Fibrinolytic Gene Polymorphism and Ischemic Stroke
Background and Purpose— The tissue-type plasminogen activator (tPA) −7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G >5G polymorphisms influence transcriptional activity. Both variants have been associated with myocardial infarction, with increased risk for the T and 4G...
Saved in:
| Published in | Stroke (1970) Vol. 36; no. 10; pp. 2077 - 2081 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
Lippincott Williams & Wilkins
01.10.2005
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 0039-2499 1524-4628 1524-4628 |
| DOI | 10.1161/01.STR.0000183617.54752.69 |
Cover
| Abstract | Background and Purpose—
The tissue-type plasminogen activator (tPA) −7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G >5G polymorphisms influence transcriptional activity. Both variants have been associated with myocardial infarction, with increased risk for the T and 4G allele, respectively. In this study we investigated the possible association between these polymorphisms, the respective plasma protein levels, and ischemic stroke.
Methods—
In the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), 600 patients with acute ischemic stroke aged 18 to 69 years and 600 matched community controls were recruited. Stroke subtype was determined using Trial of Org 10172 in Acute Treatment criteria.
Results—
There were no associations between individual genetic variants and ischemic stroke. The multivariate-adjusted odds ratio for overall ischemic stroke was 1.11 (95% CI 0.87 to 1.43) for tPA T allele carriers, and 0.84 (95% CI, 0.64 to 1.11) for subjects homozygous for the PAI-1 4G allele. When genotypes were combined, a protective effect for the tPA CC/PAI-1 4G4G genotype combination was observed (odds ratio 0.65, 95% CI 0.43 to 0.98;
P
<0.05). Plasma levels of tPA and PAI-1 antigen at follow-up were independently associated with overall ischemic stroke. tPA-antigen differed by stroke subtype and was highest among those with large-vessel disease and cardioembolic stroke.
Conclusions—
Neither the tPA −7351C>T nor the PAI-1 to 675 4G >5G polymorphism showed significant association with ischemic stroke. For the tPA CC/PAI-1 4G4G genotype combination, a protective effect was observed. Collectively, these results are consistent with a more complex role for tPA and PAI-1 in the brain as compared with the heart. |
|---|---|
| AbstractList | The tissue-type plasminogen activator (tPA) -7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G>5G polymorphisms influence transcriptional activity. Both variants have been associated with myocardial infarction, with increased risk for the T and 4G allele, respectively. In this study we investigated the possible association between these polymorphisms, the respective plasma protein levels, and ischemic stroke.BACKGROUND AND PURPOSEThe tissue-type plasminogen activator (tPA) -7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G>5G polymorphisms influence transcriptional activity. Both variants have been associated with myocardial infarction, with increased risk for the T and 4G allele, respectively. In this study we investigated the possible association between these polymorphisms, the respective plasma protein levels, and ischemic stroke.In the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), 600 patients with acute ischemic stroke aged 18 to 69 years and 600 matched community controls were recruited. Stroke subtype was determined using Trial of Org 10172 in Acute Treatment criteria.METHODSIn the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), 600 patients with acute ischemic stroke aged 18 to 69 years and 600 matched community controls were recruited. Stroke subtype was determined using Trial of Org 10172 in Acute Treatment criteria.There were no associations between individual genetic variants and ischemic stroke. The multivariate-adjusted odds ratio for overall ischemic stroke was 1.11 (95% CI 0.87 to 1.43) for tPA T allele carriers, and 0.84 (95% CI, 0.64 to 1.11) for subjects homozygous for the PAI-1 4G allele. When genotypes were