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Öğe Diyarbakır ve Bingöl illerinin Dytiscidae (Coleoptera) faunasına ait bazı türlerin moleküler yapılarının araştırılması(2017) Üzen, Ramazan; Güven, Kemal; Aykut, MedeniBu çalışmada, Bingöl ve Diyarbakır illerinden Eylül 2016 ile Mayıs 2017 dönemlerinde toplanan Dytiscidae familyasının 9 cinsine ait 19 türün PCR yöntemiyle MtDNA örnekleri elde edilerek moleküler düzeyde araştırılmıştır. Bu türlerin mitokondriyal COI genlerinin mükleotit sekansları ve PCR genomik dizileri moleküler belirteç olarak kullanıldı. Mitokondriyal DNA dizi analizleri BLAST taraması yoluyla yapıldı. 19 türe ait mitokondriyal COI gen dizileri, türlerin tanımlamasında kullanılan MEGA 7.0 programı yardımı ile filogenetik soy ağacı oluşturularak benzerlikleri karşılaştırıldı. Türlerin yakınlık dereceleri, Neighbour Joining (NJ) ve Minimum Evolution (ME) soy ağaçları kullanılarak belirlenmeye çalışıldı. Analiz sonuçlarına göre; Agabus faldermanni Zaitzev (1927) sisteme kayıtlı nükleotid dizileriyle %100 örtüşürken, bu değer; Agabus biguttatus (Olivier, 1795), Agabus bipustulatus (Linnaeus, 1767), Agabus conspersus (Marsham, 1802), Agabus glacialis Hochhuth, 1846, Agabus nebulosus (Forster, 1771), Bidessus calabricus Guignot, 1957, Hydroglyphus geminus (Fabricius, 1792), Hydroporus planus (Fabricius, 1782), Hydroporus pubescens (Gyllenhal, 1808), Ilybius chalconatus (Panzer, 1796), Laccophilus minutus (Linnaeus, 1758), Laccophilus poecilus Klug, 1834 ve Nebrioporus stearinus suavis (Sharp, 1882) türlerinde %99; Hydroporus discretus Fairmaire and Brisout, 1859, Hydroporus tessellatus (Drapiez, 1819) ve Scarodytes halensis halensis (Fabricius, 1787) türlerinde %98; Hydroporus palustris (Linnaeus, 1761) ve Liopterus haemorrhoidalis (Fabricius, 1787) türlerinde %97 olarak belirlenmiştir. Anahtar Kelimeler: Bingöl, Diyarbakır, Dytiscidae, COI, Moleküler tanımlamaÖğe Investigation of the Asp299Gly and Thr399Ile polymorphisms of TLR4 gene in rheumatoid arthritis(Dicle Üniversitesi Tıp Fakültesi, 2019) Yıldırım, İbrahim Halil; Üzen, RamazanObjective: Rheumatoid arthritis (RA) is a chronic and inflammatory disease characterized by synovial inflammation that causes cartilage and bone destruction as well as systemic defects, including cardiovascular, pulmonary, psychological, and skeletal disorders. The etiology of RA is unclear. Evidence suggests that RA is influenced by both genetic and environmental factors and the inflammatory and autoimmune activities take important roles in the development of this disease. In the onset of RA, an interaction between the resident cells of synovium and cells of the innate and adaptive immune system reported. Fibroblast-like synoviocytes (FLS) are one of the resident cells and they play a central role, with a tumor-like behavior, in joint destruction and development of chronic inflammation. Toll-like receptors (TLRs) are transmembrane glycoproteins that are related to inflammation via synthesis of proinflammatory cytokines like TNF-α, IL-6, and IL-1β. Some studies report an association between the activation of FLS and the cytokine environment, cell-to-cell contacts, or the activation of TLR2, TLR4, and TLR3. TLRs and especially TLR4 is involved in the recognition of endogenous molecules released by injured tissues and necrotic cells. TLR4 gene involved in a wide variety of both infectious and non-infectious diseases and two polymorphisms of TLR4, Asp299Gly and Thr399Ile, changed the binding capacity and electrical charge of the protein. There are conflicting or even contradictory results about these polymorphisms and we aimed to determine the distribution of the allele frequencies of these polymorphisms and compare the result of RA patients with healthy subjects. Methods: DNA extraction was realized by salting out method from peripheral blood lymphocytes of RA patients and healthy controls. PCR amplification carried out with appropriate primer pairs against the related DNA sequences. Genotyping performed by the restriction fragment length polymorphism method. Results and Conclusion: According to the results obtained from RA patients and healthy controls, we have not found any statistical difference between both groups. Including the other polymorphisms of the TLR family into this type of studies, will give more information about the role of TLR family in rheumatoid arthritis.