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Factor V Leiden and its relation to left ventricular thrombus in acute myocardial infarction
Objective - The genetic defect of coagulation factor V, known as factor V Leiden, produces a resistance to degradation by activated protein C (APC) and increases the risk of venous thrombosis. However, the role of factor V Leiden in the formation of left ventricular (LV) thrombus has not been studie...
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Published in: | Acta Cardiologica 2001-02, Vol.56 (1), p.1-6 |
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creator | Çelik, Şükrü Ovali, Ercüument Baykan, Merih UÇar, Fahri ErdÖl, Cevdet Durmusş, Ismet Kaplan, Şahin |
description | Objective - The genetic defect of coagulation factor V, known as factor V Leiden, produces a resistance to degradation by activated protein C (APC) and increases the risk of venous thrombosis. However, the role of factor V Leiden in the formation of left ventricular (LV) thrombus has not been studied.We investigated whether factor V Leiden is a risk factor for LV thrombus in patients with acute myocardial infarction (AMI).
Methods and results - We have analyzed clinical, echocardiographic and biochemical data in 135 consecutive patients (aged 58 ± 13 years; 31 women) with first anterior AMI. Two-dimensional echocardiographic examination was performed on days I, 3, 7, 15 and 30; LV thrombus was detected in 33 (24.4%) of 135 patients with AMI. The study also included 95 control subjects. Healthy age and sex-matched subjects without a personal or family history of ischaemic heart disease, stroke or thromboembolic disease served as a control group. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. In addition, concentrations of fibrinogen, von Willebrand factor (vWF), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-I (PAI-1) and D-dimer were measured in 135 patients. There was no significant difference in the prevalence of factor V Leiden between patients and control subjects. The prevalence of the factor V mutation was 9% (3/33) in patients with thrombus, and 7.7% (8/103) in patients without thrombus. The prevalence of factor V Leiden was 7.3% (7/95) in control subjects. No significant differences in plasma fibrinogen (480 ± 195 vs. 444 ± 179 mg/dl, p = 0.6), D-dimer (471 ± 256 vs. 497 ± 293 ng/dl, p = 0.7), vWF (112 ± 18 vs. 103 ± 15%, p = 0.5), PAI-I (26.7 ± 9.8 vs. 28.1 ± 10.2 ng/dl, p = 0.6), and t-PA (19.8 ± 8.7 vs. 17.2 ± 9.1 ng/dl, p = 0.7), levels are found in patients with LV thrombus when compared with those without LV thrombus. Multivariate analyses showed that peak creatine kinase level (p = 0.002) and LV wall motion score index (p = 0.003) were independent predictors of LV thrombus formation.
Conclusion - Factor V Leiden mutation is not a risk factor for LV thrombus formation in patients with AMI. (Acta Cardiol 2001; 56(1 ): 1-6) |
doi_str_mv | 10.2143/AC.56.1.2005587 |
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Methods and results - We have analyzed clinical, echocardiographic and biochemical data in 135 consecutive patients (aged 58 ± 13 years; 31 women) with first anterior AMI. Two-dimensional echocardiographic examination was performed on days I, 3, 7, 15 and 30; LV thrombus was detected in 33 (24.4%) of 135 patients with AMI. The study also included 95 control subjects. Healthy age and sex-matched subjects without a personal or family history of ischaemic heart disease, stroke or thromboembolic disease served as a control group. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. In addition, concentrations of fibrinogen, von Willebrand factor (vWF), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-I (PAI-1) and D-dimer were measured in 135 patients. There was no significant difference in the prevalence of factor V Leiden between patients and control subjects. The prevalence of the factor V mutation was 9% (3/33) in patients with thrombus, and 7.7% (8/103) in patients without thrombus. The prevalence of factor V Leiden was 7.3% (7/95) in control subjects. No significant differences in plasma fibrinogen (480 ± 195 vs. 444 ± 179 mg/dl, p = 0.6), D-dimer (471 ± 256 vs. 497 ± 293 ng/dl, p = 0.7), vWF (112 ± 18 vs. 103 ± 15%, p = 0.5), PAI-I (26.7 ± 9.8 vs. 28.1 ± 10.2 ng/dl, p = 0.6), and t-PA (19.8 ± 8.7 vs. 17.2 ± 9.1 ng/dl, p = 0.7), levels are found in patients with LV thrombus when compared with those without LV thrombus. Multivariate analyses showed that peak creatine kinase level (p = 0.002) and LV wall motion score index (p = 0.003) were independent predictors of LV thrombus formation.