combined, a protective effect for the tPA CC/PAI-1 4G4G genotype combination was observed (odds ratio 0.65, 95% CI 0.43 to 0.98; P<0.05). Plasma levels of tPA and PAI-1 antigen at follow-up were independently associated with overall ischemic stroke. tPA-antigen differed by stroke subtype and was highest among those with large-vessel disease and cardioembolic stroke.RESULTSThere were no associations between individual genetic variants and ischemic stroke. The multivariate-adjusted odds ratio for overall ischemic stroke was 1.11 (95% CI 0.87 to 1.43) for tPA T allele carriers, and 0.84 (95% CI, 0.64 to 1.11) for subjects homozygous for the PAI-1 4G allele. When genotypes were combined, a protective effect for the tPA CC/PAI-1 4G4G genotype combination was observed (odds ratio 0.65, 95% CI 0.43 to 0.98; P<0.05). Plasma levels of tPA and PAI-1 antigen at follow-up were independently associated with overall ischemic stroke. tPA-antigen differed by stroke subtype and was highest among those with large-vessel disease and cardioembolic stroke.Neither the tPA -7351C>T nor the PAI-1 to 675 4G>5G polymorphism showed significant association with ischemic stroke. For the tPA CC/PAI-1 4G4G genotype combination, a protective effect was observed. Collectively, these results are consistent with a more complex role for tPA and PAI-1 in the brain as compared with the heart.CONCLUSIONSNeither the tPA -7351C>T nor the PAI-1 to 675 4G>5G polymorphism showed significant association with ischemic stroke. For the tPA CC/PAI-1 4G4G genotype combination, a protective effect was observed. Collectively, these results are consistent with a more complex role for tPA and PAI-1 in the brain as compared with the heart. BACKGROUND AND PURPOSE: The tissue-type plasminogen activator (tPA) -7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G>5G polymorphisms influence transcriptional activity. Both variants have been associated with myocardial infarction, with increased risk for the T and 4G allele, respectively. In this study we investigated the possible association between these polymorphisms, the respective plasma protein levels, and ischemic stroke. METHODS: In the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), 600 patients with acute ischemic stroke aged 18 to 69 years and 600 matched community controls were recruited. Stroke subtype was determined using Trial of Org 10172 in Acute Treatment criteria. RESULTS: There were no associations between individual genetic variants and ischemic stroke. The multivariate-adjusted odds ratio for overall ischemic stroke was 1.11 (95% CI 0.87 to 1.43) for tPA T allele carriers, and 0.84 (95% CI, 0.64 to 1.11) for subjects homozygous for the PAI-1 4G allele. When genotypes were combined, a protective effect for the tPA CC/PAI-1 4G4G genotype combination was observed (odds ratio 0.65, 95% CI 0.43 to 0.98; P<0.05). Plasma levels of tPA and PAI-1 antigen at follow-up were independently associated with overall ischemic stroke. tPA-antigen differed by stroke subtype and was highest among those with large-vessel disease and cardioembolic stroke. CONCLUSIONS: Neither the tPA -7351C>T nor the PAI-1 to 675 4G>5G polymorphism showed significant association with ischemic stroke. For the tPA CC/PAI-1 4G4G genotype combination, a protective effect was observed. Collectively, these results are consistent with a more complex role for tPA and PAI-1 in the brain as compared with the heart. BACKGROUND AND PURPOSE: The tissue-type plasminogen activator (tPA) -7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G>5G polymorphisms influence transcriptional activity. Both variants have been associated with myocardial infarction, with increased risk for the T and 4G allele, respectively. In this study we investigated the possible association between these polymorphisms, the respective plasma protein levels, and ischemic stroke. METHODS: In the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), 600 patients with acute ischemic stroke aged 18 to 69 years and 600 matched community controls were recruited. Stroke subtype was determined