Person: ÖZER, SIDIKA AYŞE
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ÖZER
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SIDIKA AYŞE
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Publication Metadata only Impact of glucocorticoid receptor gene (NR3C1) polymorphisms in Turkish patients with metabolic syndrome(SPRINGER, 2016) AKKİPRİK, MUSTAFA; Kaya, Z.; Caglayan, S.; Akkiprik, M.; Aral, C.; Ozisik, G.; Ozata, M.; Ozer, A.Background The metabolic syndrome (MetS) is characterized by a cluster of metabolic factors, including insulin resistance and type-2 diabetes, abdominal obesity, dyslipidemia, hypertension and microalbuminuria. Impaired glucocorticoid receptor (GR) activity also plays an important role in the etiology of MetS. The objective of our study is to evaluate the effects of GR gene polymorphisms (BclI, N363S, TthIII1 and ER22/23EK) in Turkish patients with MetS. Materials and methods Seventy subjects with MetS and 185 healthy controls were enrolled in the study. PCR-RFLP analysis was used for genotyping. Results for each polymorphism have been verified by allele-specific oligonucleotide analysis. Results BclI GG genotype was significantly associated with an increased risk of MetS (p = 0.02). Also, only in women, the G allele carriers were significantly associated with higher C-peptide. T allele carriers of TthIII1 polymorphism were significantly associated with higher C-peptide, triglyceride, insulin and C-reactive protein (CRP, p value 0.048, 0.022, 0.005 and 0.022, respectively), and lower fasting blood glucose (FBG, p = 0.02). The combined carriers of BclI polymorphism G allele and TthIII1 polymorphism T allele were significantly associated with higher diastolic blood pressure in all patients, and lower FBG and postprandial blood glucose in only men. All the ER22/23EK polymorphisms coexisted with polymorphic variant of TthIII1 (p = 0.0058). Conclusion The presence of homozygote polymorphic variant of BclI might be good predictive markers for the disease susceptibility. The BclI and the TthIII1 polymorphism are associated with sex-specific clinical parameters. Our findings also suggest that the combination of BclI and TthIII1 polymorphisms may play a protective role in blood glucose.Publication Metadata only 17Beta-estradiol modulates endothelin-1 expression and release in human endothelial cells(2000) ÖZER, SIDIKA AYŞE; Bilsel, A. S.; Moini, H.; Tetik, E.; Aksungar, F.; Kaynak, B.; Ozer, A.OBJECTIVE: In this study the role of 17beta-estradiol (E2) in the regulation of endothelin-1 (ET-1) mRNA expression and secretion was investigated in cultured human umbilical vein endothelial cells (HUVECs). METHODS: Endothelial cells were either deprived of or treated with 17beta-estradiol (10(-9), 10(-7) M) for 48 h. After the incubation, the effect of E2 on ET-1 gene expression was evaluated by Northern blot analysis. ET-1 release into the media was measured by radioimmunoassay after 6 h of incubation under basal conditions and upon stimulation with thrombin (4 U/ml). In addition, the cyclic guanosine 5'-monophosphate (cGMP) content of cells was assayed by immunoassay. In order to exclude the role of nitric oxide (NO) in E2-induced effects on endothelin-1 gene expression and secretion, nitric oxide synthase (NOS) inhibitor, N-nitro L-arginine methyl ester (1 mM) (L-NAME) was added to the media of some cultures. RESULTS: Incubation of HUVECs with 10(-9) and 10(-7) M E2 for 48 h resulted in a 30 and 47% inhibition of ET-1 mRNA expression, respectively. Incubation with E2 also decreased the basal and thrombin-stimulated ET-1 release while increasing the cGMP content of cells significantly. NOS inhibitor L-NAME increased the release of ET-1 from E2-incubated cells but did not alter the ET-1 release from hormone-deprived cells. However, ET-1 secretion of E2-treated cells were significantly less than the deprived ones. Northern blot analyses also demonstrated that inhibition of NOS only partly attenuated the effect of E2 on ET-1 gene expression. In the presence of L-NAME, treatment with 10(-7) M E2 caused a 12% decrease in ET-1 gene expression. CONCLUSION: The results demonstrate that E2 may play both direct and indirect role in regulation of ET-1 gene