Conclusion - Factor V Leiden mutation is not a risk factor for LV thrombus formation in patients with AMI. (Acta Cardiol 2001; 56(1 ): 1-6)</description><identifier>ISSN: 0001-5385</identifier><identifier>EISSN: 1784-973X</identifier><identifier>EISSN: 0001-5385</identifier><identifier>DOI: 10.2143/AC.56.1.2005587</identifier><identifier>PMID: 11315119</identifier><identifier>CODEN: ACCAAQ</identifier><language>eng</language><publisher>Bruxelles: Taylor & Francis</publisher><subject>acutemyocardial infarction ; Analysis of Variance ; Biological and medical sciences ; Cardiology. Vascular system ; Case-Control Studies ; Chi-Square Distribution ; Coronary heart disease ; Factor V - genetics ; Factor V - physiology ; factor V Leiden ; Female ; Heart ; Heart Diseases - blood ; Heart Diseases - etiology ; Heart Diseases - genetics ; Heart Ventricles ; Humans ; left ventricular thrombus ; Logistic Models ; Male ; Medical sciences ; Middle Aged ; Mutation ; Myocardial Infarction - blood ; Myocardial Infarction - complications ; Prospective Studies ; Risk Factors ; Thrombosis - blood ; Thrombosis - etiology ; Thrombosis - genetics</subject><ispartof>Acta Cardiologica, 2001-02, Vol.56 (1), p.1-6</ispartof><rights>2001 Taylor and Francis Group LLC 2001</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c374t-31f096259df8f8a190a21859ef4d6d75e88d57e24b35b6228a174d8e679620293</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13932780$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11315119$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Çelik, Şükrü</creatorcontrib><creatorcontrib>Ovali, Ercüument</creatorcontrib><creatorcontrib>Baykan, Merih</creatorcontrib><creatorcontrib>UÇar, Fahri</creatorcontrib><creatorcontrib>ErdÖl, Cevdet</creatorcontrib><creatorcontrib>Durmusş, Ismet</creatorcontrib><creatorcontrib>Kaplan, Şahin</creatorcontrib><title>Factor V Leiden and its relation to left ventricular thrombus in acute myocardial infarction</title><title>Acta Cardiologica</title><addtitle>Acta Cardiol</addtitle><description>Objective - The genetic defect of coagulation factor V, known as factor V Leiden, produces a resistance to degradation by activated protein C (APC) and increases the risk of venous thrombosis. However, the role of factor V Leiden in the formation of left ventricular (LV) thrombus has not been studied.We investigated whether factor V Leiden is a risk factor for LV thrombus in patients with acute myocardial infarction (AMI).
Methods and results - We have analyzed clinical, echocardiographic and biochemical data in 135 consecutive patients (aged 58 ± 13 years; 31 women) with first anterior AMI. Two-dimensional echocardiographic examination was performed on days I, 3, 7, 15 and 30; LV thrombus was detected in 33 (24.4%) of 135 patients with AMI. The study also included 95 control subjects. Healthy age and sex-matched subjects without a personal or family history of ischaemic heart disease, stroke or thromboembolic disease served as a control group. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. In addition, concentrations of fibrinogen, von Willebrand factor (vWF), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-I (PAI-1) and D-dimer were measured in 135 patients. There was no significant difference in the prevalence of factor V Leiden between patients and control subjects. The prevalence of the factor V mutation was 9% (3/33) in patients with thrombus, and 7.7% (8/103) in patients without thrombus. The prevalence of factor V Leiden was 7.3% (7/95) in control subjects. No significant differences in plasma fibrinogen (480 ± 195 vs. 444 ± 179 mg/dl, p = 0.6), D-dimer (471 ± 256 vs. 497 ± 293 ng/dl, p = 0.7), vWF (112 ± 18 vs. 103 ± 15%, p = 0.5), PAI-I (26.7 ± 9.8 vs. 28.1 ± 10.2 ng/dl, p = 0.6), and t-PA (19.8 ± 8.7 vs. 17.2 ± 9.1 ng/dl, p = 0.7), levels are found in patients with LV thrombus when compared with those without LV thrombus. Multivariate analyses showed that peak creatine kinase level (p = 0.002) and LV wall motion score index (p = 0.003) were independent predictors of LV thrombus formation.