using Trial of Org 10172 in Acute Treatment criteria. RESULTS: There were no associations between individual genetic variants and ischemic stroke. The multivariate-adjusted odds ratio for overall ischemic stroke was 1.11 (95% CI 0.87 to 1.43) for tPA T allele carriers, and 0.84 (95% CI, 0.64 to 1.11) for subjects homozygous for the PAI-1 4G allele. When genotypes were combined, a protective effect for the tPA CC/PAI-1 4G4G genotype combination was observed (odds ratio 0.65, 95% CI 0.43 to 0.98; P T nor the PAI-1 to 675 4G>5G polymorphism showed significant association with ischemic stroke. For the tPA CC/PAI-1 4G4G genotype combination, a protective effect was observed. Collectively, these results are consistent with a more complex role for tPA and PAI-1 in the brain as compared with the heart. The tissue-type plasminogen activator (tPA) -7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G>5G polymorphisms influence transcriptional activity. Both variants have been associated with myocardial infarction, with increased risk for the T and 4G allele, respectively. In this study we investigated the possible association between these polymorphisms, the respective plasma protein levels, and ischemic stroke. In the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), 600 patients with acute ischemic stroke aged 18 to 69 years and 600 matched community controls were recruited. Stroke subtype was determined using Trial of Org 10172 in Acute Treatment criteria. There were no associations between individual genetic variants and ischemic stroke. The multivariate-adjusted odds ratio for overall ischemic stroke was 1.11 (95% CI 0.87 to 1.43) for tPA T allele carriers, and 0.84 (95% CI, 0.64 to 1.11) for subjects homozygous for the PAI-1 4G allele. When genotypes were combined, a protective effect for the tPA CC/PAI-1 4G4G genotype combination was observed (odds ratio 0.65, 95% CI 0.43 to 0.98; P<0.05). Plasma levels of tPA and PAI-1 antigen at follow-up were independently associated with overall ischemic stroke. tPA-antigen differed by stroke subtype and was highest among those with large-vessel disease and cardioembolic stroke. Neither the tPA -7351C>T nor the PAI-1 to 675 4G>5G polymorphism showed significant association with ischemic stroke. For the tPA CC/PAI-1 4G4G genotype combination, a protective effect was observed. Collectively, these results are consistent with a more complex role for tPA and PAI-1 in the brain as compared with the heart. Background and Purpose— The tissue-type plasminogen activator (tPA) −7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G >5G polymorphisms influence transcriptional activity. Both variants have been associated with myocardial infarction, with increased risk for the T and 4G allele, respectively. In this study we investigated the possible association between these polymorphisms, the respective plasma protein levels, and ischemic stroke. Methods— In the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), 600 patients with acute ischemic stroke aged 18 to 69 years and 600 matched community controls were recruited. Stroke subtype was determined using Trial of Org 10172 in Acute Treatment criteria. Results— There were no associations between individual genetic variants and ischemic stroke. The multivariate-adjusted odds ratio for overall ischemic stroke was 1.11 (95% CI 0.87 to 1.43) for tPA T allele carriers, and 0.84 (95% CI, 0.64 to 1.11) for subjects homozygous for the PAI-1 4G allele. When genotypes were combined, a protective effect for the tPA CC/PAI-1 4G4G genotype combination was observed (odds ratio 0.65, 95% CI 0.43 to 0.98; P <0.05). Plasma levels of tPA and PAI-1 antigen at follow-up were independently associated with overall ischemic stroke. tPA-antigen differed by stroke subtype and was highest among those with large-vessel disease and cardioembolic stroke. Conclusions— Neither the tPA −7351C>T nor the PAI-1 to 675 4G >5G polymorphism showed significant association with ischemic stroke. For the tPA CC/PAI-1 4G4G genotype combination, a protective effect was observed. Collectively, these results are consistent with a more complex role for tPA and PAI-1 in the brain as compared with the heart. |
| Author | Nilsson, Staffan Jood, Katarina Ladenvall, Per Ladenvall, Claes Tjärnlund-Wolf, Anna Jern, Christina Blomstrand, Christian Andersson, Maria |
| Author_xml | – sequence: 1 givenname: Katarina surname: Jood fullname: Jood, Katarina organization: From the Institute of Clinical Neuroscience (K.J., A.T.-W., C.L., C.B., C.J.) and the Clinical Experimental Research Laboratory, Cardiovascular Institute (P.L., M.A.), the Sahlgrenska Academy at Göteborg University; the Department of Clinical Genetics, Sahlgrenska University Hospital/Östra (A.T.-W., C.L., C.J.); the Department of Mathematical Statistics (S.N.), Chalmers University of Technology, Göteborg, Sweden – sequence: 2 givenname: Per surname: Ladenvall fullname: Ladenvall, Per organization: From the Institute of Clinical Neuroscience (K.J., A.T.-W., C.L., C.B., C.J.) and the Clinical Experimental Research Laboratory, Cardiovascular Institute (P.L., M.A.), the Sahlgrenska Academy at Göteborg University; the Department of Clinical Genetics, Sahlgrenska University Hospital/Östra (A.T.-W., C.L., C.J.); the Department of Mathematical Statistics (S.N.), Chalmers University of Technology, Göteborg, Sweden – sequence: 3 givenname: Anna surname: Tjärnlund-Wolf fullname: Tjärnlund-Wolf, Anna organization: From the Institute of Clinical Neuroscience (K.J., A.T.-W., C.L., C.B., C.J.) and the Clinical Experimental Research Laboratory, Cardiovascular Institute (P.L., M.A.), the Sahlgrenska Academy at Göteborg University; the Department of Clinical Genetics, Sahlgrenska University Hospital/Östra (A.T.-W., C.L., C.J.); the Department of Mathematical Statistics (S.N.), Chalmers University of Technology, Göteborg, Sweden – sequence: 4 givenname: Claes surname: Ladenvall fullname: Ladenvall, Claes organization: From the Institute of Clinical Neuroscience (K.J., A.T.-W., C.L., C.B., C.J.) and the Clinical Experimental Research Laboratory, Cardiovascular Institute (P.L., M.A.), the Sahlgrenska Academy at Göteborg University; the Department of Clinical Genetics, Sahlgrenska University Hospital/Östra (A.T.-W., C.L., C.J.); the Department of Mathematical Statistics (S.N.), Chalmers University of Technology, Göteborg, Sweden – sequence: 5 givenname: Maria surname: Andersson fullname: Andersson, Maria organization: From the Institute of Clinical Neuroscience (K.J., A.T.-W., C.L., C.B., C.J.) and the Clinical Experimental Research Laboratory, Cardiovascular Institute (P.L., M.A.), the Sahlgrenska Academy at Göteborg University; the Department of Clinical Genetics, Sahlgrenska University Hospital/Östra (A.T.-W., C.L., C.J.); the Department of Mathematical Statistics (S.N.), Chalmers University of Technology, Göteborg, Sweden – sequence: 6 givenname: Staffan surname: Nilsson fullname: Nilsson, Staffan organization: From the Institute of Clinical Neuroscience (K.J., A.T.-W., C.L., C.B., C.J.) and the Clinical Experimental Research Laboratory, Cardiovascular Institute (P.L., M.A.), the Sahlgrenska Academy at Göteborg University; the Department of Clinical Genetics, Sahlgrenska University Hospital/Östra (A.T.-W., C.L., C.J.); the Department of Mathematical Statistics (S.N.), Chalmers University of Technology, Göteborg, Sweden – sequence: 7 givenname: Christian surname: Blomstrand fullname: Blomstrand, Christian organization: From the Institute of Clinical Neuroscience (K.J., A.T.-W., C.L., C.B., C.J.) and the Clinical Experimental Research Laboratory, Cardiovascular Institute (P.L., M.A.), the Sahlgrenska Academy at Göteborg University; the Department of Clinical Genetics, Sahlgrenska University Hospital/Östra (A.T.-W., C.L., C.J.); the Department of Mathematical Statistics (S.N.), Chalmers University of Technology, Göteborg, Sweden – sequence: 8 givenname: Christina surname: Jern fullname: Jern, Christina organization: From the Institute of Clinical Neuroscience (K.J., A.T.-W., C.L., C.B., C.J.) and the Clinical Experimental Research Laboratory, Cardiovascular Institute (P.L., M.A.), the Sahlgrenska Academy at Göteborg University; the Department of Clinical Genetics, Sahlgrenska University Hospital/Östra (A.T.-W., C.L., C.J.); the Department of Mathematical Statistics (S.N.), Chalmers University of Technology, Göteborg, Sweden |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17204095$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/16179568$$D View this record in MEDLINE/PubMed https://gup.ub.gu.se/publication/41562$$DView record from Swedish Publication Index https://research.chalmers.se/publication/41562$$DView record from Swedish Publication Index |