expression and production in human endothelial cells. E2-induced increase in NO but decrease in ET-1 production may partly explain the mechanism of the protective effects of the hormone on the cardiovascular system.Publication Metadata only Effect of BCG vaccination on cytokine mRNA expression in atopic children with asthma(2003) ÖZER, SIDIKA AYŞE; Ozer, Ayse; Tükenmez, Faruk; Biricik, Anil; Barlan, Isil B.; Cirakoglu, Beyazit; Başaran, Müjdat M.BACKGROUND: To investigate whether a preexisting T(H2)-type immune response could be suppressed by BCG immunization in atopic children with asthma. METHODS AND RESULTS: We have used PCR to amplify reverse transcribed (RT) IFN-gamma and IL-5 mRNA expressed by peripheral blood mononuclear cells (PBMCs) in response to in vitro phytohemagglutinin A, purified protein derivative and Dermatophagoides pteronyssinus II stimulation from nine atopic children, both before and 8 weeks after BCG vaccination. We have demonstrated that IFN-gamma expression was induced in response to all stimulants (IFN-gamma/beta-actin) after the vaccination, whereas there was no expression before (P<0.001). Although there was a tendency to diminish in the expression of IL-5 mRNA in response to the stimulants, only PHA rendered a statistically significant decrease after the vaccination. CONCLUSIONS: These results provide some evidence of TH1 dominance after BCG administration in atopic children.Publication Metadata only Mutation distributions and clinical correlations of PIK3CA gene mutations in breast cancer(SAGE PUBLICATIONS LTD, 2016) AKKİPRİK, MUSTAFA; Dirican, Ebubekir; Akkiprik, Mustafa; Ozer, AyseBreast cancer (BCa) is the most common cancer and the second cause of death among women. Phosphoinositide 3-kinase (PI3K) signaling pathway has a crucial role in the cellular processes such as cell survival, growth, division, and motility. Moreover, oncogenic mutations in the PI3K pathway generally involve the activation phosphatidylinositol-4,5-bisphosphate 3-kinase-catalytic subunit alpha (PIK3CA) mutation which has been identified in numerous BCa subtypes. In this review, correlations between PIK3CA mutations and their clinicopathological parameters on BCa will be described. It is reported that PIK3CA mutations which have been localized mostly on exon 9 and 20 hot spots are detected 25-40 % in BCa. This relatively high frequency can offer an advantage for choosing the best treatment options for BCa. PIK3CA mutations may be used as biomarkers and have been major focus of drug development in cancer with the first clinical trials of PI3K pathway inhibitors currently in progress. Screening of PIK3CA gene mutations might be useful genetic tests for targeted therapeutics or diagnosis. Increasing data about PIK3CA mutations and its clinical correlations with BCa will help to introduce new clinical applications in the near future.Publication Metadata only PIK3CA and TP53 MUTATIONS and SALL4, PTEN and PIK3R1 GENE EXPRESSION LEVELS in BREAST CANCER(WALTER DE GRUYTER GMBH, 2020) KAYA, HANDAN; Dirican, Ebubekir; Seven, Ipek Erbarut; Kaya, Handan; Ugurlu, M. Umit; Peker, Irem; Gulluoglu, Bahadir M.; Ozer, Ayse; Akkiprik, MustafaObjective: A high frequency of PI3K signalling pathway abnormalities and TP53 mutations are critical in the development and progression of breast cancer (BCa). We aimed to detect PIK3CA and TP53 mutations via an expression analysis of PIK3R1, PTEN and SALL4 and correlate the expression of these genes with clinical parameters of BCa. Materials and methods: PIK3CA and TP53 mutations in BCa samples were analysed by High-Resolution Melting (HRM) analysis, followed by Sanger sequencing, and the expression levels of PIK3R1, PTEN and SALL4 were evaluated by RT-PCR methods. Results: The frequency of PIK3CA and TP53 mutations was 42% and 38% according to the HRM and Sanger sequencing. There was a significantly high frequency of these mutations in ER(+), N0 and HER2(-) tumour samples. PIK3R1 and PTEN expression levels were high in tumour samples, whereas SALL4 expression was low. In patients with TP53 mutations, PIK3R1 expression was low, and this finding was statistically significant. PIK3R1 and PTEN expression levels showed statistically significant, respectively