Polymorphism of the cytokine genes and IgA nephropathy
Polymorphism of the cytokine genes and IgA nephropathy. IgA nephropathy (IgAN) is a form of chronic glomerulonephritis of unknown etiology and pathogenesis. Cytokine gene polymorphisms regulate cytokine production and play a role in immune and inflammatory responses; these immunological responses th...
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| Veröffentlicht in: | Kidney international 2002-03, Vol.61 (3), p.1079-1085 |
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| description | Polymorphism of the cytokine genes and IgA nephropathy.
IgA nephropathy (IgAN) is a form of chronic glomerulonephritis of unknown etiology and pathogenesis. Cytokine gene polymorphisms regulate cytokine production and play a role in immune and inflammatory responses; these immunological responses thus are possibly involved in the etiology and pathogenesis of IgAN.
We studied by polymerase chain reaction (PCR) polymorphisms of important cytokine genes of inflammation interleukin-1 (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1 receptor antagonist (IL-1Ra) in 167 patients with IgAN and 400 healthy blood donor controls. IgAN patients had been followed up for 6 to 17 (median 11) years from renal biopsy.
Carriage of the IL-1β allele 2 (IL1β2) or IL-1Ra allele 2 (IL1RN*2) was associated with an increased risk of IgAN. These alleles were highly linked and the odds ratio (OR) of IgAN for carriage of both alleles was 1.8 (95% confidence interval 1.2 to 2.6; P = 0.002). Carriage of the TNF-α allele 2 (TNF2) was associated with a decreased risk of IgAN (OR 0.5, range 0.3 to 0.7; P = 0.001). The risk of IgAN was found to be highest in those carrying IL1β2 and IL1RN*2 but not TNF2 as compared to those who did not carry both of these IL-1 cluster genes and were carriers of TNF2 (OR 5.0 (2.4–10.3); P < 0.001). None of the polymorphisms studied was associated with poor prognosis.
Carriage of IL1β2 and IL1RN*2 together with non-carriage of TNF2 is associated with increased susceptibility, but not with a prognosis of IgAN. |
| doi_str_mv | 10.1046/j.1523-1755.2002.00193.x |
| format | Article |
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IgA nephropathy (IgAN) is a form of chronic glomerulonephritis of unknown etiology and pathogenesis. Cytokine gene polymorphisms regulate cytokine production and play a role in immune and inflammatory responses; these immunological responses thus are possibly involved in the etiology and pathogenesis of IgAN.
We studied by polymerase chain reaction (PCR) polymorphisms of important cytokine genes of inflammation interleukin-1 (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1 receptor antagonist (IL-1Ra) in 167 patients with IgAN and 400 healthy blood donor controls. IgAN patients had been followed up for 6 to 17 (median 11) years from renal biopsy.
Carriage of the IL-1β allele 2 (IL1β2) or IL-1Ra allele 2 (IL1RN*2) was associated with an increased risk of IgAN. These alleles were highly linked and the odds ratio (OR) of IgAN for carriage of both alleles was 1.8 (95% confidence interval 1.2 to 2.6; P = 0.002). Carriage of the TNF-α allele 2 (TNF2) was associated with a decreased risk of IgAN (OR 0.5, range 0.3 to 0.7; P = 0.001). The risk of IgAN was found to be highest in those carrying IL1β2 and IL1RN*2 but not TNF2 as compared to those who did not carry both of these IL-1 cluster genes and were carriers of TNF2 (OR 5.0 (2.4–10.3); P < 0.001). None of the polymorphisms studied was associated with poor prognosis.
Carriage of IL1β2 and IL1RN*2 together with non-carriage of TNF2 is associated with increased susceptibility, but not with a prognosis of IgAN.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1046/j.1523-1755.2002.00193.x</identifier><identifier>PMID: 11849463</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adolescent ; Adult ; Aged ; Biological and medical sciences ; Child ; Disease Progression ; gene polymorphism ; Genotype ; Glomerulonephritis ; Glomerulonephritis, IGA - complications ; Glomerulonephritis, IGA - genetics ; Glomerulonephritis, IGA - physiopathology ; Hematuria - etiology ; Humans ; Hypertension - etiology ; IgA nephropathy ; IL-6 ; immune response ; Interleukin 1 Receptor Antagonist Protein ; interleukin-1 ; Interleukin-1 - genetics ; Medical sciences ; Middle Aged ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Polymorphism, Genetic ; progressive renal disease ; Proteinuria - etiology ; renoprotection ; Sialoglycoproteins - genetics ; tumor necrosis factor ; Tumor Necrosis Factor-alpha - genetics</subject><ispartof>Kidney international, 2002-03, Vol.61 (3), p.1079-1085</ispartof><rights>2002 International Society of Nephrology</rights><rights>2002 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Mar 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c594t-2c04a5c98b122b0b7b49b3104db3cc36cc9e1ea971775ab34998a9e6d995fe453</citedby><cites>FETCH-LOGICAL-c594t-2c04a5c98b122b0b7b49b3104db3cc36cc9e1ea971775ab34998a9e6d995fe453</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/210119483?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>309,310,314,780,784,789,790,23930,23931,25140,27924,27925,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13582252$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11849463$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Syrjänen, Jaana</creatorcontrib><creatorcontrib>Hurme, Mikko</creatorcontrib><creatorcontrib>Lehtimäki, Terho</creatorcontrib><creatorcontrib>Mustonen, Jukka</creatorcontrib><creatorcontrib>Pasternack, Amos</creatorcontrib><title>Polymorphism of the cytokine genes and IgA nephropathy</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Polymorphism of the cytokine genes and IgA nephropathy.