Conclusion - Factor V Leiden mutation is not a risk factor for LV thrombus formation in patients with AMI. (Acta Cardiol 2001; 56(1 ): 1-6)</description><subject>acutemyocardial infarction</subject><subject>Analysis of Variance</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Case-Control Studies</subject><subject>Chi-Square Distribution</subject><subject>Coronary heart disease</subject><subject>Factor V - genetics</subject><subject>Factor V - physiology</subject><subject>factor V Leiden</subject><subject>Female</subject><subject>Heart</subject><subject>Heart Diseases - blood</subject><subject>Heart Diseases - etiology</subject><subject>Heart Diseases - genetics</subject><subject>Heart Ventricles</subject><subject>Humans</subject><subject>left ventricular thrombus</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Myocardial Infarction - blood</subject><subject>Myocardial Infarction - complications</subject><subject>Prospective Studies</subject><subject>Risk Factors</subject><subject>Thrombosis - blood</subject><subject>Thrombosis - etiology</subject><subject>Thrombosis - genetics</subject><issn>0001-5385</issn><issn>1784-973X</issn><issn>0001-5385</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><recordid>eNp1kEuLFDEURoMoTjPO2p1ko7vqyaPyctc0jg40uFFxIYR0HhhJVcYkpfS_N02XzGpWl3s55-PyAfAaoy3BI73d7beMb_GWIMSYFM_ABgs5DkrQ78_BBiGEB0YluwI3tf46rwgzxceX4ApjihnGagN-3BnbcoHf4MFH52doZgdjq7D4ZFrMM2wZJh8a_OPnVqJdkimw_Sx5Oi4Vxi7YpXk4nbI1xUWT-i2YYs_uK_AimFT9zTqvwde7D1_2n4bD54_3-91hsFSMbaA4IMUJUy7IIA1WyBAsmfJhdNwJ5qV0THgyHik7ckI6IkYnPRfdQkTRa_DukvtQ8u_F16anWK1Pycw-L1ULgbhAjHfw9gLakmstPuiHEidTThojfe5U7_aacY312mk33qzRy3Hy7pFfG-zA2xUw1ZoUipltrI8cVZQIiTr3_sL1enKZzN9cktPNnFIu_yX61Bf_AGjgkNo</recordid><startdate>20010201</startdate><enddate>20010201</enddate><creator>Çelik, Şükrü</creator><creator>Ovali, Ercüument</creator><creator>Baykan, Merih</creator><creator>UÇar, Fahri</creator><creator>ErdÖl, Cevdet</creator><creator>Durmusş, Ismet</creator><creator>Kaplan, Şahin</creator><general>Taylor & Francis</general><general>Acta cardiologica</general><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>7X8</scope></search><sort><creationdate>20010201</creationdate><title>Factor V Leiden and its relation to left ventricular thrombus in acute myocardial infarction</title><author>Çelik, Şükrü ; Ovali, Ercüument ; Baykan, Merih ; UÇar, Fahri ; ErdÖl, Cevdet ; Durmusş, Ismet ; Kaplan, Şahin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c374t-31f096259df8f8a190a21859ef4d6d75e88d57e24b35b6228a174d8e679620293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>acutemyocardial infarction</topic><topic>Analysis of Variance</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Case-Control Studies</topic><topic>Chi-Square Distribution</topic><topic>Coronary heart disease</topic><topic>Factor V - genetics</topic><topic>Factor V - physiology</topic><topic>factor V Leiden</topic><topic>Female</topic><topic>Heart</topic><topic>Heart Diseases - blood</topic><topic>Heart Diseases - etiology</topic><topic>Heart Diseases - genetics</topic><topic>Heart Ventricles</topic><topic>Humans</topic><topic>left ventricular thrombus</topic><topic>Logistic Models</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Myocardial Infarction - blood</topic><topic>Myocardial Infarction - complications</topic><topic>Prospective Studies</topic><topic>Risk Factors</topic><topic>Thrombosis - blood</topic><topic>Thrombosis - etiology</topic><topic>Thrombosis - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Çelik, Şükrü</creatorcontrib><creatorcontrib>Ovali, Ercüument</creatorcontrib><creatorcontrib>Baykan, Merih</creatorcontrib><creatorcontrib>UÇar, Fahri</creatorcontrib><creatorcontrib>ErdÖl, Cevdet</creatorcontrib><creatorcontrib>Durmusş, Ismet</creatorcontrib><creatorcontrib>Kaplan, Şahin</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>Acta Cardiologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Çelik, Şükrü</au><au>Ovali, Ercüument</au><au>Baykan, Merih</au><au>UÇar, Fahri</au><au>ErdÖl, Cevdet</au><au>Durmusş, Ismet</au><au>Kaplan, Şahin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Factor V Leiden and its relation to left ventricular thrombus in acute myocardial infarction</atitle><jtitle>Acta Cardiologica</jtitle><addtitle>Acta Cardiol</addtitle><date>2001-02-01</date><risdate>2001</risdate><volume>56</volume><issue>1</issue><spage>1</spage><epage>6</epage><pages>1-6</pages><issn>0001-5385</issn><eissn>1784-973X</eissn><eissn>0001-5385</eissn><coden>ACCAAQ</coden><abstract>Objective - The genetic defect of coagulation factor V, known as factor V Leiden, produces a resistance to degradation by activated protein C (APC) and increases the risk of venous thrombosis. However, the role of factor V Leiden in the formation of left ventricular (LV) thrombus has not been studied.We investigated whether factor V Leiden is a risk factor for LV thrombus in patients with acute myocardial infarction (AMI).
Methods and results - We have analyzed clinical, echocardiographic and biochemical data in 135 consecutive patients (aged 58 ± 13 years; 31 women) with first anterior AMI. Two-dimensional echocardiographic examination was performed on days I, 3, 7, 15 and 30; LV thrombus was detected in 33 (24.4%) of 135 patients with AMI. The study also included 95 control subjects. Healthy age and sex-matched subjects without a personal or family history of ischaemic heart disease, stroke or thromboembolic disease served as a control group. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. In addition, concentrations of fibrinogen, von Willebrand factor (vWF), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-I (PAI-1) and D-dimer were measured in 135 patients. There was no significant difference in the prevalence of factor V Leiden between patients and control subjects. The prevalence of the factor V mutation was 9% (3/33) in patients with thrombus, and 7.7% (8/103) in patients without thrombus. The prevalence of factor V Leiden was 7.3% (7/95) in control subjects. No significant differences in plasma fibrinogen (480 ± 195 vs. 444 ± 179 mg/dl, p = 0.6), D-dimer (471 ± 256 vs. 497 ± 293 ng/dl, p = 0.7), vWF (112 ± 18 vs. 103 ± 15%, p = 0.5), PAI-I (26.7 ± 9.8 vs. 28.1 ± 10.2 ng/dl, p = 0.6), and t-PA (19.8 ± 8.7 vs. 17.2 ± 9.1 ng/dl, p = 0.7), levels are found in patients with LV thrombus when compared with those without LV thrombus. Multivariate analyses showed that peak creatine kinase level (p = 0.002) and LV wall motion score index (p = 0.003) were independent predictors of LV thrombus formation.
Conclusion - Factor V Leiden mutation is not a risk factor for LV thrombus formation in patients with AMI. (Acta Cardiol 2001; 56(1 ): 1-6)</abstract><cop>Bruxelles</cop><pub>Taylor & Francis</pub><pmid>11315119</pmid><doi>10.2143/AC.56.1.2005587</doi><tpages>6</tpages></addata></record> |
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subjects | acutemyocardial infarction Analysis of Variance Biological and medical sciences Cardiology. Vascular system Case-Control Studies Chi-Square Distribution Coronary heart disease Factor V - genetics Factor V - physiology factor V Leiden Female Heart Heart Diseases - blood Heart Diseases - etiology Heart Diseases - genetics Heart Ventricles Humans left ventricular thrombus Logistic Models Male Medical sciences Middle Aged Mutation Myocardial Infarction - blood Myocardial Infarction - complications Prospective Studies Risk Factors Thrombosis - blood Thrombosis - etiology Thrombosis - genetics |
title | Factor V Leiden and its relation to left ventricular thrombus in acute myocardial infarction |
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