in G3 grades, ER(+), (PR)(+), HER2(+) and ER(+). Conclusions: We suggest that these candidate genes could be potential prognostic biomarkers of BCa and that they should be considered in the evaluation of clinical parameters of BCa.Publication Metadata only Association of ACP1 genotypes and clinical parameters in patients with metabolic syndrome(TUBITAK SCIENTIFIC & TECHNICAL RESEARCH COUNCIL TURKEY, 2011) AKKİPRİK, MUSTAFA; Akkiprik, Mustafa; Sertoglu, Filiz Ozdemir; Caglayan, Sinan; Aral, Cenk; Ozisik, Gokhan; Atabey, Zebra; Ozata, Metin; Ozer, Sidika AyseAim: Acid phosphatase locus 1 (ACP1) encodes a polymorphic enzyme and has potential implications for the development of metabolic syndrome (MS) by altering insulin sensitivity. The aim of this study was to determine whether a relationship exists between ACP1 genotypes and various metabolic syndrome risk factors. Materials and methods: We employed a PCR-RFLP based genotyping of ACP1 in a cohort of 70 patients with MS and 168 healthy individuals. Results: When compared to controls, genotypes associated with low enzyme activity were observed at significantly lower frequencies in both sexes. Of note, high enzyme activity genotypes were more common in patients with MS when compared with medium and low enzyme activity genotypes. *A allele frequency was not different between patients and controls even considering sex; however, there was a good correlation of the presence of the allele with body composition, serum cortisol levels and suppressibility of cortisol, particularly in women with MS. Conclusion: Our findings suggest that low enzyme activity genotypes seem to be associated with a protective effect for the development of MS. Additionally, *A allele carriage affects body composition in women but not in men, and the presence of this allele might modulate serum cortisol levels as well as its suppressibility in both sexes, in an inverse manner.Publication Metadata only Analysis of p53 Gene Polymorphisms and Protein Over-expression in Patients with Breast Cancer(SPRINGER, 2009) KAYA, HANDAN; Akkiprik, Mustafa; Sonmez, Ozgur; Gulluoglu, Bahadir M.; Caglar, Hale B.; Kaya, Handan; Demirkalem, Pakize; Abacioglu, Ufuk; Sengoz, Meric; Sav, Aydin; Ozer, Aysep53 polymorphic variants play an important role in the determination of tumor phenotype and characteristics in breast cancer. In this study, we examined three common polymorphisms in p53 gene and their haplotype combinations to assess their potential association with inherited predisposition to breast cancer development, in relations with the protein over-expression and patients' demographic data. A total of 99 patients with breast cancer and 107 age-matched healthy controls were included in the study. Genotypes were determined using PCR-RFLP and DNA sequencing techniques. Evaluation of p53 protein overexpression was also examined by immunohistochemistry. Among three polymorphisms, increased codon 72 Pro allele frequency (p=0.0067) and the presence of Pro allele were found to be significantly associated with breast cancer (p=0.013). A significant risk was also found in subjects with combinations of specific haplotypes and genotypes. Most of breast cancer women especially younger than 50 years carry at least one p53 polymorphism (p=0.001). There was no any association between these three p53 polymorphisms and the protein over-expression, separately or in interaction, with breast cancer. In conclusion, presence of proline allele at codon 72 alone, and its special combinations with other two polymorphisms appear to be a significant risk factor for breast cancer. Determination of well-known p53 polymorphisms might be a good predictor for breast cancer development especially in women younger than 50 years.Publication Metadata only R72P Polymorphism of TP53 in Ulcerative Colitis Patients is Associated with the Incidence of Colectomy, Use of Steroids and the Presence of a Positive Family History(SPRINGER, 2010) ÇELİKEL, ÇİĞDEM; Eren, Fatih; Akkiprik, Mustafa; Atug, Ozlen; Sonmez, Ozgur; Tahan, Gulgun; Ozdemir, Filiz; Hamzaoglu, Hulya Over; Celikel, Cigdem Ataizi; Imeryuz, Nese; Avsar, Erol; Ozer, AyseP53 tumor suppressor protein is one of the pivotal regulators for genome integrity, cell