levels (23.00 ± 13.81 ng/ml) with respect to C/C (16.77 ± 11.97 ng/ml) and G/G (10.47 ± 7.07 ng/ml) genotype carriers (
P
= 0.036). The
PAI-1
Hin
dIII polymorphism was not associated with RA susceptibility. However, the C/G genotype is associated with high PAI-1 plasma levels in RA patients.</description><identifier>ISSN: 1591-8890</identifier><identifier>EISSN: 1591-9528</identifier><identifier>DOI: 10.1007/s10238-009-0038-0</identifier><identifier>PMID: 19238514</identifier><identifier>CODEN: CEMLBA</identifier><language>eng</language><publisher>Milan: Springer Milan</publisher><subject>Arthritis, Rheumatoid - pathology ; Deoxyribonuclease HindIII - metabolism ; Disease Susceptibility ; Enzyme-Linked Immunosorbent Assay - methods ; Gene Frequency ; Hematology ; Humans ; Internal Medicine ; Medicine ; Medicine & Public Health ; Oncology ; Original Article ; Plasma - chemistry ; Plasminogen Activator Inhibitor 1 - blood ; Plasminogen Activator Inhibitor 1 - genetics ; Polymerase Chain Reaction - methods ; Polymorphism ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; Protease inhibitors ; Rheumatoid arthritis</subject><ispartof>Clinical and experimental medicine, 2009-09, Vol.9 (3), p.223-228</ispartof><rights>Springer-Verlag 2009</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c400t-72d9a7736de20c19402542c45536a37f844cd96f5ec1da584c394a23ce2d899d3</citedby><cites>FETCH-LOGICAL-c400t-72d9a7736de20c19402542c45536a37f844cd96f5ec1da584c394a23ce2d899d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10238-009-0038-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10238-009-0038-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19238514$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Torres-Carrillo, Norma</creatorcontrib><creatorcontrib>Torres-Carrillo, Nora Magdalena</creatorcontrib><creatorcontrib>Martínez-Bonilla, Gloria Esther</creatorcontrib><creatorcontrib>Vázquez-Del Mercado, Mónica</creatorcontrib><creatorcontrib>Palafox-Sánchez, Claudia Azucena</creatorcontrib><creatorcontrib>Oregón-Romero, Edith</creatorcontrib><creatorcontrib>Bernard-Medina, Ana Guilaisne</creatorcontrib><creatorcontrib>Rangel-Villalobos, Héctor</creatorcontrib><creatorcontrib>Muñoz-Valle, José Francisco</creatorcontrib><title>Plasminogen activator inhibitor-1 C/G polymorphism in relation to plasma levels in rheumatoid arthritis</title><title>Clinical and experimental medicine</title><addtitle>Clin Exp Med</addtitle><addtitle>Clin Exp Med</addtitle><description>Plasminogen activator inhibitor type 1 (PAI-1) is an inhibitor of plasmin production. Plasmin can directly or indirectly to degrade cartilage and bone matrix. The
PAI-1
Hin
dIII polymorphism has been associated with high PAI-1 plasma levels in myocardial infarction patients and control populations. Furthermore, it has been associated with the angiographic extent of coronary artery disease, but their involvement in other diseases is still uncertain. Here, we assessed the relationship between
PAI-1
Hin
dIII polymorphism and PAI-1 plasma levels in rheumatoid arthritis (RA). One hundred and twenty-five RA patients and 132 control subjects (CS) were included. Genotypes were identified by the polymerase chain reaction-restriction fragment length polymorphism technique and PAI-1 plasma levels were quantified using an ELISA kit. Not significant differences in genotype and allele frequencies between both studied groups were observed (
P
> 0.05). RA patients showed lower PAI-1 plasma levels (18.92 ± 12.94 ng/ml) than CS (23.68 ± 23.38 ng/ml), without significant difference (
P
= 0.299). However, in RA patients the C/G genotype carriers showed higher PAI-1 plasma levels (23.00 ± 13.81 ng/ml) with respect to C/C (16.77 ± 11.97 ng/ml) and G/G (10.47 ± 7.07 ng/ml) genotype carriers (
