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Öğe Bilateral Papillophlebitis in a Patient with Mutation of Metilenetetrahydrofolate Reductase Enzyme(TURKISH OPHTHALMOLOGICAL SOC, 2016) Guzel, Huseyin; Ozturk, Banu Turgut; Gedik, Sansal; Bakbak, Berker; Beyoglu, Abdullah; Kocak, NadirPapillophlebitis is known as central retinal vein occlusion seen in young patients. It usually presents as unilateral optic disc edema with cotton wool spots and hemorrhage in the peripapillary region. As it may be due to many autoimmune and inflammatory causes, a thorough systemic evaluation of the patient is warranted. In this case report we describe a bilateral, simultaneous papillophlebitis case thought to be related to hyperhomocysteinemia secondary to C677T polymorphism of methylenetetrahyrofolate reductase enzyme.Öğe Desmoplastic non-infantile astrocytic tumor with BRAF V600E mutation(SPRINGER JAPAN KK, 2014) Karabagli, Pinar; Karabagli, Hakan; Kose, Dogan; Kocak, Nadir; Etus, Volkan; Koksal, Yavuz[Abstract not Available]Öğe First molecular evidence of ocular transmission of Encephalitozoonosis during the intrauterine period in rabbits(ELSEVIER IRELAND LTD, 2019) Ozkan, Ozcan; Karagoz, Alper; Kocak, NadirMany reports have been published on the suspected vertical transmission of Encephalitozoon cuniculi; however, prior to 2003, these reports were based on circumstantial evidence, such as histopathological, immunohistochemical, or serological diagnosis of the infection. In 2003, vertical transmission of the parasite was confirmed by detection of E. cuniculi DNA in fetuses with the nested polymerase chain reaction (PCR) technique. However, the passage of the parasite to eyes of fetus during the intrauterine stage still requires verification. In the current study, natively infected with parasite spores female rabbits were mated with non-infected males. All resulting offspring that died before ten postpartum days were investigated using molecular techniques to confirm the intrauterine transmission of the parasite to the offspring' eyes. In total, 119 DNA samples from rabbit offspring tissues were collected from blood, kidney, brain, eye (both eyes were used as single samples), lung, placenta, liver and heart were used for PCR. Parasitic DNA in the eyes of offspring was detected (54%) 6 of 11 naturally seropositive mother rabbits. PCR results were found to be positive for the eyes of 63% (19/30) of the offsprings from seropositive rabbits. Therefore, mother rabbits naturally infected with E. cuniculi showed the molecular presence of the parasite in their offspring' eyes. Sequence analysis confirmed the partial DNA sequence data of E. cuniculi and blast analysis identified the agent as genotype I. These results confirm transmission of E. cuniculi to rabbit offspring' eyes in the intrauterine period. This is the first molecular evidence to show ocular transmission of the infection via an intrauterine route in rabbits.Öğe Investigation of autophagic effects of melatonin on breast cancer stem cells(ALLIED ACAD, 2017) Donmez, Huseyin; Kocak, Nadir; Yildirim, Ibrahim HalilAutophagy plays important roles in physiologic cellular events and also in cancers. It has been reported that cells escaped from death via autophagy and if autophagy inhibited, cells conducted to apoptosis. In some studies, protective effects of the melatonin on induced autophagy in cancer cells reported. In this study, we aimed to evaluate the autophagic effect of melatonin in cancer stem cells. For this purpose, CD44+/CD24-phenotype cells sorted from melatonin-treated and untreated MCF-7 and HEK293 cells. Effect of melatonin on autophagy was analysed by immunofluorescence and western blot analysis. Results showed that melatonin-induced LC3 (Microtubule-associated protein 1A/1B-light chain 3) aggregation and formation of autophagic vacuoles in MCF-7 derived cancer stem cells and also induced LC3-I to LC3-II conversion in these stem cells when compared to untreated control group. In conclusion, melatonin showed a pro-autophagic effect in CD44+/CD24-stem cells derived from MCF-7 cells and anti-autophagic effect in CD44+/CD24-stem cells obtained from HEK293 cells.Öğe Is obesity genetic disease?(2017) Duran, Tugce; Zainalbden, Hasanain Akram; Kocak, NadirObesity is a complex disease that has unfavorable impacts for all ethnic populations in worldwide. Genetics, environment and lifestyle are among aetiological factors of this disease. Genetic contribution associated with this disease is generally classified into 2 types: monogenic syndromes that display severe obesity, and the polygenic model of common obesity. Single-gene mutations can cause severe obesity resulting from alteration in central and peripheral appetite control mechanisms. Candidate gene and genome-wide association studies have led to the identification of nine loci associated with Mendelian forms of obesity and 58 loci contributing to polygenic obesity. These loci explain a small fraction of the heritability for obesity and many genes remain to be identified. The interaction of several polymorphisms and epigenetic modifications open a new research field for common obesity. As a result, still remains to be a mystery.