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    Association between MMP-3 and MMP-9 polymorphisms and coronary artery disease
    (SPANDIDOS PUBL LTD, 2016) Beton, Osman; Arslan, Serdal; Acar, Burak; Ozbilum, Nil; Berkan, Ocal
    Matrix metalloproteinase (MMP)-3 and MMP-9 polymorphisms are characterized by plaque stability in coronary arteries. The aim of the current study was to investigate the 5A/6A polymorphism in the MMP-3 gene and C/T polymorphism in the MMP-9 gene in patients with coronary artery disease (CAD). The study population consisted of 400 patients who underwent coronary angiography. There were two groups consisting of 200 consecutive patients with CAD, presenting with stable angina pectoris, and 200 consecutive patients exhibiting normal coronary arteries. Two single nucleotide polymorphisms in the MMP gene, MMP-3 and MMP-9, were detected using a polymerase chain reaction-restriction fragment length polymorphism assay. Mean age, gender distribution, smoking status, presence of diabetes mellitus and hypercholesterolemia were identified to be similar between the groups. One hundred and twenty seven (63.5%) patients had hypertension in the CAD group, whereas only 55 (27.5%) patients had hypertension in the control group (P< 0.001). No significant difference in frequency of alleles and genotypes of MMP-9 C -> T between the CAD and control groups was identified. The 5A allele frequency of MMP-3 in the CAD group was significantly higher when compared with the control group (P< 0.001; odds ratio=2.18). The genotype frequency of MMP-3 5A/5A in the CAD group was significantly higher when compared with the controls (P=0.005). When compared with the homozygous wild-type (6A/6A) genotype of the MMP-3 gene, the cumulative frequency of heterozygote and homozygote genotypes of the MMP-3 gene was significantly higher in the CAD compared with the control group (P<0.001). Thus, the present study demonstrated that the 5A/5A and 6A/5A+5A/5A genotypes of the MMP-3 gene were associated with an increased risk of CAD.
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    Association between NF-kappa BI and NF-kappa BIA polymorphisms and coronary artery disease
    (SPANDIDOS PUBL LTD, 2015) Arslan, Serdal; Korkmaz, Ozge; Ozbilum, Nil; Berkan, Ocal
    Coronary artery disease (CAD) is the leading cause of fatalities worldwide. Nuclear factor (NF)-kappa B is a transcription factor that controls cell proliferation, differentiation and immunity. To the best of our knowledge, the present study is the first investigation of the association between CAD and NF-kappa B1 -94 W/D/NF-kappa BIA 3'-untranslated region (3'-UTR) A -> G polymorphisms. The study population comprised 226 CAD patients and 201 controls. There was no significant difference in NF-kappa B1A 3'-UTR A -> G in the allele and genotype frequencies between case and control populations. The D allele frequency of NF-kappa B1 -94 in the case group was significantly higher compared to the control group (P= 0.028, odds ratio= 1.37). The genotype frequency of NF-kappa B1 -94 DD in the case group was significantly higher compared to the controls (P= 0.028). Linkage analysis showed a close linkage among these 2 genes (P< 0.001 for case and control), and AD and GD haplotypes were associated with CAD (P< 0.001; P= 0.015, respectively). NF-kappa B1 -94 DD genotype can be a significant risk factor for the development of CAD.
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    Ateroskleroz hastalarının Koroner Arter plaklarında uzun kodlama yapmayan RNA’ ların (lncRNAs) ifade düzeylerinin araştırılması
    (2016) Arslan, Serdal; Berkan, Öcal; Korkmaz, Özge; Göksel, Sabahattin; Çetin, Nilgün
