The exon 3-deleted/full-length growth hormone receptor polymorphism and response to growth hormone therapy in growth hormone deficiency and Turner syndrome: a multicenter study.

Background/aim: The exon 3-deleted/full-length (d3/fl) growth hormone (GH) receptor (GHR) polymorphism has been associated with responsiveness to GH therapy in some diagnostic groups. However, there are still controversies on this issue. To evaluate the effect of the GHR exon 3 polymorphism on growth after 1 and 2 years of GH therapy in Turkish patients with GH deficiency (GHD) and Turner's syndrome (TS) and the distribution of GHR exon 3 isoforms.

The distribution of exon 3-deleted/full-length growth hormone receptor polymorphism in the Turkish population.

Objective: The exon 3-deleted/full-length (d3/fl) growth hormone receptor (d3/fl-GHR) polymorphism has been associated with responsiveness to GH therapy in some children and also with adult height variation in the general population. We aimed to evaluate the distribution of d3/fl-GHR polymorphism in a Turkish population.

Methods: The study included 477 (54 females/423 males) healthy adults with a mean±SD age of 31.

Effects of myeloperoxidase -463 G/A gene polymorphism and plasma levels on coronary artery disease.

Myeloperoxidase is a lysosomal enzyme of polymorphonuclear leucocytes that contributes to inflammatory responses. In previous studies it was shown that MPO was synthesized in atherosclerotic lesions responsible of lipoprotein oxidations. We aimed to determine the MPO -463 G/A gene polymorphism distribution in Turkish population and evaluate the effects of it on myeloperoxidase levels.

Comparison of lipid profiles in relation to APOB EcoRI polymorphism in obese children with hyperlipidemia.

Background: We aimed to evaluate apolipoprotein B-100 (APOB) EcoRI polymorphism and plasma lipid parameters together in children and adolescents. This is the first such study in Turkey to determine possible relationships of these parameters.

Materials And Methods: Three separate groups were studied: a group of obese children with hyperlipidemia, a group of obese children without hyperlipidemia, and a group of healthy children neither with hyperlipidemia nor obesity.

Bladder cancer and polymorphisms of DNA repair genes (XRCC1, XRCC3, XPD, XPG, APE1, hOGG1).

Carcinogenic molecules from cigarettes are known to cause DNA damage to bladder epithelial cells, but such damage can be corrected by some DNA repair mechanisms such as base and nucleotide excision repair, double-strand repair and mismatch repair. Various gene products play a role in these DNA repair systems. The aim of this study was to investigate six of these genes (XRCC1, XRCC3, XPD, XPG, APE1, hOGG1) each of which has a separate role in these repair mechanisms.

APE1 and XRCC3 polymorphisms and myocardial infarction.

Background: In most cells, DNA is regularly damaged by mutagens. Different DNA repair mechanisms operate on specific types of damaged DNA. When DNA damage resulting from free radicals is not repaired, it might lead to deteriorated gene expression, the development of a number of diseases such as cancer, diabetes, vascular diseases, and aging.

Effects of manganase superoxide dismutase Ala-9Val polymorphism on prostate cancer: a case-control study.

Background: Manganese superoxide dismutase (MnSOD) is a major enzyme that is responsible for the detoxification of reactive oxygen species in the mitochondria. Mitochondrial DNA damage may contribute to carcinogenesis as an important risk factor. The aim of this study was to investigate the relationship between prostate cancer and MnSOD Ala-9Val polymorphism in Turkish men with prostate cancer.