dc.contributor.author | Aydin, Murat | |
dc.contributor.author | Katrancioglu, Nurkay | |
dc.contributor.author | Manduz, Sinasi | |
dc.contributor.author | Atahan, Erhan | |
dc.contributor.author | Karahan, Oguz | |
dc.contributor.author | Ozdemir, Ozturk | |
dc.contributor.author | Berkan, Ocai | |
dc.date.accessioned | 2019-07-27T12:10:23Z | |
dc.date.accessioned | 2019-07-28T10:07:16Z | |
dc.date.available | 2019-07-27T12:10:23Z | |
dc.date.available | 2019-07-28T10:07:16Z | |
dc.date.issued | 2010 | |
dc.identifier.issn | 1301-5680 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12418/9782 | |
dc.description | WOS: 000283410700007 | en_US |
dc.description.abstract | Background: In this study, we aimed to investigate the relationship between abdominal aortic aneurysm (AAA) and chemokine receptor 5 Delta 32 (CCR5) gene polymorphism as a risk factor. Methods: Fifty-eight patients (41 males, 17 females; mean age 62.9 +/- 6.5 years; range 45 to 78 years) operated on our clinic between May 2008 and March 2009 with the diagnosis of AAA, and 58 healthy volunteers (38 males, 20 females; mean age 58.8 +/- 11.6 years; range 30 to 79 years) with normal aortic diameters measured by computed tomography were included in this study. Thirty-two base p deletions in the CCR5 gene were screened after obtaining genomic DNAs from peripheral blood samples of the patients. Results: When the groups were compared with the predisposing risk factors for the development of AAA, no significant difference was observed (p>0.05). Eleven patients (19.0%) had heterozygote CCR5 gene mutation in the AAA group, however, only one patient (1.7%) had heterozygote CCR5 gene mutation in the control group. While the CCR5 homozygote was normal in 47 (81.0%) patients, the CCR5 homozygote was normal in 57 (98.3%) volunteers in the control group. Chemokine receptor 5 Delta 32 heterozygote gene mutation was significantly higher in the AAA group. (p=0.004). Conclusion: Consequently, a relationship between CCR5 gene polymorphism and AAA was demonstrated in this study. We think that hereditary factors considered between unchanged etiologic factors play a role in the development of AAA and we believe that AAA can be treated before serious complications occur with frequent clinical check ups in people with hereditary predisposition. | en_US |
dc.language.iso | tur | en_US |
dc.publisher | BAYCINAR MEDICAL PUBL-BAYCINAR TIBBI YAYINCILIK | en_US |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.subject | Abdominal aortic aneurysm | en_US |
dc.subject | CCR5 | en_US |
dc.subject | chemokine | en_US |
dc.subject | gene polymorphism | en_US |
dc.subject | 32 base p deletion | en_US |
dc.title | Chemokine receptor 5 Delta 32 gene polymorphism and abdominal aortic aneurysms | en_US |
dc.type | article | en_US |
dc.relation.journal | TURK GOGUS KALP DAMAR CERRAHISI DERGISI-TURKISH JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY | en_US |
dc.contributor.department | [Aydin, Murat -- Katrancioglu, Nurkay -- Manduz, Sinasi -- Atahan, Erhan -- Karahan, Oguz -- Berkan, Ocai] Cumhuriyet Univ, Tip Fak, Kalp & Damar Cerrahisi Anabilim Dali, TR-58140 Sivas, Turkey -- [Ozdemir, Ozturk] Tibbi Genet Anabilim Dali, Sivas, Turkey | en_US |
dc.contributor.authorID | Karahan, Oguz -- 0000-0003-0044-9476 | en_US |
dc.identifier.volume | 18 | en_US |
dc.identifier.issue | 4 | en_US |
dc.identifier.endpage | 289 | en_US |
dc.identifier.startpage | 284 | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |