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    Evaluation of Superoxide Dismutase and Glutathione Peroxidase Enzyme Polymorphisms in Familial Mediterranean Fever Patients
    (Modestum Ltd, 2015) Akbas, Ali; Ozyurt, Huseyin; Sahin, Semsettin; Benli, Ismail; Saylan, Oguzhan; Aydogan, Leyla; Ekici, Fatih
    Familial Mediterranean Fever (FMF) is a fairly common inflammatory disease in communities with mediterranean origin. It is characterized with autosomal recessive, recurrent short-term episodes of fever, peritoneal, pleural, synovial membrane involvement and skin lesions. The aim of the present study was to investigate possible associations between FMF and Ala-9Val polymorphism of MnSOD and Pro198Leu polymorphism of GPx1. The study included 129 FMF patients who has mutations (E148Q, P369S, F479L, M680I(G/C), M680I(G/A), I692del, M694V, M694I, K695R, V726A, A744S, R761H) in the heterozygous or homozygous form and 95 healthy subjects. To identify MnSOD Ala-9Val and GPx1 Pro198Leu SNPs, genotyping was performed using PCR amplification, and polymorphisms were detected with hybridization probes labeled with fluorescent dyes. Genotype and allele frequencies of Ala-9Val polymorphism of MnSOD and Pro198Leu polymorphism of GPx1 were detected. The MnSOD Val allele frequency is 132 (51.16%) in the FMF and 115 (60.52%) in the control group (p<0.05). The GPx1 Leu allele is 83 (32.17%) in the FMF and 61 (32.11%) in the control group (p=0.988). No significant differences were found between genotype frequencies of GPx1 and MnSOD polymorphisms. According to our findings MnSOD Val allele may be a genetic factor involved in the pathogenesis of FMF. The fact that there are only few studies in literature, we need more patients, other enzyme levels and works about polymorphism to support our study.
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    The gene expression and protein profiles of ADAMTS and TIMP in human chondrosarcoma cell lines induced by insulin: The potential mechanisms for skeletal and articular abnormalities in diabetes
    (Modestum Ltd, 2020) Akyol, Sumeyya; Karagoz, Zehra; Inan, Nuran Dingil; Butun, Ilknur; Benli, Ismail; Demircan, Kadir; Yigitoglu, Muhammet Ramazan
    Background: The delay in wound healing, decrease in the long bones resilience to fracture, and delay in fracture healing are among common complications diabetes mellitus (DM) patients, and they still remain as challenging issues to be solved. The mechanism has not been fully understood yet, but high sugar and/or insulin deficiency or unresponsiveness to insulin in blood are potential causes to blame. Extracellular matrix degradation/remodeling is one of the important mechanisms whereby cell differentiation, bone remodeling and wound repair can be regulated. A disintegrin and metalloproteinase with a thrombospondin type 1 motif (ADAMTS) proteins play important roles in cartilage/bone metabolism. This study aimed to determine whether ADAMTS/Tissue inhibitors of metalloproteinases (TIMP) proteins were affected by insulin application in OUMS-27 (chondrosarcoma) cells. Material and Methods: OUMS-27 cells were induced by 10 mu g/mL insulin for 1, 3, 7, and 11 days. Cells were harvested, mRNA and protein extractions were performed. Total mRNA and cDNA levels were measured by qRT-PCR and protein levels were detected by WB. Results: ADAMTS1,5, and 7 levels were significantly decreased, while TIMP-3 levels were detected increased (mRNA/protein concentrations). Conclusion: Pathologies and disturbances of cartilage/bone metabolism, delayed fracture healing in particular, in patients with DM may result from insulin deficiency. ADAMTS genes that play a role in healing process are increased during insulin deficiency, which consequently interrupts healing process by causing cartilage extracellular matrix (ECM) degradation.