    Koroner arter hastalığı dünyadaki ölümlerin önde gelen sebebini oluşturan yaygın kompleks bir hastalıktır. Koroner arter hastalığının en yaygın sebebi koroner arterlerdeki aterosklerozdur. Ateroskleroz damar duvarının yaralanmasına cevap olarak gelişen kronik inflamatuar bir hastalık olarak kabul edilir. Ateroskleroz Türkiye? deki ölümlerin de %40? ını oluştururken, 65 yaş üstü Avrupalı erkeklerde birincil ölüm nedeni kadınlarda ise ikincil ölüm nedeni olmaktadır. Kodlama yapmayan RNA aracılı epigenetik düzenlemeler uzun kodlama yapmayan RNA?lar (Long noncodingRNA, lncRNA) ve kısa kodlama yapmayan RNA?lar tarafından gerçekleştirilir. lncRNA? ların gen düzenleme mekanizmaları hem gen ekspresyonunun aktivasyonu hem de inhibisyonu içermesi açısından daha kompleks bir yapıya sahiptir. Bu çalışmada dünyada ilk defa ateroskleroz hastalarının koroner arter plaklarında bazı uzun kodlama yapmayan RNA?ların ifade düzeyleri araştırılmıştır. Son yıllarda yapılan klinik çalışmalarda internal mamalial arter greftlerinin bugün için koroner arter bypass cerrahisinde ideal greftlere en yakın greft olduğu belirlenmiştir. Bu çalışmada koroner arter by-pass cerrahisi sırasında aterosklerotik koroner arter ve internal mamalial arterden alınan doku örnekleri kullanılmıştır. Total RNA doku örneklerinin homojenizasyonundan sonra izole edilmiştir. Doku örneklerinde beş adet uzun kodlama yapmayan RNA?ların ifade düzeyleri RT-PCR kullanılarak ölçülmüştür. Mevcut çalışmada kardiyak patolojiyle ilişkili olduğundan şüphelenilen beş adet uzun kodlama yapmayan RNA araştırılmıştır. Bu lncRNA? lar hipoksi indüklenebilen faktör 1A antisens RNA 2 (aHIF2), siklin bağımlı kinaz inhibitör 2B antisens RNA 1 (ANRIL), Potasyum voltaj-kapılı kanal, KQTbenzeri alt familyası,üye1 ters zincir/antisens transkript 1 (KCNQ1OT1), MI-İlişkili transkript (MIAT) ve Metastaz ilişkili akciğer adenokarsinom transkript 1 (MALAT1) dır. Bu çalışmada aterosklerotik koroner arter ve aterosklerotik olmayan internal mamalial arter arasındaki uzun kodlama yapmayan RNA?ların ifade düzeyleri arasındaki farklılık karşılaştırılmıştır. ANRIL, MIAT,MALAT1 in koroner arter plaklarındaki ifade dağılımları internal mamalial arterdekine göre istatistiksel olarak anlamlı bulunmuştur. KCNQ ve HIF ın ifade dağılımları istatistiksel olarak anlamlı olmamakla birlikte kontrol grubuna göre iki genin ifadeside artmıştır. ANRIL, MIAT,MALAT1 in koroner arter plak gelişimi açısından belirteç olma özelliğindedir.
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    Aterosklerozlu hastalarda koroner arter ve internal mamarian arterlerin yapısal ve patolojik açıdan karşılaştırılması
    (2017) Berkan, Öcal; Eğilmez, Hatice Reyhan; Arslan, Serdal; Korkmaz, Özge; Çetin, Nilgün
    Koroner arter hastalığı dünyadaki ölümlerin önde gelen sebebini oluşturan yaygın kompleks bir hastalıktır. Koroner arter hastalığının en yaygın sebebi koroner arterlerdeki aterosklerozdur. Ateroskleroz damar duvarının yaralanmasına cevap olarak gelişen kronik inflamatuar bir hastalık olarak kabul edilir. Ateroskleroz Türkiye’ deki ölümlerin de %40’ ını oluştururken, 65 yaş üstü Avrupalı erkeklerde birincil ölüm nedeni kadınlarda ise ikincil ölüm nedeni olmaktadır. Kodlama yapmayan RNA aracılı epigenetik düzenlemeler uzun kodlama yapmayan RNA’lar ve kısa kodlama yapmayan RNA’lar (mikroRNA) tarafından gerçekleştirilir. Mikro RNA’lar 19-25 nükleotid uzunluğunda, mRNA stabilitesinin ve translasyonunun düzenlenmesinde görev alan kodlama yapmayan RNA’lardır. Mikro RNA lar aterosklerozun patogenezinde anahtar rol oynamaktadır. Bu çalışmada dünyada ilk defa ateroskleroz hastalarının koroner arter plaklarında bazı uzun kodlama yapmayan RNA’ların ifade düzeyleri araştırılmıştır. Çalışmamızda koroner bay-pass sırasında alınan koroner arter ve internal mamalial arterlerde patolojik incelemeler yapılmıştır. Dokular homojenize edilmiş ve RNA izolasyonu gerçekleştirilmiştir. Mikroarray ile mikro RNA ekspresyon çalışması için 2500 mi RNA için geliştirilmiş probu bulunan mir Base Ver 21 kullanılmıştır. Mikroarray ekspresyon sonuçları beş adet miRNA için RT-PCR ile doğrulanmıştır. MiRNA ekspresyon sonuçları Genespring (Ver 3.0) kullanarak analiz edilmiştir. Analiz sonucunda yalnız koroner arter plaklarına ifade olan 49 adet mi RNA bulunmuştur. Koroner arter ve internal mamalial arterlerde ifade olan mi RNA ların karşilaştırılması sonucu 32 adet miRNA istatistiksel olarak anlamlı ifade olduğu tespit edilmiştir (p?0.05). Bu 32 miRNA nın 15 adedi yukarı düzenlenmiş, 17 adedi ise aşağı düzenlenmiştir. Biyoinformatik analizlerle istatistiksel olarak önemli ifade olan miRNA ların hedef genleri bulunmuştur. Bu çalışma verileri, koroner arterlerdeki aterosklerotik sürecin, patolojik temelinde rol oynayan epigenetik mekanizmaların açıklanmasına katkı sağlayacaktır. Ayrıca, ilerde mikro RNA’lar kullanılarak geliştirilecek olan, aterosklerotik plak gelişimini önlemeye yönelik ilaçların geliştirilmesi sürecinde önemli bir veri kaynağı olacaktır.