P
= 0.036). The
PAI-1
Hin
dIII polymorphism was not associated with RA susceptibility. However, the C/G genotype is associated with high PAI-1 plasma levels in RA patients.</description><subject>Arthritis, Rheumatoid - pathology</subject><subject>Deoxyribonuclease HindIII - metabolism</subject><subject>Disease Susceptibility</subject><subject>Enzyme-Linked Immunosorbent Assay - methods</subject><subject>Gene Frequency</subject><subject>Hematology</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Plasma - chemistry</subject><subject>Plasminogen Activator Inhibitor 1 - blood</subject><subject>Plasminogen Activator Inhibitor 1 - genetics</subject><subject>Polymerase Chain Reaction - methods</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Polymorphism, Restriction Fragment Length</subject><subject>Protease inhibitors</subject><subject>Rheumatoid arthritis</subject><issn>1591-8890</issn><issn>1591-9528</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkUtLAzEUhYMo1tcPcCPBhbvRm9dkspTiCwRd6DrETNqmzEzGZEbovze1hYIgLkIunO-cy-UgdE7gmgDIm0SAsqoAUPmthz10RIQihRK02t_OVaVggo5TWgIQUTE4RBOisk8QfoTmr41Jre_C3HXY2MF_mSFE7LuF__B5Kgie3jzgPjSrNsR-4VObRRxdYwYfOjwE3K8TDG7cl2vSj7hwY5tjfI1NHBbRDz6dooOZaZI72_4n6P3-7m36WDy_PDxNb58LywGGQtJaGSlZWTsKligOVHBquRCsNEzOKs5trcqZcJbURlTcMsUNZdbRulKqZifoapPbx_A5ujTo1ifrmsZ0LoxJl5JLWUr1L0iB5tUlyeDlL3AZxtjlIzRlUEopOM8Q2UA2hpSim-k--tbElSag113pTVc6d6XXXWnInott8PjRunrn2JaTAboBUpa6uYu7zX-nfgNbqJ60</recordid><startdate>20090901</startdate><enddate>20090901</enddate><creator>Torres-Carrillo, Norma</creator><creator>Torres-Carrillo, Nora Magdalena</creator><creator>Martínez-Bonilla, Gloria Esther</creator><creator>Vázquez-Del Mercado, Mónica</creator><creator>Palafox-Sánchez, Claudia Azucena</creator><creator>Oregón-Romero, Edith</creator><creator>Bernard-Medina, Ana Guilaisne</creator><creator>Rangel-Villalobos, Héctor</creator><creator>Muñoz-Valle, José Francisco</creator><general>Springer Milan</general><general>Springer Nature B.V</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>7T5</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7QP</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20090901</creationdate><title>Plasminogen activator inhibitor-1 C/G polymorphism in relation to plasma levels in rheumatoid arthritis</title><author>Torres-Carrillo, Norma ; Torres-Carrillo, Nora Magdalena ; Martínez-Bonilla, Gloria Esther ; Vázquez-Del Mercado, Mónica ; Palafox-Sánchez, Claudia Azucena ; Oregón-Romero, Edith ; Bernard-Medina, Ana Guilaisne ; Rangel-Villalobos, Héctor ; Muñoz-Valle, José Francisco</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c400t-72d9a7736de20c19402542c45536a37f844cd96f5ec1da584c394a23ce2d899d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Arthritis, Rheumatoid - pathology</topic><topic>Deoxyribonuclease HindIII - metabolism</topic><topic>Disease Susceptibility</topic><topic>Enzyme-Linked Immunosorbent Assay - methods</topic><topic>Gene Frequency</topic><topic>Hematology</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Plasma - chemistry</topic><topic>Plasminogen Activator Inhibitor 1 - blood</topic><topic>Plasminogen Activator Inhibitor 1 - genetics</topic><topic>Polymerase Chain Reaction - methods</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Polymorphism, Restriction Fragment Length</topic><topic>Protease inhibitors</topic><topic>Rheumatoid arthritis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Torres-Carrillo, Norma</creatorcontrib><creatorcontrib>Torres-Carrillo, Nora Magdalena</creatorcontrib><creatorcontrib>Martínez-Bonilla, Gloria