Effect Of G2706A and G1051A polymorphisms of the ABCA1 gene on the lipid, oxidative stress and homocystein levels in Turkish patients with polycystıc ovary syndrome

<p>Abstract</p> <p>Background</p> <p>Obesity, insulin resistance and hyperandrogenism, crucial parameters of Polycystic ovary syndrome (PCOS) play significant pathophysiological roles in lipidemic aberrations associated within the syndrome. Parts of the metabolic syndrome (low HDL and insulin resistance) appeared to facilitate the association between PCOS and coronary artery disease, independently of obesity. ABCA1 gene polymorphism may be altered this components in PCOS patients.</p> <p>In this study, we studied 98 PCOS patients and 93 healthy controls. All subjects underwent venous blood drawing for complete hormonal assays, lipid profile, glucose, insulin, malondialdehyde, nitric oxide, disulfide levels and ABCA genetic study.</p> <p>Results</p> <p>In PCOS group fasting glucose, DHEAS, 17-OHP, free testosterone, total-cholesterol, triglyceride, LDL-cholesterol and fibrinogen were significantly different compare to controls. The genotype ABCA G2706A distribution differed between the control group (GG 60.7%, GA 32.1%, AA 7.1%) and the PCOS patients (GG 8.7%, GA 8.7%, AA 76.8%). The frequency of the A allele (ABCAG2706A) was higher in PCOS patients than control group with 13,0% and 23,2%, respectively. In this study, the homocystein and insulin levels were significantly higher in PCOS patients with ABCA G1051A mutant genotype than those with heterozygote and wild genotypes.</p> <p>Conclusions</p> <p>We found higher percentage of AA genotype and A allele of ABCA G2706A in PCOS patients compare to controls. The fasting insulin and homocystein levels were significantly higher in PCOS patients with ABCA G1051A mutant genotype than those with heterozygote and wild genotypes.</p

Determining in vitro anticancer activity of mitomycin C loaded microemulsion

European Biotechnology Congress -- SEP 28-OCT 01, 2011 -- Istanbul, TURKEYWOS: 000295310800409European Biotechnol Themat Network Asso

Preparation and characterization of lipid nanoparticle/pDNA complexes for STAT3 downregulation and overcoming chemotherapy resistance in lung cancer cells

WOS: 000401112300012PubMed ID: 28428090Developments in the field of molecular oncology have revealed that resistance to chemotherapeutics is acqured through several mechanisms including overexpression of common oncogenic proteins. Signal Transducer and Activator of Transcription 3 (STAT3) is one of these oncogenes that is overexpressed in many cancer types. RNA interference (RNAi) is proven powerful tool for downregulating STAT3, allowing re-sensitization of resistant cancer cells. However, delivery of RNA interference-mediating molecules for STAT3 downregulation in lung cancer cells is limited to a small number of studies most of which employ commercially available transfection kits. The aim of this study was to develop and evaluate cationic solid lipid nanoparticles for delivery of RNAi-mediating plasmid DNA in order to down regulate STAT3 in cisplatin resistant lung cancer cells. We focused on obtaining cSLN:plasmid DNA complexes with size below or equal to 100 nm, and a positive zeta potential. Two successful candidate cSLN: plasmid DNA complexes (K2 and K3) were selected for in vitro tests and cell culture studies. These formulations have particle sizes of 98 and 93 nm, and zeta potential values of 10.5 and 8.9 mV, respectively. Plasmid DNA in these complexes was protected against DNaseI and serum-mediated degradation. Substantial part of DNA retained its supercoiled and circular conformation. TEM images showed nearly spherical complex structure. Both formulations reduced STAT3 expression by approx. 5-fold in cisplatin resistant Calu1 cell line and increased the sensitivity of cells to cisplatin. (C) 2017 Elsevier B.V. All rights reserved.Ege UniversityEge University [12-ECZ-006]This study was supported by the scientific fund of the Ege University (Project no. 12-ECZ-006). We thank to Dr. Tugba Erdogan from Transmission Electron Microscopy Facility of the Middle East Technical University for her help with TEM imaging experiments, and Assoc. Prof. Timur Kose from the Biostatistics Department, Ege University for providing consultancy with statistical analyses

Cytotoxicity of Dental Implants: The Effects of Ultrastructural Elements

WOS: 000417113300011PubMed ID: 29140372Purpose: In this in vitro study, the purpose was to assess the cytotoxicity profiles of seven commercial dental implant materials by using cell culture methods on an osteoblastic cell line. Materials and Methods: The microstructure of seven commercial dental implants (each given a letter code) was investigated via scanning electron microscopy and energy-dispersive x-ray analysis. Medium extracts were collected on the first and fifth days for each group and tested using MC3T3-E1 cell line. Cytotoxicity was evaluated with Xcelligance System and XTT reagent, and apoptosis was determined by Annexin-V staining. One-way analysis of variance (ANOVA) and Tukey's multiple range tests were used for statistical analyses. In all tests, P was set as .05. Results: ANOVA results disclosed that Ti (P = .001), Na (P = .001), Ca (P = .019), Al (P = .024), and P (P = .020) amounts were significantly different between test materials. Cytotoxicity and apoptosis analyses revealed that implant materials (C) and (E) were the materials with the lowest cell vitality and the highest apoptosis rates among the test materials. Phosphorus was the only element that presented the highest amount in C and E (14.23% and 12.29%, respectively) compared with the other implant materials tested. (F) and (G) had favorable results for all experiments. Conclusion: The results suggest that pure dental implant materials with a lower number of additional elements may possess fewer cytotoxic effects than the other implant materials tested in this study

Suppression of STAT3 by chemically modified siRNAs increases the chemotherapeutic sensitivity of parental and cisplatin-resistant non-small cell lung cancer cells

WOS: 000334153000021PubMed ID: 24659656Purpose: Increased activation of the JAK-STAT signaling pathway is frequently observed in several primary cancers as well as cancer cell lines. Thus, targeting JAK-STAT pathway components by different molecular-biologic approaches in the search for new anticancer therapies has become widespread and resulted in encouraging outcomes. In this study, the effects of chemically modified anti-STAT3 small interfering (si)RNAs on cell viability, proliferation and apoptosis of parental and cisplatin resistant non-small cell lung cancer (NSCLC) cells were investigated with the aim to provide a new therapeutic strategy for overcoming cisplatin resistance in lung cancer. Methods: The parental NSCLC cell line Calu1 and its cisplatin-resistant subline CR-Calu1 were used to study the effects of STAT3 suppression with chemically modified anti-STAT3 siRNAs. STAT3 gene and protein expressions were analyzed by real-time (RT) quantitative (q) PCR and Western blot, respectively. Apoptosis was evaluated by Caspase-3 activity and cell death assays. Results: STAT3 messenger (m)RNA and protein expression were significantly increased in CR-Calu1 cells and suppressing its expression with specific siRNAs increased the rate of apoptosis through Caspase-3 activation. STAT3 suppression also significantly increased cisplatin sensitivity of Calu1 and CR-Calu1 cells after transfection with STAT3 siRNAs. Conclusions: NSCLC cells could be sensitized to cisplatin by targeting STAT3 with chemically modified siRNAs together, a fact which was accompanied with increased apoptosis