Browsing by Author "Terzi, Yunus Kasim"

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Associations between IL-1 alpha, IL-1 beta, TNF alpha, and IL-6 variations, and susceptibility to transposition of the great arteries
(2022) Atasoy Karakas, Latife; Tugrul, Duygu; Sahin Uysal, Nihal; Esin, Sertac; Tokel, Niyazi Kursat; Terzi, Yunus Kasim; 35590253; AEY-5060-2022
Background: To evaluate the relationship between IL-1 alpha-889UT (rs1800587), IL-1 beta -511 C >T (rs16944), TNF alpha-308G > A (rs1800629), TNF alpha-238G > A (rs361525), IL-6 -174G> C (rs1800795), and IL-6 -572G > C (rs1800796) polymorphisms and the susceptibility to transposition of the great arteries (TGA). Methods: A prospective analysis was performed on mothers whose newborns were diagnosed as having TGA. For each case of TGA, a mother who gave birth to a healthy neonate in the same period was randomly selected for the control group. The sample size was calculated before planning the study with 80% power and 5% alpha. Results: Twenty-seven mothers whose newborn had TGA anomalies (group 1) and 27 mothers whose newborn had no TGA (group 2) were included in the study. There were no significant differences between the groups in terms of maternal age, pregestational body mass index, gestational age at birth and infant sex (p> 0.05). The genotype and allele distributions of IL-1 alpha -889C/T (rs1800587), IL-1 beta -511C >T (rs16944), TNF alpha -308G >A (rs1800629), TNF alpha -238G > A (rs361525), IL-6 -174G> C (rs1800795) and IL-6 -572G > C (rs1800796) gene variants were not different between the two groups (p> 0.05). Conclusions: There was no relation between IL-1 alpha, IL-1 beta, IL-6, and TNF alpha promoter gene polymorphisms and TGA occurrence in our study group.
beta-Adrenoreceptor antagonists reduce cancer cell proliferation, invasion, and migration
(2014) Iseri, Ozlem Darcansoy; Sahin, Feride Iffet; Terzi, Yunus Kasim; Yurtcu, Erkan; Erdem, S. Remzi; Sarialioglu, Faik; 25026350
Context: Propranolol, atenolol, and ICI118,551 are non-selective beta-adrenergic receptor (AR), beta(1)-AR, and beta(2)-AR antagonists, respectively. Objective: We investigated the efficacy of propranolol, atenolol, and ICI118,551 on proliferation, migration, and invasion of non-stimulated breast (MCF7), colon (HT-29), and hepatocellular (HepG2) cancer cells. Materials and methods: beta-AR expression profiling of cells was performed by real time PCR. Cell proliferation was determined by MTT. Boyden chamber and scratch assays were performed to evaluate invasion and migration. Results and discussion: All cell lines expressed beta-ARs. ICI118,551 was the most cytotoxic, whereas atenolol was the least effective beta-AR antagonist for 24, 48, and 72 h. Cell invasion was inhibited by ICI118,551 (45, 46, and 50% for MCF7, HT29, and HepG2, respectively) and propranolol (72, 65, and 90% for MCF7, HT29, and HepG2, respectively). Propranolol, atenolol, and ICI118,551 reduced migration of MCF7, HT-29, and HepG2 cells to varying extents depending on the application concentration and duration. Propranolol and atenolol reduced migration of MCF7 and HT-29 in a concentration-dependent manner, whereas migration of these cells decreased after 48 and 72 h of ICI118,551 applications. Conclusion: Beta(2)-AR antagonist seemed to be the most cytotoxic beta-blocker on non-stimulated cancer cells. Propranolol and ICI118,551 were more effective than atenolol in inhibiting invasion and migration of non-stimulated MCF7 and HT-29 cells; ICI118,551 being the most potent. Concordantly, beta(2)-selective blockage seemed to be more effective for non-stimulated cells. Effect of the selective beta-AR antagonists showed variation depending on the concentration, incubation time, and histological origin of cells.
Biochemical, Radiologic, Ultrastructural, and Genetic Evaluation of Iron Overload in Acute Leukemia and Iron-chelation Therapy
(2014) Olcay, Lale; Hazirolan, Tuncay; Yildirmak, Yildiz; Erdemli, Esra; Terzi, Yunus Kasim; Arda, Kemal; Ozturkmen, Seda; Akyay, Arzu; Kaymak-Cihan, Meric; Bicakci, Zafer; Bal, Ceylan; https://orcid.org/0000-0001-5612-9696; https://orcid.org/0000-0002-4480-7784; 23887025; B-4372-2018; ABI-7551-2020
Iron overload in hereditary hemochromatosis and hematologic malignancy has unfavorable effects on morbidity. Herein, 53 children (age 108.4 +/- 58.3 mo, 25 girls and 28 boys) with acute myeloblastic and lymphoblastic leukemia, who received 4 different chemotherapy protocols, were evaluated for iron overload throughout chemotherapy. Iron overload arose: (1) before chemotherapy, which was dependent on neither chemotherapy nor packed red blood cell transfusions and (2) after chemotherapy, which was dependent on the duration and nature of chemotherapy and partially on transfusion of packed red blood cells. Iron overload was documented in 75% of patients with a ferritin level >1000 ng/mL, by liver and heart magnetic resonance imaging, and they were administered iron-chelation therapy with success. Three of 10 radiologically iron-overloaded patients were heterozygous for H63D mutation. Aminolevulinic acid and porphobilinogen levels were normal. Light microscopic examination of the bone marrow revealed increased iron granules in erythroblasts, platelets, and megakaryocytes, iron-laden macrophages, free iron in the matrix, dyshematopoiesis, and apoptotic cells. Electron microscopic examination revealed iron-laden secondary lysosomes and autolysosomes in normoblasts and iron-laden primary granules in promyelocytes, irrelevant to the ferritin level, implying autophagia due to chemotherapy as a source of the excess iron. We think that iron overload, which is an important complication of acute leukemia, should be evaluated separately from transfusion overload, and the management principles specific to leukemia should be implemented.