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    Catalyzing Transcriptomics Research in Cardiovascular Disease: The CardioRNA COST Action CA17129
    (MDPI, 2019) Gomes, Clarissa Pedrosa da Costa; Agg, Bence; Andova, Andrejaana; Arslan, Serdal; Baker, Andrew; Bartekova, Monika; Beis, Dimitris; Betsou, Fay; Wettinger, Stephanie Bezzina; Bugarski, Branko; Condorelli, Gianluigi; da Silva, Gustavo Jose Justo; Danilin, Sabrina; de Gonzalo-Calvo, David; Buil, Alfonso; Carmo-Fonseca, Maria; Enguita, Francisco J.; Felekkis, Kyriacos; Ferdinandy, Peter; Gyoengyoesi, Mariann; Hackl, Matthias; Karaduzovic-Hadziabdic, Kanita; Hellemans, Jan; Heymans, Stephane; Hlavackova, Marketa; Hoydal, Morten Andre; Jankovic, Aleksandra; Jusic, Amela; Kardassis, Dimitris; Kerkela, Risto; Kuster, Gabriela M.; Lakkisto, Paivi; Leszek, Przemyslaw; Lustrek, Mitja; Maegdefessel, Lars; Martelli, Fabio; Novella, Susana; O'Brien, Timothy; Papaneophytou, Christos; Pedrazzini, Thierry; Pinet, Florence; Popescu, Octavian; Potocnjak, Ines; Robinson, Emma; Sasson, Shlomo; Scholz, Markus; Simionescu, Maya; Stoll, Monika; Varga, Zoltan V.; Vinciguerra, Manlio; Xuereb, Angela; Yilmaz, Mehmet Birhan; Emanueli, Costanza; Devaux, Yvan
    Cardiovascular disease (CVD) remains the leading cause of death worldwide and, despite continuous advances, better diagnostic and prognostic tools, as well as therapy, are needed. The human transcriptome, which is the set of all RNA produced in a cell, is much more complex than previously thought and the lack of dialogue between researchers and industrials and consensus on guidelines to generate data make it harder to compare and reproduce results. This European Cooperation in Science and Technology (COST) Action aims to accelerate the understanding of transcriptomics in CVD and further the translation of experimental data into usable applications to improve personalized medicine in this field by creating an interdisciplinary network. It aims to provide opportunities for collaboration between stakeholders from complementary backgrounds, allowing the functions of different RNAs and their interactions to be more rapidly deciphered in the cardiovascular context for translation into the clinic, thus fostering personalized medicine and meeting a current public health challenge. Thus, this Action will advance studies on cardiovascular transcriptomics, generate innovative projects, and consolidate the leadership of European research groups in the field. COST (European Cooperation in Science and Technology) is a funding organization for research and innovation networks (www.cost.eu).
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    Determination of chemical profile, antioxidant, DNA damage protection and antiamoebic activities of Teucrium polium and Stachys iberica
    (ELSEVIER SCIENCE BV, 2011) Tepe, Bektas; Degerli, Serpil; Arslan, Serdal; Malatyali, Erdogan; Sarikurkcu, Cengiz
    This work deals with the evaluation of in vitro antioxidant, DNA preventing and antiamoebic activities of the water extracts of Teucrium polium and Stachys iberica. In all systems, T. polium extract exhibited excellent activity potential than that of S. iberica. The amount of total phenolics and flavonoids were high in this extract. In the presence of 40 mg/ml T. polium extract, a significant protection was observed for native super coiled DNA of pBR322 plasmid DNA. In the presence of 32 mg/ml of T polium extract, no trophozoite was after the 24th hour. (C) 2010 Elsevier B.V. All rights reserved.
