Yazar "Isik, M. R." seçeneğine göre listele

Listeleniyor 1 - 2 / 2
  • [ X ]
    Öğe
    CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND PARAOXONASE-1 192 AND 55 GENE POLYMORPHISMS
    (Taylor & Francis Ltd, 2010) Tekes, S.; Isik, B.; Yildiz, T.; Simsek, S.; Isik, M. R.; Budak, T.
    Chronic obstructive pulmonary disease (COPD) is a leading cause of chronic morbidity and mortality. The oxidative stress is increased in COPD patients. Paraoxonase (PON1) in the lung may have a role to protect from oxidative stress. We have investigated a possible relationship between PON1 55 and PON1 192 gene polymorphisms in COPD patients and control subjects. A Total of 62 inpatients of COPD, 45 non-smokers and 35 smokers without COPD were included in the study The serum levels of PON1 were measured. The PON1 genotypes were determined by PCR amplification of the region containing the polymorphism followed by restriction enzyme digestion. The serum levels of PON1 were significantly low in the COPD patients group (p<0.001). There were no statistical differences between the COPD and control groups for PON1 55 polymorphism. The PON1 192 QQ and QR genotypes occurred with similar frequencies in the COPD and control groups with no significant differences while a significant difference was found between the PON1 192 RR allele frequencies (p<0.05) of all groups. PON1 192 gene polymorphism may be considered associated with COPD. PON1 polymorphisms and low PON1 activity levels might be considered as an independent risk factor for COPD.
  • [ X ]
    Öğe
    The insertion/deletion polymorphism in the ACE gene and chronic obstructive pulmonary disease
    (Funpec-Editora, 2013) Simsek, S.; Tekes, S.; Oral, D.; Turkyilmaz, A.; Isik, B.; Isik, M. R.; Akkoc, H.
    An insertion/deletion (I/D) polymorphism was identified in intron 16 of the gene encoding the human angiotensin I-converting enzyme (ACE), a candidate gene for chronic obstructive pulmonary disease (COPD). We investigated the relationship between this polymorphism in the ACE gene and the risk of developing COPD. Sixty-six COPD in-patients and 40 non-smoking control individuals were recruited for this study. The distribution of ACE genotypes in these individuals was studied. The frequencies of ACE genotypes were found to be 47.0% for DD, 30.3% for ID, and 22.7% for II in the COPD group and 32.5% for DD, 47.5% for ID, and 20.0% for II in the control group. The allele frequencies were found to be 0.62% for the D allele and 0.38% for the I allele in the COPD group and 0.56% for the D allele and 0.44% for the I allele in the control group. A significant difference was found between I and D allele frequencies (P < 0.05) of the study and control groups. Our results suggest that this ACE polymorphism may be associated with the development of COPD.