| BookMark | eNqFkl1vFCEUhompsdvqXzAbE71yRmCAYbzSNLY2aaJx6_UJA4cuOl-FmZj-e1l3bRMTUy4gwMNzCLwn5GgYByTkFaMlY4q9o6zcXH8raW5MV4rVpRS15KVqnpAVk1wUQnF9RFaUVk3BRdMck5OUfmSeV1o-I8fZUjdS6RXh56GNYRi7uznY9QUOuP6aJ_0Yp21I_doMbn2Z7Bb7vL2Z4_gTn5On3nQJXxzGU_L9_NP12efi6svF5dnHq8JKTeeCWUG9p7mg946hQ1FVlWeorTOGOo21UkpKx-uaSmbzhTSruPU1UuQm06dks_emXzgtLUwx9CbewWgCRExoot2C3Zqux5ggITSCojAOQWjhc-cNaCFraB3axrkWpTLZ-va_1ptlgrx0s-xsgknFM_5mj09xvF0wzdCHZLHrzIDjkkBpJfK7ykdBVu84oTL48gAubY_u_gJ__yQDrw-ASdZ0PprBhvTA1ZwK2uwqfthzNo4pRfRgw2zmMA5zNKEDRmEXF6AMclzgIS7wJy6gmqx4_4_ivsrjh38DubnEjQ |
| CODEN | SJCCA7 |
| CitedBy_id | crossref_primary_10_1007_BF03256279 crossref_primary_10_3109_07853890_2010_507601 crossref_primary_10_1097_MBC_0000000000000274 crossref_primary_10_1016_j_ahj_2007_05_021 crossref_primary_10_1016_j_ccell_2008_01_001 crossref_primary_10_1586_14737159_8_4_495 crossref_primary_10_1016_j_jstrokecerebrovasdis_2007_03_002 crossref_primary_10_1155_2014_514891 crossref_primary_10_1016_j_thromres_2012_06_015 crossref_primary_10_1016_j_jstrokecerebrovasdis_2007_02_002 crossref_primary_10_1136_bmjopen_2015_009827 crossref_primary_10_1159_000438494 crossref_primary_10_3892_ijmm_2013_1234 crossref_primary_10_1007_s11825_008_0109_8 crossref_primary_10_1160_TH10_10_0682 crossref_primary_10_1007_s00415_012_6477_7 crossref_primary_10_1111_j_1538_7836_2010_04134_x crossref_primary_10_3390_ijms23031497 crossref_primary_10_3390_ijms25094931 crossref_primary_10_1016_j_gene_2011_12_046 crossref_primary_10_5482_HAMO_13_08_0041 crossref_primary_10_1016_j_neuri_2022_100068 crossref_primary_10_1097_MOH_0b013e3280dce557 crossref_primary_10_1016_j_thromres_2008_07_018 crossref_primary_10_1016_j_neulet_2013_01_041 crossref_primary_10_1089_gtmb_2018_0130 crossref_primary_10_1136_jnnp_2012_304834 crossref_primary_10_3109_10408361003791520 crossref_primary_10_3171_2008_7_JNS08272 crossref_primary_10_1016_S1474_4422_07_70028_5 crossref_primary_10_1097_MBC_0b013e3281ec4eee crossref_primary_10_1177_1076029617705728 crossref_primary_10_1186_s12872_016_0456_3 crossref_primary_10_1111_j_1538_7836_2006_02124_x crossref_primary_10_1177_1076029619869500 crossref_primary_10_1089_gte_2008_0025 crossref_primary_10_1002_humu_20666 crossref_primary_10_36502_2020_ASJBCCR_6209 crossref_primary_10_1017_cjn_2015_45 crossref_primary_10_1371_journal_pone_0053558 crossref_primary_10_1002_art_22598 crossref_primary_10_3390_ijms24108716 crossref_primary_10_1160_TH15_12_0938 crossref_primary_10_1007_s11033_007_9106_2 crossref_primary_10_1016_j_cca_2010_02_071 crossref_primary_10_1016_j_jstrokecerebrovasdis_2014_05_025 crossref_primary_10_1007_s00424_017_2014_y crossref_primary_10_14712_18059694_2020_13 crossref_primary_10_1016_j_jstrokecerebrovasdis_2009_10_011 crossref_primary_10_1055_s_0044_1789596 crossref_primary_10_1186_s12872_024_04406_9 crossref_primary_10_1016_j_bbacli_2014_12_004 crossref_primary_10_1016_j_jstrokecerebrovasdis_2022_106974 crossref_primary_10_1183_09031936_00055107 crossref_primary_10_1007_s13167_019_00162_5 crossref_primary_10_1021_acsomega_4c05204 |
| Cites_doi | 10.1161/str.31.1.26 10.1161/01.str.0000098004.26252.eb 10.1016/j.tins.2003.12.011 10.1055/s-0037-1613990 10.1161/atvb.19.2.454 10.1161/circ.104.25.3063 10.1080/01616412.1999.11741005 10.1161/01.cir.0000066908.82782.3a 10.1055/s-0038-1656042 10.1097/00043798-200204000-00009 10.1055/s-0037-1613481 10.1016/S0140-6736(94)90064-7 10.1038/sj.ejhg.5201011 10.1046/j.1365-2141.2000.02164.x 10.1093/cvr/27.5.882 10.1055/s-0037-1614532 10.1055/s-0037-1612951 10.1161/01.str.0000124123.76658.6c 10.1161/01.str.0000169944.46025.09 10.1161/circ.103.2.e13 10.1161/str.29.11.2261 10.1073/pnas.92.6.1851 10.1161/01.CIR.101.1.67 10.1161/atvb.19.11.2801 10.1161/str.27.6.1066 10.1111/j.1749-6632.1992.tb51622.x 10.1160/TH03-11-0693 |