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    Effect of TLR10 (2322A/G, 720A/C, and 992T/A) polymorphisms on the pathogenesis of Crimean Congo hemorrhagic fever disease
    (WILEY, 2018) Kizildag, Sibel; Arslan, Serdal; Ozbilum, Nil; Engin, Aynur; Bakir, Mehmet
    Crimean Congo hemorrhagic fever (CCHF) is a tick-borne disease caused by the Crimean Congo hemorrhagic fever virus (CCHFV). Toll-like receptors (TLRs) are type 1 transmembrane proteins of immune cells that play a critical role in innate and adaptive immunity. The present study first time aims to investigate the relation between TLR10 gene polymorphisms (720A/C, 992T/A, and 2322A/G), severity/non-severity, fatality/non-fatality, and CCFH disease by using PCR-RFLP assay in a Turkish population. TLR10 720A/C polymorphism was determined to be statistically significant both genotype and allele frequency (P=0,011, P=0.015, respectively). TLR10 992T/A polymorphism was found statistically significant relationships between patient and control (P=0.026) and individual with AA genotype have approximately three times greater risk than TT genotype (OR=2.93). There was not a significant difference in 2322A/G genotype distribution (P=0.152). There were also statistically significant associations between both TLR10 992T/A and 2322A/G polymorphism and patient mortality (P=0.001 and P=0.008, respectively). We have not found statistically any linkage among TLR10 haplotype, but individual AAA and GAT haplotype have higher risk than individual AAT haplotype (OR=3.22, OR=1.93, respectively). Consequently, this study shows that pathogenesis of CCHF disease is associated with the TLR10 720A/C and 992T/A polymorphisms. There is a statistically significant association in fatal/non-fatal patients with TLR10 720A/C and 992T/A. The TLR10 992AA genotype might increase and TLR10 720CC genotype might decrease susceptibility to pathogenesis of CCHF disease. TLR 10 polymorphisms may be also an important biomarker for CCHF susceptibility and fatality rate.
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    Effects of MPO-463G/A and -129G/A polymorphisms on coronary artery disease risk and patient survival in a Turkish population
    (SPANDIDOS PUBL LTD, 2017) Arslan, Serdal; Berkan, Ocal; Bayyurt, Burcu; Beton, Osman; Sahin, Nil Ozbilum; Aydemir, Eylem Itir
    Myeloperoxidase (MPO) is an oxidative hemoprotein compound expressed in polymorphonuclear leukocytes that contributes to inflammatory responses. Coronary artery disease (CAD), as the most prevalent form of heart disease, is considered to originate from an interaction between genetic and environmental factors. In the present study, the potential associations between MPO-463G/A and -129G/A polymorphisms with CAD were investigated in a Turkish population using a polymerase chain reaction-based restriction fragment length polymorphism (RFLP) assay technique. To the best of our knowledge, the study was the first to examine the association of MPO-463G/A and -129G/A with patient survival rate in a Turkish population. The study population consisted of 201 patients with CAD and 201 healthy controls. The results indicated that there was a significant association of the GA genotype of MPO-463G/A with the case population (P=0.048). Meanwhile, in the patients with CAD, the frequency distributions of the MPO-129A allele (P=0.006) and GA genotype (P=0.001) were significantly increased compared with the G allele and GG genotype, respectively, in CAD patients. Additionally, compared with the GG genotype, the frequency distribution of MPO-129A was significantly increased in the patient group regarding smoking status (P=0.001) and the presence of hypercholester-olemia (P=0.028). However, survival analysis did not detect an effect of either polymorphism on the survival rate of the CAD patients (P>0.05). Therefore, the MPO-129GA genotype may be a significant risk factor for the development of CAD.
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    Examination of IL-6 -174 gene polymorphism in patients diagnosed with primary knee osteoarthritis: A case-control study
    (2022) Keskinbıçkı, Mehmet Vakıf; Öztemur, Zekeriya; Öztürk, Hayati; Kılınç, Seyran; Bulut, Okay; Arslan, Serdal; Pazarcı, Özhan
    Degenerative osteoarthritis (OA) is the most common joint disease. However, its etiology has not been clearly understood. We aimed to investigate the association between the IL-6-174G/C gene variant responsible for regulating IL-6 functions and primary knee osteoarthritis (PKOA). Patients older than 40 years who presented between February 2012 and April 2013 and were diagnosed with PKOA and had grade 3 (i.e., moderate) or 4 (i.e., severe) disease constituted the case group. Healthy volunteers formed the control group. Genomic DNA was extracted from blood leukocytes in both case and control groups, and the IL6-174 G/C genotypes were determined. Two groups were compared regarding demographic, clinical, radiological findings, and IL-6-174 genotyping results. Both case and control groups included 90 patients each. No statistically significant difference was found between the two groups regarding gender distribution, patient age, and body weight. The frequency of the mutant base pairs GC and CC in the IL-6-174 promoter region were significantly higher in controls than in cases. Women with genotypes including C alleles were genetically protect ed against the clinical disease. Similar findings were not detected in the male patient group. The IL6-174 G/C gene polymorphism does not increase the risk of PKOA. However, the mutant C allele can be protective against PKOA in female patients. Studies conducted on larger patient populations from different ethnic backgrounds are needed to confirm our findings since our sample size is relatively small.
