Show simple item record

dc.contributor.authorAydin, Murat
dc.contributor.authorKatrancioglu, Nurkay
dc.contributor.authorManduz, Sinasi
dc.contributor.authorAtahan, Erhan
dc.contributor.authorKarahan, Oguz
dc.contributor.authorOzdemir, Ozturk
dc.contributor.authorBerkan, Ocai
dc.date.accessioned2019-07-27T12:10:23Z
dc.date.accessioned2019-07-28T10:07:16Z
dc.date.available2019-07-27T12:10:23Z
dc.date.available2019-07-28T10:07:16Z
dc.date.issued2010
dc.identifier.issn1301-5680
dc.identifier.urihttps://hdl.handle.net/20.500.12418/9782
dc.descriptionWOS: 000283410700007en_US
dc.description.abstractBackground: 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.isoturen_US
dc.publisherBAYCINAR MEDICAL PUBL-BAYCINAR TIBBI YAYINCILIKen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAbdominal aortic aneurysmen_US
dc.subjectCCR5en_US
dc.subjectchemokineen_US
dc.subjectgene polymorphismen_US
dc.subject32 base p deletionen_US
dc.titleChemokine receptor 5 Delta 32 gene polymorphism and abdominal aortic aneurysmsen_US
dc.typearticleen_US
dc.relation.journalTURK GOGUS KALP DAMAR CERRAHISI DERGISI-TURKISH JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERYen_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, Turkeyen_US
dc.contributor.authorIDKarahan, Oguz -- 0000-0003-0044-9476en_US
dc.identifier.volume18en_US
dc.identifier.issue4en_US
dc.identifier.endpage289en_US
dc.identifier.startpage284en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

Show simple item record