| ContentType | Journal Article |
| Copyright | 2005 INIST-CNRS |
| Copyright_xml | – notice: 2005 INIST-CNRS |
| DBID | AAYXX CITATION IQODW CGR CUY CVF ECM EIF NPM 7TK 8FD FR3 P64 RC3 7X8 ADTPV AOWAS F1U F1S |
| DOI | 10.1161/01.STR.0000183617.54752.69 |
| DatabaseName | CrossRef Pascal-Francis Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Neurosciences Abstracts Technology Research Database Engineering Research Database Biotechnology and BioEngineering Abstracts Genetics Abstracts MEDLINE - Academic SwePub SwePub Articles SWEPUB Göteborgs universitet SWEPUB Chalmers tekniska högskola |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Genetics Abstracts Engineering Research Database Technology Research Database Neurosciences Abstracts Biotechnology and BioEngineering Abstracts MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic MEDLINE CrossRef Genetics Abstracts |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1524-4628 |
| EndPage | 2081 |
| ExternalDocumentID | oai_research_chalmers_se_940e4ade_484f_48fa_8457_bdec9ddbe56a oai_gup_ub_gu_se_41562 16179568 17204095 10_1161_01_STR_0000183617_54752_69 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GroupedDBID | --- .3C .55 .GJ .XZ .Z2 01R 0R~ 123 1J1 2WC 3O- 40H 4Q1 4Q2 4Q3 53G 5RE 5VS 6PF 71W 77Y 7O~ A9M AAAAV AAAXR AAFWJ AAGIX AAHPQ AAIQE AAJCS AAMOA AAMTA AAQKA AAQQT AARTV AASCR AASOK AAUEB AAXQO AAYEP AAYJJ AAYXX ABASU ABBUW ABDIG ABJNI ABPXF ABQRW ABVCZ ABXVJ ABXYN ABZAD ABZZY ACCJW ACDDN ACDOF ACEWG ACGFS ACGOD ACILI ACLDA ACWDW ACWRI ACXJB ACXNZ ACZKN ADBBV ADFPA ADGGA ADGHP ADHPY ADKSD ADNKB ADSXY AE3 AE6 AEBDS AEETU AENEX AFBFQ AFDTB AFEXH AFFNX AFMBP AFNMH AFSOK AFUWQ AGINI AHMBA AHOMT AHQNM AHQVU AHRYX AHVBC AIJEX AINUH AJCLO AJIOK AJNWD AJNYG AJZMW AKCTQ AKULP ALKUP ALMA_UNASSIGNED_HOLDINGS ALMTX AMJPA AMKUR AMNEI AOHHW AOQMC AYCSE BAWUL BCGUY BOYCO BQLVK BS7 C45 CITATION CS3 DIK DIWNM DU5 DUNZO E.X E3Z EBS EEVPB EJD ERAAH EX3 F2K F2L F2M F2N F5P FCALG FL- FW0 GNXGY GQDEL GX1 H0~ H13 HLJTE HZ~ IKREB IKYAY IN~ IPNFZ J5H JF9 JG8 JK3 JK8 K8S KD2 KMI KQ8 L-C L7B M18 N4W N9A N~7 N~B N~M O9- OAG OAH OB3 OCUKA ODA ODMTH OGROG OHYEH OK1 OL1 OLG OLH OLU OLV OLY OLZ OPUJH ORVUJ OUVQU OVD OVDNE OVIDH OVLEI OVOZU OWBYB OWU OWV OWW OWX OWY OWZ OXXIT P-K P2P PQQKQ R58 RAH RIG RLZ S4R S4S T8P TEORI TSPGW V2I VVN W3M W8F WH7 WOQ WOW X3V X3W X7M XXN XYM YFH YHZ YQJ YYP ZB8 ZGI ZZMQN IQODW ACIJW AWKKM CGR CUY CVF ECM EIF NPM OJAPA OLW RHF YCJ 7TK 8FD FR3 P64 RC3 7X8 ADTPV AOWAS F1U F1S |
| ID | FETCH-LOGICAL-c580t-1c40ff0385ffd1ede4333f1e8cdaa0d8e766655d277051c1798132cf7e0e2ae43 |
| ISSN | 0039-2499 1524-4628 |
| IngestDate | Wed Sep 10 02:26:39 EDT 2025 Tue Sep 09 23:21:13 EDT 2025 Wed Oct 01 13:41:43 EDT 2025 Sun Sep 28 06:18:06 EDT 2025 Wed Feb 19 01:42:36 EST 2025 Mon Jul 21 09:14:41 EDT 2025 Wed Oct 01 03:45:06 EDT 2025 Thu Apr 24 22:53:07 EDT 2025 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 10 |
| Keywords | ischemic stroke subtypes Cerebral infarction Stroke Nervous system diseases Serine endopeptidases Enzyme Cardiovascular disease t-Plasminogen activator Cerebral disorder plasminogen activator inhibitor type 1 Vascular disease Peptidases Plasminogen activator inhibitor 1 Central nervous system disease Hydrolases tissue-type plasminogen activator Cerebrovascular disease Fibrinolytic Polymorphism |
| Language | English |
| License | CC BY 4.0 |
| LinkModel | OpenURL |
| MergedId | FETCHMERGED-LOGICAL-c580t-1c40ff0385ffd1ede4333f1e8cdaa0d8e766655d277051c1798132cf7e0e2ae43 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| OpenAccessLink | https://www.ahajournals.org/doi/pdf/10.1161/01.STR.0000183617.54752.69 |
| PMID | 16179568 |
| PQID | 17400046 |
| PQPubID | 23462 |
| PageCount | 5 |