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    FOXP3 rs3761548 polymorphism is associated with knee osteoarthritis in a Turkish population
    (WILEY, 2018) Cekin, Nilgun; Pinarbasi, Ergun; Bildirici, Aslihan Esra; Donmez, Gonca; Oztemur, Zekeriya; Bulut, Okay; Arslan, Serdal
    Aim: Functional polymorphisms located in FOXP3 intron 1 was recently found to be associated with rheumatoid arthritis (RA). Although RA is an autoimmune disease, there is supporting evidence that activated maladaptive responses including pro-inflammatory pathways play roles in osteoarthritis (OA), similar to RA. The aim of this study was to explore the relationship between rs2232365 (-924A/G) and rs3761548 (-3279A/C) polymorphisms as well as possible changes in the 600 bp promoter region of FOXP3 and knee OA. Methods: Patients with primary knee OA (n = 300) and healthy individuals (n = 300) were examined for rs3761548 and rs2232365 FOXP3 gene polymorphisms by the polymerase chain reaction-restriction fragment-length polymorphism method. The 600 bp promoter region (between -500 and +100) of the gene was also sequenced with direct sequencing in 50 knee OA patients and 50 healthy individuals. Results: There were no sequence variants in the promoter region tested both in OA patients and healthy controls. The SNP rs2232365 showed no association with OA susceptibility and severity and the results of other genetic models were also nonsignificant. On the other hand, rs3761548 AC (P = 0.003), AA + CC (P = 0.0014) as well as AC + AA (P = 0.40) genotypes showed association with Grade 4 knee OA patients. Conclusion: Our findings indicated that the association between FOXP3 rs2232365 polymorphism and knee OA tended to yield negative results but the FOXP3 rs3761548 C allele was associated with elevated risk of OA in Grade 4 knee OA patients in a Turkish population.
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    Genetic Polymorphisms of Sulfotransferases (SULT1A1 and SULT1A2) in a Turkish Population
    (SPRINGER/PLENUM PUBLISHERS, 2010) Arslan, Serdal
    Sulfotransferases (SULTs) play a significant role in the biotransformation of a variety of xenobiotics and endogenous compounds. SULTs are genetically polymorphic enzymes; to date, 12 human cytosolic SULT isoforms have been identified. This study investigated SULT1A1 and SULT1A2 gene polymorphism using a PCR-RFLP method (n = 303). The frequency of the SULT1A1*1 allele was 76.2% and SULT1A1*2 was 23.8%. The SULT1A1*3 allele could not be identified. The SULT1A2 frequencies were 69.2% (SULT1A2*1), 18.3% (SULT1A2*2), and 12.5% (SULT1A2*3). The SULT1A1 and SULT1A2 loci were in Hardy-Weinberg equilibrium (SULT1A1 chi(2) = 0.58, P = 0.44; SULT1A2 chi(2) = 7.28, P = 0.06). Linkage analysis indicated a close linkage between these two genes (chi(2) = 5.31, P < 0.01); therefore, the statistical hypothesis that SULT1A1 and SULT1A2 alleles are independently distributed was rejected. Additionally, a strongly positive linkage was detected between SULT1A1*2 and SULT1A2*2 alleles in this population (D' = 0.79, chi(2) = 33.33).
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    Genetic Structure of Brown Trout (Salmo trutta) Populations from Turkey Based on Microsatellite Data
    (SPRINGER/PLENUM PUBLISHERS, 2010) Arslan, Serdal; Bardakci, Fevzi
    This present study investigated micro- and macro-geographic microsatellite DNA variations using five polymorphic microsatellite loci from 27 brown trout populations in Turkey. Average number of alleles and average observed heterozygosity were 7.4 and 0.254, respectively. Even populations from the same sea basin and river system (the so called micro-geographic regions) had unique alleles. Genetic variation among the populations from macro-geographic regions (different sea basins and river systems) was 45.78%. The mtDNA lineages of brown trout that have previously been identified by mtDNA analyses were supported by the analysis of the microsatellite DNA data in general. The Catak population, which belongs to the Tigris lineage, was clustered together with the Euphrates populations within the Adriatic mtDNA lineage, based on microsatellite data. Both mitochondrial and microsatellite DNA analyses have made it possible to determine a secondary contact between Adriatic and Tigris lineages.