IgA nephropathy (IgAN) is a form of chronic glomerulonephritis of unknown etiology and pathogenesis. Cytokine gene polymorphisms regulate cytokine production and play a role in immune and inflammatory responses; these immunological responses thus are possibly involved in the etiology and pathogenesis of IgAN.
We studied by polymerase chain reaction (PCR) polymorphisms of important cytokine genes of inflammation interleukin-1 (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1 receptor antagonist (IL-1Ra) in 167 patients with IgAN and 400 healthy blood donor controls. IgAN patients had been followed up for 6 to 17 (median 11) years from renal biopsy.
Carriage of the IL-1β allele 2 (IL1β2) or IL-1Ra allele 2 (IL1RN*2) was associated with an increased risk of IgAN. These alleles were highly linked and the odds ratio (OR) of IgAN for carriage of both alleles was 1.8 (95% confidence interval 1.2 to 2.6; P = 0.002). Carriage of the TNF-α allele 2 (TNF2) was associated with a decreased risk of IgAN (OR 0.5, range 0.3 to 0.7; P = 0.001). The risk of IgAN was found to be highest in those carrying IL1β2 and IL1RN*2 but not TNF2 as compared to those who did not carry both of these IL-1 cluster genes and were carriers of TNF2 (OR 5.0 (2.4–10.3); P < 0.001). None of the polymorphisms studied was associated with poor prognosis.
Carriage of IL1β2 and IL1RN*2 together with non-carriage of TNF2 is associated with increased susceptibility, but not with a prognosis of IgAN.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Child</subject><subject>Disease Progression</subject><subject>gene polymorphism</subject><subject>Genotype</subject><subject>Glomerulonephritis</subject><subject>Glomerulonephritis, IGA - complications</subject><subject>Glomerulonephritis, IGA - genetics</subject><subject>Glomerulonephritis, IGA - physiopathology</subject><subject>Hematuria - etiology</subject><subject>Humans</subject><subject>Hypertension - etiology</subject><subject>IgA nephropathy</subject><subject>IL-6</subject><subject>immune response</subject><subject>Interleukin 1 Receptor Antagonist Protein</subject><subject>interleukin-1</subject><subject>Interleukin-1 - genetics</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Polymorphism, Genetic</subject><subject>progressive renal disease</subject><subject>Proteinuria - etiology</subject><subject>renoprotection</subject><subject>Sialoglycoproteins - genetics</subject><subject>tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkE1v1DAQhi0EosvCTwBFSHBL8GdsH9uKj0qV4ABny3EmXS-JHewEdf89XnbVSlw4jUbzzKuZB6GK4IZg3n7YN0RQVhMpREMxpg3GRLPm_gnaPAyeog3GStRUMHWBXuS8x6XXDD9HF4QornnLNqj9FsfDFNO883mq4lAtO6jcYYk_fYDqDgLkyoa-urm7rALMuxRnu-wOL9GzwY4ZXp3rFv349PH79Zf69uvnm-vL29oJzZeaOsytcFp1hNIOd7LjumPlhb5jzrHWOQ0ErJZESmE7xrVWVkPbay0G4IJt0ftT7pzirxXyYiafHYyjDRDXbCThXAopC_j2H3Af1xTKbYYSTIjmihVInSCXYs4JBjMnP9l0MASbo1izN0d_5ujPHMWav2LNfVl9c85fuwn6x8WzyQK8OwM2OzsOyQbn8yPHhKK0ZG_R6xMX7LImeAA411SVoC26Os2haP3tIZnsPAQHvU_gFtNH__9r_wCUE567</recordid><startdate>20020301</startdate><enddate>20020301</enddate><creator>Syrjänen, Jaana</creator><creator>Hurme, Mikko</creator><creator>Lehtimäki, Terho</creator><creator>Mustonen, Jukka</creator><creator>Pasternack, Amos</creator><general>Elsevier Inc</general><general>Nature Publishing</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</scope><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>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20020301</creationdate><title>Polymorphism of the cytokine genes and IgA nephropathy</title><author>Syrjänen, Jaana ; Hurme, Mikko ; Lehtimäki, Terho ; Mustonen, Jukka ; Pasternack, Amos</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c594t-2c04a5c98b122b0b7b49b3104db3cc36cc9e1ea971775ab34998a9e6d995fe453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Child</topic><topic>Disease Progression</topic><topic>gene polymorphism</topic><topic>Genotype</topic><topic>Glomerulonephritis</topic><topic>Glomerulonephritis, IGA - complications</topic><topic>Glomerulonephritis, IGA - genetics</topic><topic>Glomerulonephritis, IGA - physiopathology</topic><topic>Hematuria - etiology</topic><topic>Humans</topic><topic>Hypertension - etiology</topic><topic>IgA nephropathy</topic><topic>IL-6</topic><topic>immune response</topic><topic>Interleukin 1 Receptor Antagonist Protein</topic><topic>interleukin-1</topic><topic>Interleukin-1 - genetics</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Polymorphism, Genetic</topic><topic>progressive renal disease</topic><topic>Proteinuria - etiology</topic><topic>renoprotection</topic><topic>Sialoglycoproteins - genetics</topic><topic>tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Syrjänen, Jaana</creatorcontrib><creatorcontrib>Hurme, Mikko</creatorcontrib><creatorcontrib>Lehtimäki, Terho</creatorcontrib><creatorcontrib>Mustonen, Jukka</creatorcontrib><creatorcontrib>Pasternack, Amos</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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 China</collection><collection>MEDLINE - Academic</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Syrjänen, Jaana</au><au>Hurme, Mikko</au><au>Lehtimäki, Terho</au><au>Mustonen, Jukka</au><au>Pasternack, Amos</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Polymorphism of the cytokine genes and IgA nephropathy</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2002-03-01</date><risdate>2002</risdate><volume>61</volume><issue>3</issue><spage>1079</spage><epage>1085</epage><pages>1079-1085</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Polymorphism of the cytokine genes and IgA nephropathy.
IgA nephropathy (IgAN) is a form of chronic glomerulonephritis of unknown etiology and pathogenesis. Cytokine gene polymorphisms regulate cytokine production and play a role in immune and inflammatory responses; these immunological responses thus are possibly involved in the etiology and pathogenesis of IgAN.
We studied by polymerase chain reaction (PCR) polymorphisms of important cytokine genes of inflammation interleukin-1 (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1 receptor antagonist (IL-1Ra) in 167 patients with IgAN and 400 healthy blood donor controls. IgAN patients had been followed up for 6 to 17 (median 11) years from renal biopsy.
Carriage of the IL-1β allele 2 (IL1β2) or IL-1Ra allele 2 (IL1RN*2) was associated with an increased risk of IgAN. These alleles were highly linked and the odds ratio (OR) of IgAN for carriage of both alleles was 1.8 (95% confidence interval 1.2 to 2.6; P = 0.002). Carriage of the TNF-α allele 2 (TNF2) was associated with a decreased risk of IgAN (OR 0.5, range 0.3 to 0.7; P = 0.001). The risk of IgAN was found to be highest in those carrying IL1β2 and IL1RN*2 but not TNF2 as compared to those who did not carry both of these IL-1 cluster genes and were carriers of TNF2 (OR 5.0 (2.4–10.3); P < 0.001). None of the polymorphisms studied was associated with poor prognosis.
Carriage of IL1β2 and IL1RN*2 together with non-carriage of TNF2 is associated with increased susceptibility, but not with a prognosis of IgAN.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>11849463</pmid><doi>10.1046/j.1523-1755.2002.00193.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescent Adult Aged Biological and medical sciences Child Disease Progression gene polymorphism Genotype Glomerulonephritis Glomerulonephritis, IGA - complications Glomerulonephritis, IGA - genetics Glomerulonephritis, IGA - physiopathology Hematuria - etiology Humans Hypertension - etiology IgA nephropathy IL-6 immune response Interleukin 1 Receptor Antagonist Protein interleukin-1 Interleukin-1 - genetics Medical sciences Middle Aged Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Polymorphism, Genetic progressive renal disease Proteinuria - etiology renoprotection Sialoglycoproteins - genetics tumor necrosis factor Tumor Necrosis Factor-alpha - genetics |
| title | Polymorphism of the cytokine genes and IgA nephropathy |
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