| ParticipantIDs | swepub_primary_oai_research_chalmers_se_940e4ade_484f_48fa_8457_bdec9ddbe56a swepub_primary_oai_gup_ub_gu_se_41562 proquest_miscellaneous_68640005 proquest_miscellaneous_17400046 pubmed_primary_16179568 pascalfrancis_primary_17204095 crossref_citationtrail_10_1161_01_STR_0000183617_54752_69 crossref_primary_10_1161_01_STR_0000183617_54752_69 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2005-10-01 |
| PublicationDateYYYYMMDD | 2005-10-01 |
| PublicationDate_xml | – month: 10 year: 2005 text: 2005-10-01 day: 01 |
| PublicationDecade | 2000 |
| PublicationPlace | Hagerstown, MD |
| PublicationPlace_xml | – name: Hagerstown, MD – name: United States |
| PublicationTitle | Stroke (1970) |
| PublicationTitleAlternate | Stroke |
| PublicationYear | 2005 |
| Publisher | Lippincott Williams & Wilkins |
| Publisher_xml | – name: Lippincott Williams & Wilkins |
| References | e_1_3_2_27_2 e_1_3_2_28_2 e_1_3_2_29_2 (e_1_3_2_30_2) 1999; 69 e_1_3_2_21_2 e_1_3_2_22_2 e_1_3_2_23_2 e_1_3_2_24_2 e_1_3_2_25_2 (e_1_3_2_6_2) 2005; 105 e_1_3_2_9_2 e_1_3_2_15_2 e_1_3_2_8_2 e_1_3_2_16_2 e_1_3_2_7_2 e_1_3_2_17_2 e_1_3_2_18_2 e_1_3_2_19_2 e_1_3_2_1_2 e_1_3_2_10_2 e_1_3_2_31_2 e_1_3_2_5_2 e_1_3_2_11_2 e_1_3_2_4_2 e_1_3_2_12_2 e_1_3_2_3_2 e_1_3_2_13_2 e_1_3_2_2_2 e_1_3_2_14_2 (e_1_3_2_26_2) 1998; 80 (e_1_3_2_20_2) 2004; 91 |
| References_xml | – ident: e_1_3_2_25_2 doi: 10.1161/str.31.1.26 – ident: e_1_3_2_16_2 doi: 10.1161/01.str.0000098004.26252.eb – ident: e_1_3_2_23_2 doi: 10.1016/j.tins.2003.12.011 – volume: 80 start-page: 632 year: 1998 ident: e_1_3_2_26_2 publication-title: Thromb Haemost – ident: e_1_3_2_5_2 doi: 10.1055/s-0037-1613990 – ident: e_1_3_2_4_2 doi: 10.1161/atvb.19.2.454 – ident: e_1_3_2_10_2 doi: 10.1161/circ.104.25.3063 – ident: e_1_3_2_29_2 doi: 10.1080/01616412.1999.11741005 – ident: e_1_3_2_31_2 doi: 10.1161/01.cir.0000066908.82782.3a – volume: 69 start-page: 43 year: 1999 ident: e_1_3_2_30_2 publication-title: Int J Hematol – ident: e_1_3_2_11_2 doi: 10.1055/s-0038-1656042 – ident: e_1_3_2_15_2 doi: 10.1097/00043798-200204000-00009 – ident: e_1_3_2_19_2 doi: 10.1055/s-0037-1613481 – ident: e_1_3_2_24_2 doi: 10.1016/S0140-6736(94)90064-7 – ident: e_1_3_2_17_2 doi: 10.1038/sj.ejhg.5201011 – ident: e_1_3_2_12_2 doi: 10.1046/j.1365-2141.2000.02164.x – ident: e_1_3_2_22_2 doi: 10.1093/cvr/27.5.882 – ident: e_1_3_2_2_2 doi: 10.1055/s-0037-1614532 – ident: e_1_3_2_7_2 doi: 10.1055/s-0037-1612951 – ident: e_1_3_2_8_2 doi: 10.1161/01.str.0000124123.76658.6c – ident: e_1_3_2_18_2 doi: 10.1161/01.str.0000169944.46025.09 – ident: e_1_3_2_14_2 doi: 10.1161/circ.103.2.e13 – ident: e_1_3_2_28_2 doi: 10.1161/str.29.11.2261 – ident: e_1_3_2_9_2 doi: 10.1073/pnas.92.6.1851 – ident: e_1_3_2_13_2 doi: 10.1161/01.CIR.101.1.67 – ident: e_1_3_2_3_2 doi: 10.1161/atvb.19.11.2801 – volume: 105 start-page: 1060 year: 2005 ident: e_1_3_2_6_2 publication-title: Blood – ident: e_1_3_2_27_2 doi: 10.1161/str.27.6.1066 – ident: e_1_3_2_1_2 doi: 10.1111/j.1749-6632.1992.tb51622.x – ident: e_1_3_2_21_2 – volume: 91 start-page: 1019 year: 2004 ident: e_1_3_2_20_2 publication-title: Thromb Haemost doi: 10.1160/TH03-11-0693 |
| SSID | ssj0002385 |
| Score | 2.1209266 |
| Snippet | Background and Purpose—
The tissue-type plasminogen activator (tPA) −7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G >5G polymorphisms... The tissue-type plasminogen activator (tPA) -7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G>5G polymorphisms influence transcriptional... BACKGROUND: and Purpose- The tissue-type plasminogen activator (tPA) -7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G >5G polymorphisms... BACKGROUND AND PURPOSE: The tissue-type plasminogen activator (tPA) -7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G>5G polymorphisms... |
| SourceID | swepub proquest pubmed pascalfrancis crossref |
| SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source |
| StartPage | 2077 |