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    Highly Up-Regulation of Fas Ligand Gene Expression after Increasing in Oxidized Low-Density Lipoprotein
    (2025) Bayyurt, Burcu; Arslan, Serdal
    Oxidized low-density lipoprotein (ox-LDL) shows many harmful effects such as induction of apoptosis on function of endothelial cell (EC). Fas ligand (FASL) induces apoptosis in divergent pathological conditions. EC apoptosis which induced by ox-LDL is related with FASL. In this study, we aimed to determine how different ox-LDL levels affect FASL expression in ECs. We treated human umbilical vein endothelial cells (HUVECs) with two different concentration of ox-LDL. FASL gene expression in groups was detected by quantitative polymerase chain reaction (qPCR). We compared FASL gene expression level between the groups according to ∆∆Ct method. FASL gene expression was statistic significantly up-regulated in the group treated higher amounts of ox-LDL (P<0.001). We found that treatment with higher amounts of ox-LDL in HUVECs increased FASL gene expression dramatically. According to our findings, we concluded that increasing the amount of ox-LDL may be critical in inducing the FASL-dependent apoptotic pathway in ECs.
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    HULC and 7SL RNA expression levels in patients with Crimean-Congo hemorrhagic fever
    (WILEY, 2018) Bayyurt, Burcu; Arslan, Serdal; Engin, Aynur; Bakir, Mehmet
    Crimean-Congo hemorrhagic fever (CCHF) is a tick-borne disease caused by the Crimean-Congo hemorrhagic fever virus. Long non-coding RNAs (lncRNAs) are generally classified as transcripts longer than 200 nucleotides (nt). The various lncRNAs expressed in infected cells are responsible for regulating the expression of viral and host genes. This is the first study to investigate hepatocellular carcinoma upregulated long non-coding RNA (HULC) and 7SL RNA expression levels in patients with CCHF. Blood samples were taken from 100 individuals (60 patients and 40 controls), and total RNA isolation was performed. Quantitative polymerase chain reaction (qPCR) was performed using the SYBR Green method to determine HULC and 7SL RNA expression levels in the study population. Compared the patient and control groups, HULC was upregulated statistically significantly (P=0.04) and 7SL RNA was downregulated (P=0.93) in patients. Also, there was a statistically significant difference between fatal cases and surviving patients for HULC and 7SL RNA (P<0.01 and P=0.03, respectively). In addition, HULC expression was increased statistically significantly in fatal cases compared with surviving patients in terms of clinical parameters such as aspartate aminotransferase (P<0.01), alanine aminotransferase (P<0.01), international normalized ratio (P=0.05), prothrombin time (P=0.01), active partial thromboplastin time (P<0.01), and lactate dehydrogenase (P<0.01). These findings highlighted that HULC and 7SL RNA could be important mediators for studying the pathogenesis of CCHF and significant therapeutic targets of the disease.
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    Identification of potential microRNA markers related to Crimean-Congo hemorrhagic fever disease
    (Wiley, 2019) Arslan, Serdal; Engin, Aynur; Aydemir, Eylem Itir; Sahin, Nil Ozbilum; Bayyurt, Burcu; Sari, Ismail; Cosgun, Yasemin
    Crimean-Congo hemorrhagic fever (CCHF) is a tick-borne disease caused by the arbovirus Crimean-Congo hemorrhagic fever virus (CCHFV). The CCHFV has a single-stranded RNA genome of negative sense. MicroRNAs (miRNAs) are key players in virus-host interactions and viral pathogenesis. We investigated the miRNA gene expression profiles in patients with CCHF using microarray for the first time in the world. Microarray analysis was performed using mirBase Ver 21 (Agilent Technologies, Santa Clara, CA). All statistical analyses were performed across the case-control, fatal-control, and fatal-nonfatal case groups using Genespring (Ver 3.0). Fifteen miRNAs were statistical significant in patients with CCHF compared with the controls (5 were upregulated, 10 were downregulated). Seventy-five and sixty-six miRNAs are in fatal compared with control and nonfatal case, respectively (fold change ([FC] >= 50) were statistically significant. In this study, the target genes of important miRNAs were identified and Gene Ontology analyses were performed across all groups. As a result of this study, we propose that the detection of miRNAs in patients with CCHF will allow the determination of therapeutic targets in diseases. CCHF is an important public health problem that can often be fatal. In this study, we investigated miRNA expression in case-control, fatal-control, and fatal-nonfatal case groups. Significant miRNAs associated with fatality were detected in CCHF. This study will serve as a source of data for the development of an antagomir-based therapy against CCHF using miRNAs in the future.