cycle and apoptosis. The most commonly and extensively studied single nucleotide polymorphism (SNP) of p53 is Arg>Pro substitution on codon 72 (R72P). Although we know that the SNP has unique functional effects on the protein, its clinical significance is not clearly identified yet. Aim of the study was to access the relationship between R72P genotype distribution and clinical variables in patients with ulcerative colitis (UC) and colorectal cancer (CRC). Genomic DNA samples were extracted from 95 UC, 50 CRC, and 219 healthy controls. R72P genotype analysis was carried out with polymerase chain reaction following by restriction enzyme digestion. We observed that Pro allele carriage is a strong risk factor for CRC (OR=3.03; 95%CI=1.91-2.40; p=0.003), but only modest association with UC (OR=1.61; 95%CI=0.98-2.65; p =0.059) (Pro/Pro and Pro/Arg genotypes vs. Arg/Arg genotype). We did not find any correlation between genotype distribution of the polymorphism and clinical parameters of CRC, but in UC, Pro/Pro genotype was significantly related to an inflammatory bowel disease family history (OR=8.0; 95%CI=1.68-38.08, p=0.015), and Arg/Pro genotype was significantly associated with the history of disease-related colectomy (OR=17.77; 95%CI=0.98-323.34, p=0.012) and steroid use (OR=10.14; 95%CI=2.63-39.12, p=0.0002). Our data suggest that R72P variant seems to be associated with high risk for development of CRC but carries low risk for development of UC. R72P genotypes might be a useful predictive marker for surgical and medical treatment of UC.Publication Metadata only Treatment with either obestatin or ghrelin attenuates mesenteric ischemia-reperfusion-induced oxidative injury of the ileum and the remote organ lung(ELSEVIER SCIENCE INC, 2015) YEGEN, BERRAK; Sen, Leyla Semiha; Karakoyun, Berna; Yegen, Cumhur; Akkiprik, Mustafa; Yuksel, Meral; Ercan, Feriha; Ozer, Ayse; Yegen, Berrak C.To evaluate the effects of exogenous ghrelin or obestatin on intestinal injury and accompanying pulmonary injury, intestinal ischemia-reperfusion (I/R) was induced in rats by obstructing the superior mesenteric artery for 60 min, whereas laparotomy was performed in the sham group. At the beginning of the 90-min reperfusion period, the rats were injected with obestatin (100 mu g/kg), ghrelin (10 ng/kg), or saline intravenously (iv). At the end of reperfusion, the blood, ileum, and lung samples were taken for the histological and biochemical assays. In the saline-treated I/R group, the increased serum interleukin (IL)-1 beta level, high damage scores, and elevated tissue malondialdehyde level and collagen content in both tissues were significantly reduced by obestatin or ghrelin. Increased ileal myeloperoxidase activity of the saline-treated I/R group was reduced by treatment with obestatin or ghrelin, whereas increased pulmonary myeloperoxidase activity was reduced with administration of obestatin. Increased DNA fragmentation in the ileum of the saline-treated I/R group was reduced by both peptides. Elevated luminol-lucigenin chemiluminescence levels and nuclear factor kappa B (NF-kappa B) messenger RNA ( mRNA) expression in the ileum of the saline-treated-I/R group were significantly decreased by obestatin or ghrelin treatment. I/R-induced depletion of the antioxidant glutathione in both ileal and pulmonary tissues was prevented with either obestatin or ghrelin treatment. Administration of either obestatin or ghrelin exerts similar protective effects against I/R-induced ileal and pulmonary injury, thus warranting further investigation for their possible use against ischemic intestinal injury. (C) 2015 Elsevier Inc. All rights reserved.Publication Metadata only Targeted custom gene panel sequencing for cardiac ion channelopathies: Efficiently detects candidate pathogenic mutations in Long QT syndrome(ELSEVIER SCIENCE BV, 2017) ÖZER, SIDIKA AYŞE; Temel, S. G.; Turkgenc, B.; Karadag, O.; Aykan, H. H.; Uysal, F.; Bastuhan, I. Y.; Sulu, A.; Atik, S. U.; Cinar, B.; Dedeoglu, R.; Gunay, E.; Ramoglu, M.; Cilsal, E.; Sahin, M.; Mese, T.; Ciftci, O.; Oztunc, F.; Karagoz, T.; Baspinar, O.; Bostan, O. M.; Akalin, F.; Kervanoglu, M.; Ayabakan, C.; Cil, E.; Alanay, Y.; Celiker, A.; Ozer, S. A.; Yakicier, M. C.