| SubjectTerms | Adolescent Adult Aged Alleles Biological and medical sciences Blood. Blood coagulation. Reticuloendothelial system Brain - metabolism Brain Ischemia - genetics Case-Control Studies Cerebrovascular Accident/diagnosis/genetics Dermatologi och venereologi Dermatology and Venereal Diseases Female Fibrinolysis - genetics Genetic Genotype Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Homozygote Humans Male Medical sciences Middle Aged Models, Statistical Multivariate Analysis Myocardial Infarction - genetics Myocardium - metabolism Nervous system (semeiology, syndromes) Neurology Non-U.S. Gov't Odds Ratio Pharmacology. Drug treatments Plasminogen Activator Inhibitor 1 - blood Plasminogen Activator Inhibitor 1 - genetics Plasminogen Activator Inhibitor 1/blood/genetics Polymorphism Polymorphism, Genetic Regression Analysis Research Support Risk Factors Statistical Stroke - diagnosis Stroke - genetics Thrombosis - diagnosis Thrombosis - genetics Thrombosis/diagnosis/genetics Tissue Plasminogen Activator - blood Tissue Plasminogen Activator - genetics Tissue Plasminogen Activator/blood/genetics Transcription Transcription, Genetic Vascular diseases and vascular malformations of the nervous system |
| Title | Fibrinolytic Gene Polymorphism and Ischemic Stroke |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/16179568 https://www.proquest.com/docview/17400046 https://www.proquest.com/docview/68640005 https://gup.ub.gu.se/publication/41562 https://research.chalmers.se/publication/41562 |
| Volume | 36 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| journalDatabaseRights | – providerCode: PRVAFT databaseName: Open Access Digital Library customDbUrl: eissn: 1524-4628 dateEnd: 99991231 omitProxy: true ssIdentifier: ssj0002385 issn: 1524-4628 databaseCode: KQ8 dateStart: 19700101 isFulltext: true titleUrlDefault: http://grweb.coalliance.org/oadl/oadl.html providerName: Colorado Alliance of Research Libraries – providerCode: PRVBFR databaseName: Free Medical Journals customDbUrl: eissn: 1524-4628 dateEnd: 20241001 omitProxy: true ssIdentifier: ssj0002385 issn: 1524-4628 databaseCode: DIK dateStart: 19700101 isFulltext: true titleUrlDefault: http://www.freemedicaljournals.com providerName: Flying Publisher – providerCode: PRVFQY databaseName: GFMER Free Medical Journals customDbUrl: eissn: 1524-4628 dateEnd: 99991231 omitProxy: true ssIdentifier: ssj0002385 issn: 1524-4628 databaseCode: GX1 dateStart: 0 isFulltext: true titleUrlDefault: http://www.gfmer.ch/Medical_journals/Free_medical.php providerName: Geneva Foundation for Medical Education and Research |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1ZbxMxELZCkRASQpwlHGUf6OOGPXzsPqKIqvRAgqaib5bXRyuINlGyeYA3_jnjtfdISUTpyyrr2COvZzz22DPfIPSOplomTNGQaZyHWBZJWNBYhdLA8kmVzW1uo5FPP9PDc3x0QS4Gg9_96JKqGMlfG-NKbsNVKAO-2ijZ_-BsSxQK4DfwF57AYXjeiMcH1l-_nE1_WtRVCyBt3dnAmIexa3JffALrtfZ_P6sWsx9rfj-upEZqylnUOxI48m44x6ICS7psFfeJACUF_XdZjzu33sl3sT8e72fZopyuShV-m00d1GO5pe14KvT6eQNpPddaHZraOxmX1mikvdpMcGijXPt61QGbNPIT9bVk5FO3aP_qsrb8rc1pXEcojM4mX2ugSdA_sOMaEcxIMqJ5t4Y19_bXlrbW4bA2dWjMo5gDLd7R4jUtTvM76G7CKLVJMI6_dIDzsKNxSTD8R3vcWqD1fnu_1vY4D-ZiCdPNuDwpmwyZayi19c5m8gg99CZJ8MHJ12M00OUTdO_UO108RUlfzAIrZkFfzAIQs6ARs8AJ1TN0fvBxMj4MfaqNUJIsqsJY4sgYe0tsjIq10jhNUxPrTCohIpVpGBpKiEoYAy0uLcodzGJpmI50IqD2c7RTzkr9AgWiIBlTmChYPXBUqCJl9qWIhDCwH1VDlDeDw6XHobfpUKb830waorRtO3doLDdqtbfGg66pzdAENsYQvW2YwkG72iszUerZagk1cB1fvb0GzaitAjR2HTc76tAHG4w7RPuOve0_FtL9cjXnUHS54kvN7SlKMkQnG-p5zK8rLq_qhEpLWz_HkcYwbznOsIGHETzDhPFCaZkrVWhCxctbjdUrdL-b9K_RTrVY6Tew7a6KvXpi_AFc68q5 |
| linkProvider | Colorado Alliance of Research Libraries |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Fibrinolytic+Gene+Polymorphism+and+Ischemic+Stroke&rft.jtitle=Stroke+%281970%29&rft.au=Jood%2C+Katarina&rft.au=Ladenvall%2C+Per&rft.au=Tja%CC%88rnlund-Wolf%2C+Anna&rft.au=Ladenvall%2C+Claes&rft.date=2005-10-01&rft.issn=0039-2499&rft.eissn=1524-4628&rft.volume=36&rft.issue=10&rft.spage=2077&rft.epage=2081&rft_id=info:doi/10.1161%2F01.STR.0000183617.54752.69&rft.externalDBID=n%2Fa&rft.externalDocID=10_1161_01_STR_0000183617_54752_69 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0039-2499&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0039-2499&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0039-2499&client=summon |