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    Investigation of hsa-miR-1908 and hsa-miR-144 Expression Levels in Crimean-Congo Hemorrhagic Fever Patients
    (Ankara Microbiology Soc, 2024) Aldemir, Ozlem; Engin, Aynur; Bayyurt, Burcu; Arslan, Serdal
    Crimean-Congo hemorrhagic fever (CCHF) is a tick-borne zoonotic viral disease. MicroRNAs (miRNAs), which play an important role in the regulation of gene expression, are involved in many processes essential for cell life such as development, differentiation, survival, apoptosis and aging. If miRNAs fail to fulfill their functions, they cause susceptibility to many diseases, including viral infections or cause the disease to be experienced in different clinical situations, such as severe or mild. In this study, we aimed to determine the expression levels of hsa-miR-144 and hsa-miR-1908 in CCHF patients and to compare the results in different clinical courses of CCHF disease. In this study, expression levels of hsa-miR-144 and hsa-miR-1908 were detected by quantitative reverse transcription polymerase chain reaction (RT-qPCR) in blood samples obtained from 60 CCHF patients and 40 healthy individuals. We also investigated the differences in the expression levels of the microRNAs between patients with severe and non-severe disease or between patients who died and survived. Quantitative polymerase chain reaction data were uploaded to the Data Analysis Center (Qiagen, Germany) and analyzed using the Delta Delta Cq (Delta Delta Ct) method. p value was calculated according to Student's t test for genes in the study groups. The expression level of hsa-miR-144 decreased (fold change= 0.09) and the expression level of hsa-miR-1908 increased 1.44-fold in CCHF patients compared to the control group. The expression of hsa-miR-144 and hsa-miR-1908 increased 2 and 2.36-fold, respectively, in severe patients compared to non-severe patients. The expression levels of hsa-miR-144 and hsa-miR-1908 were 16.3- and 14.3-fold higher, respectively, in fatal cases compared to surviving patients and these results were statistically significant. In addition, the expression level of hsa-miR-144 was significantly decreased in patients with low leukocyte counts and the expression level of hsa-miR-1908 was significantly increased in patients with prolonged prothrombin time (PT). This is the first study in the literature investigating the expression level of hsa-miR-1908 in CCHF patients. In conclusion, the data of this study suggest that hsa-miR-144 and hsa-miR-1908 may be important biomarkers in predicting the prognosis and clinical course of CCHF disease.
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    Investigation of NEAT1, IFNG-AS1, and NRIR expression in Crimean-Congo hemorrhagic fever
    (Wiley, 2021) Bayyurt, Burcu; Bakir, Mehmet; Engin, Aynur; Oksuz, Caner; Arslan, Serdal
    Crimean-Congo hemorrhagic fever (CCHF), whose causative agent is CCHF orthonairovirus (CCHFV), demonstrates different symptoms in patients. Long noncoding RNAs (lncRNAs) take part in various pathological processes of viral diseases. They are prominent regulators of antiviral immune responses. To our knowledge, this study is the first study to investigate nuclear paraspeckle assembly transcript 1 (NEAT1), interferon (IFN) gamma antisense RNA 1 (IFNG-AS1), and negative regulator of IFN response (NRIR) expression in CCHF in the literature. We selected these lncRNAs because they are related to IFN signal or IFN-stimulated genes. We investigated NEAT1, IFNG-AS1, and NRIR gene expression in patients with CCHF. Total RNA was extracted from blood samples of 100 volunteers and NEAT1, IFNG-AS1, and NRIR expression were measured using a quantitative real-time polymerase chain reaction. NRIR expression was statistically significant in cases versus controls (p < .001), fatals versus controls (p < .001), and fatals versus nonfatals (p = .01). Furthermore, NRIR was found statistically significant at some clinical parameters including alanine aminotransferase (p = .03), international normalized ratio (p = .03), prothrombin time (p = .02), and active partial thromboplastin time (p = .01) in CCHF cases. NEAT1 and IFNG-AS1 expression were downregulated in the case and fatal groups which were compared with controls. Our results demonstrate that NRIR may be important in CCHF pathogenesis and the target of CCHF treatment.