Öğe Is obesity genetic disease? -- 2(2017) Duran, Tugce; Zainalbden, Hasanain Akram; Kocak, NadirObesity is a complex disease that has unfavorable impacts for all ethnic populations in worldwide. Genetics, environment and lifestyle are among aetiological factors of this disease. Genetic contribution associated with this disease is generally classified into 2 types: monogenic syndromes that display severe obesity, and the polygenic model of common obesity. Single-gene mutations can cause severe obesity resulting from alteration in central and peripheral appetite control mechanisms. Candidate gene and genome-wide association studies have led to the identification of nine loci associated with Mendelian forms of obesity and 58 loci contributing to polygenic obesity. These loci explain a small fraction of the heritability for obesity and many genes remain to be identified. The interaction of several polymorphisms and epigenetic modifications open a new research field for common obesity. As a result, still remains to be a mystery.Öğe Methylenetetrahydrofolate Reductase Gene Polymorphisms in Children with Attention Deficit Hyperactivity Disorder(IVYSPRING INT PUBL, 2011) Gokcen, Cem; Kocak, Nadir; Pekgor, AhmetObjective: The purpose of this study was to evaluate the relationship between 5,10-methylenetetrahydrofolate reductase (MTHFR) polymorphisms and Attention Deficit Hyperactivity Disorder (ADHD) in a sample of Turkish children. Study Design: MTHFR gene polymorphisms were assessed in 40 patients with ADHD and 30 healty controls. Two mutations in the MTHFR gene were investigated using polymerase chain reactions and restriction fragment length polymorphisms. Results: Although there were no statistically significant differences in genotype distributions of the C677T alleles between the ADHD and the control groups (p=0,678) but the genotypic pattern of the distributions of the A1298C alleles was different between the ADHD patients and the controls (p=0,033). Conclusions: Preliminary data imply a possible relationship between A1298C MTHFR polymorphisms and the ADHD.Öğe Treacher collins syndrome with a novel deletion in the tcof1 gene(ERCIYES UNIV SCH MEDICINE, 2019) Cavdartepe, Busra Eser; Kocak, Nadir; Yasa, Nafiz; Cora, TulinTreacher Collins syndrome (TCS) is a rare autosomal dominant congenital disorder characterized by various craniofacial malformations. The estimated incidence is 1 in 50000 live births. Bilaterally symmetric anomalies of the structure are present within the first and second branchial arches. Characteristic facial findings includes bilateral hypoplasia of the malar bones and mandible. This syndrome most commonly results from mutations in the TCOF1 gene. Here we present a five-year-old female patient with syndromic appearance and hearing loss. The patient had various facial dysmorphic features and malformed bilateral pinnae and left ear microtia. According to the clinical features, we suspected TCS and sequence analysis of TCOF1 gene was performed. A heterozygous new mutation c. 1722_1731delCATCCTCCAG in exon 12 of the TCOF1 gene was detected. It has been determined that this mutation is pathogenic according to the in silico prediction tools. The current study further expands the TCOF1 mutation spectrum.Öğe Tunicamycin-induced endoplasmic reticulum stress reduces in vitro subpopulation and invasion of CD44+/CD24-phenotype breast cancer stem cells(ELSEVIER GMBH, 2016) Nami, Babak; Donmez, Huseyin; Kocak, NadirTunicamycin is an inhibitor of glycosylation that disturbs protein folding machinery in eukaryotic cells. Tunicamycin causes accumulation of unfolded proteins in cell endoplasmic reticulum (ER) and induces ER stress. ER stress is an essential mechanism for cellular homeostasis has role in cell death via reprogramming of protein processing, regulation of autophagy and apoptosis. In this study we show effect of tunicamycin on subpopulation and invasion of CD44+/CD24- MCF7 breast cancer stem cells. CD44+/CD24- cells were isolated from MCF7 cell line by fluorescence activated cell sorting (FACS) and treated with tunicamycin. ER stress was monitored by evaluation of X-box binding protein 1(XBP-1) mRNA splicing, cleaved activating transcription factor 6 (ATF6) nuclear translocation and CCAAT/enhancer-binding protein homologous protein (CHOP) expression. CD44+/CD24- subpopulation was analyzed using flow cytometry. Invasion was investigated by scratch assay, trypan blue staining, 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide (MTT) proliferation and in vitro migration assays. Increased level of spliced XBP-1, ATF6 nuclear translocation and CHOP protein expression were detected in CD44+/CD24- and original MCF7 cells treated with tunicamycin. Also, a significant decline in CD44+/CD24- cell subpopulation was determined in the cells treated with tunicamycin. The results also showed inhibited invasion, increased cell death, suppressed proliferation and reduced migration in the CD44+/CD24- and CD44+/CD24- rich MCF7 cell culture, under effect of tunicamycin. Our results indicate that CD44+/CD24- phenotype MCF7 cells are susceptible to tunicamycin. The results showed that tunicamycin-induced ER stress suppresses CD44+/CD24- phenotype cell subpopulation and in vitro invasion and accelerates tumorosphore formation. These results suggest that tunicamycin-induced ER stress inhibits CD44+/CD24- phenotype MCF7 breast cancer stem cells. We conclude that using ER-targeting chemicals like tunicamycin is an interesting approach to target breast cancer stem cells inside tumor. (C) 2016 Elsevier GmbH. All rights reserved.
