Association of the plasminogen activator inhibitor-1(PAI-1) gene 4G5G promoter polymorphism in Buergers disease (Tromboangiitis obliterans)英文文献资料.docVIP

Association of the plasminogen activator inhibitor-1(PAI-1) gene 4G5G promoter polymorphism in Buergers disease (Tromboangiitis obliterans)英文文献资料.doc

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Association of the plasminogen activator inhibitor-1(PAI-1) gene 4G5G promoter polymorphism in Buergers disease (Tromboangiitis obliterans)英文文献资料

Vol.2, No.5, 454-457 (2010) Health doi:10.4236/health.2010.25068 Association of the plasminogen activator inhibitor-1(PAI-1) gene 4G/5G promoter polymorphism in Buerger’s disease (Tromboangiitis obliterans) Sinasi Manduz , Nurkay Katrancioglu , Oguz Karahan , Oztürk Ozdemir * 1 1 1 2 1 2 Department of Cardiovascular Surgery, Faculty of Medicine, Cumhuriyet University, Sivas, Turkey Department of Medical Genetics, Faculty of Medicine, Cumhuriyet University, Sivas and University of COMU, Faculty of Medicine, Canakkale, Turkey; *Corresponding Author: ozdemir615@ Received 3 January 2010; revised 26 January 2010; accepted 27 January 2010. ABSTRACT Polymorphisms; PAI-1 Thromboangiitis obliterans (TAO) is an unusual tobacco-associated vasculopathy that is a non- atherosclerotic inflammatory disorder of unkn- own etiology that affects small and medium- sized vessels of the extremities. The single guanosine nucleotide deletion/insertion polym- orphism (4G/5G) at -675 bp in promoter region of the PAI-1 gene is the major genetic determi- nant of PAI-1 expression. Plasma PAI-1 level is higher in people with the homozygous 4G gen- otype than in those with the 5G/5G genotype and renders higher transcription activity. The aim of this study was to determine the status and the role of PAI-1 gene 4G/5G promoter pol- ymorphism in patients with Buerger’s disease (Thromboangiitis obliterans—TAO). The current case-control study included 30 consecutive pat- ients with Buerger’s disease (mean age 42.9 ± 14.3 years, 28 men and 2 women), and 30 heal- thy volunteers (mean age 40.9 ± 4.79 years, 27 men and 3 women) between January 2006 and September 2009. Patients and control cases were genotyped for the 4G/5G polymorphism using the multiplex PCR based stripassay reverse

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