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    Investigation of RN7SL1 Expression in Human Umbilical Vein Endothelial Cells After Oxidized Low-Density Lipoprotein Stimulation: Experimental Study
    (Turkiye Klinikleri, 2025) Bayyurt, Burcu; Arslan, Serdal
    Objective: Oxidized low-density lipoprotein (ox-LDL) dam-ages endothelial cells (ECs) and induces pathogenic processes related to atherosclerosis (AS). Long non-coding RNAs (lncRNAs) have been accepted to be transcripts code no proteins and have important roles in gene expression regulation. LncRNAs have been thought important targets in the fight against cardiovascular diseases (CVDs). RNA component of signal recognition particle (SRP) 7SL1 (RN7SL1) is a lncRNA. RN7SL1 was associated with inhibition of cell cycle arrest. Since RN7SL1 is associated with cell cycle arrest and ox-LDL affects EC cell apoptosis, hypothesis of our study is that ox-LDL may alter the expression of this lncRNA in ECs. There was no study yet on RN7SL1 and CVDs including AS. We aimed to compare RN7SL1 gene expression between ECs treated with ox-LDL and normal ECs. Material and Methods: We investigated expression level of lncRNA RN7SL1 in human umbilical vein endothelial cells (HUVECs) induced with ox-LDL in this study. We performed measurement with SYBR green dye using quantitative PCR (real-time PCR, qPCR) method. Results: We found that expression of RN7SL1 was up-regulated 6.06 fold statistic significantly in HUVECs after ox-LDL treatment (P<0.001**). RN7SL1 up-regulation may modulate EC cycle and apoptosis in AS, since ox-LDL stimulation increased expression of RN7SL1 gene in HUVECs. Conclusion: According to findings of the current study, our interest focused on that RN7SL1 may associated with vascular damage of the ECs at initation of the AS. Our results further will guide future studies related to the RN7SL1 and CVDs including AS. © 2025 by Türkiye Klinikleri.
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    An investigation of the relationship between SULT1A1 Arg(213)His polymorphism and lung cancer susceptibility in a Turkish population
    (WILEY-BLACKWELL, 2009) Arslan, Serdal; Silig, Yavuz; Pinarbasi, Hatice
    Human sulfotransferase 1A1 (SULT1A1), the most expressed isoform of the phenol SULT1 subfamily, is an important member of sulfotransferase superfamily. A transition, G to A at position 638, in SULT1A1 gene, results in Arg(213)His change. This single nucleotide polymorphism reduces the activity and thermostability of SULT1A1 enzyme. Thus, in the present study the relationship between SULT1A1 Arg(213)His polymorphism and lung cancer was investigated. One hundred and six case and 271 control samples were studied using PCR-RFLP. There was no significant difference in genotype and allele distribution between lung cancer and control populations (p=0.07; p=0.06, respectively). Compared with the SULT1A1*1/SULT1A1*1 genotype the variant SULT1A1 genotype (SULT1A1*1/SULT1A1*2 or SULT1A1*2/SULT1A1*2) was associated with a significantly increased lung cancer risk in cases (p=0.027). In male populations, there was no significant difference between case and controls (p=0.313). In female populations, however, this difference was found to be significant (p=0.04). In smoker and non-smoker populations, no significant relationship was evident between lung cancer and control population (p=0.170, p=0.065, respectively). Statistical analyses of histological types of lung cancer in comparison with the control individuals indicated a significant difference between SULT1A1 Arg(213)His polymorphism and SCC (p=0.027) and other types of cancer, (p = 0.037), except SMCC (p = 0.854). Copyright (C) 2009 John Wiley & Solis. Ltd.
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    Is There Any Relationship Between Toll-Like Receptor 3 c.1377C/T and-7C/A Polymorphisms and Susceptibility to Crimean Congo Hemorrhagic Fever?
    (WILEY-BLACKWELL, 2016) Engin, Aynur; Arslan, Serdal; Ozbilum, Nil; Bakir, Mehmet
    Crimean-Congo hemorrhagic fever (CCHF) is an infectious disease that is caused by CCHF virus. A family of transmembrane receptors called as Toll-like receptors (TLRs) selectively acts in recognizing a wide range of microbial components and endogenous molecules released by damaged tissue and have been preserved throughout evolution. TLRs initiate some signaling cascades which activate the innate immune system. Mainly four TLRs act in protection against viral infections; TLR3 is one of them. TLR3 identifies dsRNA. By producing inflammatory cytokines and type I interferons, it generates an antiviral immune response. Proper response to TLR ligands may be impaired by single nucleotide polymorphisms (SNPs) within TLR genes in some indviduals, and this can cause varied susceptibility to infections. In the present work, polymerase chain reaction-based restriction fragment length polymorphism is used to analyze the frequencies of TLR3 (c. 1377C/T and -7C/A) polymorphisms in 149 CCHF patients and 171 healthy adults as controls, in Cumhuriyet University, Sivas/Turkey. We also investigated the relation between these polymorphisms and severity or mortality of CCHF disease. This is the first study investigating the TLR3 SNPs in patients with CCHF. In the present study, the frequency of the TLR3 (c. 1377C/T and -7A/C) genotypes in fatal and non-fatal cases were comparable, however, the homozygous mutant (TT) genotype frequency of TLR3 c. 1377C/T in CCHF patients was significantly higher than that of the healthy controls. In conclusion, presence of TLR3 c. 1377 TT genotype may have a role in the susceptibility to CCHF. (C) 2016 Wiley Periodicals, Inc.