Esther</creatorcontrib><creatorcontrib>Vázquez-Del Mercado, Mónica</creatorcontrib><creatorcontrib>Palafox-Sánchez, Claudia Azucena</creatorcontrib><creatorcontrib>Oregón-Romero, Edith</creatorcontrib><creatorcontrib>Bernard-Medina, Ana Guilaisne</creatorcontrib><creatorcontrib>Rangel-Villalobos, Héctor</creatorcontrib><creatorcontrib>Muñoz-Valle, José Francisco</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and experimental medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Torres-Carrillo, Norma</au><au>Torres-Carrillo, Nora Magdalena</au><au>Martínez-Bonilla, Gloria Esther</au><au>Vázquez-Del Mercado, Mónica</au><au>Palafox-Sánchez, Claudia Azucena</au><au>Oregón-Romero, Edith</au><au>Bernard-Medina, Ana Guilaisne</au><au>Rangel-Villalobos, Héctor</au><au>Muñoz-Valle, José Francisco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plasminogen activator inhibitor-1 C/G polymorphism in relation to plasma levels in rheumatoid arthritis</atitle><jtitle>Clinical and experimental medicine</jtitle><stitle>Clin Exp Med</stitle><addtitle>Clin Exp Med</addtitle><date>2009-09-01</date><risdate>2009</risdate><volume>9</volume><issue>3</issue><spage>223</spage><epage>228</epage><pages>223-228</pages><issn>1591-8890</issn><eissn>1591-9528</eissn><coden>CEMLBA</coden><abstract>Plasminogen activator inhibitor type 1 (PAI-1) is an inhibitor of plasmin production. Plasmin can directly or indirectly to degrade cartilage and bone matrix. The
PAI-1
Hin
dIII polymorphism has been associated with high PAI-1 plasma levels in myocardial infarction patients and control populations. Furthermore, it has been associated with the angiographic extent of coronary artery disease, but their involvement in other diseases is still uncertain. Here, we assessed the relationship between
PAI-1
Hin
dIII polymorphism and PAI-1 plasma levels in rheumatoid arthritis (RA). One hundred and twenty-five RA patients and 132 control subjects (CS) were included. Genotypes were identified by the polymerase chain reaction-restriction fragment length polymorphism technique and PAI-1 plasma levels were quantified using an ELISA kit. Not significant differences in genotype and allele frequencies between both studied groups were observed (
P
> 0.05). RA patients showed lower PAI-1 plasma levels (18.92 ± 12.94 ng/ml) than CS (23.68 ± 23.38 ng/ml), without significant difference (
P
= 0.299). However, in RA patients the C/G genotype carriers showed higher PAI-1 plasma levels (23.00 ± 13.81 ng/ml) with respect to C/C (16.77 ± 11.97 ng/ml) and G/G (10.47 ± 7.07 ng/ml) genotype carriers (
P
= 0.036). The
PAI-1
Hin
dIII polymorphism was not associated with RA susceptibility. However, the C/G genotype is associated with high PAI-1 plasma levels in RA patients.</abstract><cop>Milan</cop><pub>Springer Milan</pub><pmid>19238514</pmid><doi>10.1007/s10238-009-0038-0</doi><tpages>6</tpages></addata></record> |
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source | MEDLINE; Springer Nature - Complete Springer Journals |
subjects | Arthritis, Rheumatoid - pathology Deoxyribonuclease HindIII - metabolism Disease Susceptibility Enzyme-Linked Immunosorbent Assay - methods Gene Frequency Hematology Humans Internal Medicine Medicine Medicine & Public Health Oncology Original Article Plasma - chemistry Plasminogen Activator Inhibitor 1 - blood Plasminogen Activator Inhibitor 1 - genetics Polymerase Chain Reaction - methods Polymorphism Polymorphism, Genetic Polymorphism, Restriction Fragment Length Protease inhibitors Rheumatoid arthritis |
title | Plasminogen activator inhibitor-1 C/G polymorphism in relation to plasma levels in rheumatoid arthritis |
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