BRCA1 and BRCA2 sequence variations detected with next-generation sequencing in patients with premature ovarian insufficiency
(2016) Yilmaz, Nafiye Karakas; Karagin, Peren Hatice; Terzi, Yunus Kasim; Kahyaoglu, Inci; Yilmaz, Saynur; Erkaya, Salim; Sahin, Feride Iffet; 27403073
Objective: Although the association between BRCA1 and BRCA2 gene mutations and breast and ovarian cancer is known, there is insufficient data about premature ovarian insufficiency (POI). However, several studies have reported that there might be a relationship between POI and BRCA1 and BRCA2 gene mutation. Therefore, in the present study, we aimed to investigate the role of BRCA1 and BRCA2 gene mutations in the etiology of POI in a Turkish population. Material and Methods: The cohort was classified into two groups: a study group, consisting of 56 individuals diagnosed with premature ovarian insufficiency (and who were younger than 40 years of age, had an antral follicle count <3-5, and FSH levels >12 IU/I), and a control group, consisting of 45 fertile individuals. A total of 101 individuals were analyzed by next-generation sequencing to detect BRCA1 and BRCA2 gene mutations. Results: We detected four new variations (p.T1246N and p.R1835Q in BRCA1 and p.I3312V and IVS-7T>A in BRCA2) that had not been reported before. Conclusion: We did not find an association between the BRCA1 and BRCA2 gene mutations and premature ovarian insufficiency. However, larger, functional studies are needed to clarify the association.
Chronic Tonsillitis Is Not Associated with Beta Defensin 1 Gene Polymorphisms in Turkish Population
(2015) Arslan, Fatih; Babakurban, Seda Turkoglu; Erbek, Selim S.; Sahin, Feride I.; Terzi, Yunus Kasim; 0000-0001-7308-9673; 0000-0001-5612-9696; 0000-0003-4825-3499; 0000-0001-5067-4044; 25683590; AAC-7232-2020; B-4372-2018; B-7604-2019; AAI-8856-2021
Background: Defensins are antimicrobial peptides expressed on mucosal surfaces. They function as part of the innate immune system. Palatine tonsils play important roles in innate immune system. However, our knowledge on the pathophysiology of chronic tonsils is limited. Objective: The aim of this study was to investigate the association between beta defensin 1 gene single nucleotide polymorphisms and chronic tonsillitis. Study design: Prospective, non-randomized, controlled clinical study. Setting: Tertiary referral center. Subjects and methods: Eighty six patients with chronic tonsillitis and eighty controls without history of chronic tonsillitis were enrolled in this study. Genotypes were determined by restriction fragment length polymorphism analyses after polymerase chain reaction. Results: Genotype and allele frequencies of the -20G/A (rs11362), -44C/G (rs1800972) and -52G/A (rs1799946) single nucleotide polymorphisms were not statistically different between patients and control groups (p > 0.05). Conclusion: In this study, we found that DEFB1 gene -20G/A, -44C/G and -52G/A single nucleotide polymorphisms were not associated with chronic tonsillitis. Studies, which analyse other polymorphism of the beta defensin 1 gene in large case series, should be conducted to understand the role of DEFB1 gene on chronic tonsillitis. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
Clinical Findings and Mutation Analysis of NF1 Patients in Turkey
(2018) Terzi, Yunus Kasim; Oguzkan-Balci, Sibel; Anlar, Banu; Varan, Ali; Ersoy-Evanse, Sibel; Sharafif, Parisa; Ayter, Sukriye; https://orcid.org/0000-0001-5612-9696; B-4372-2018
Neurofibromatosis type 1 (NF1) is an autosomal dominant disease that is caused by mutations of the NF1 gene. NF1 is clinically characterized by neurofibromas, pigmentation anomalies, and an increased risk of malignant tumors. The mutation rate of NF1 is one of the highest known for human disorders: approximately 50% of all affected individuals are sporadic cases and carry de novo mutations Therefore mutation analysis of NF1 may be an important tool in early diagnosis and genetic counseling. This is the first large NF1 study performed in Turkey. The data collected in this study enabled us to overview the genetic and clinical aspects of NF1 molecular diagnostics. The patients, who were clinically diagnosed for NF1, were included in this study. These patients were clinically evaluated, and subgroup of them genotyped or DNA sequenced for mutations in NF1, either to confirm the clinical diagnosis or to identify pathogenic mutations. The mutation detection rate was 52%, based on analysis of only genomic DNA. We observed that frameshift mutations were the largest proportion of the identified mutations (38.5%). The frequency of microdeletions was 26.9% and the splice site and nonsense mutations were 11.5% in this cohort. Turkish NF1 patients have similar NF1 germline mutations compared to other populations. Considering that some of these detected mutations belonged to the patients who did not fulfill the NIH criteria for NF1 diagnosis, mutation analysis of NF1 is an important tool in early diagnosis and genetic counseling.
The differences in the expression of fractalkine and its receptor in conditions of tonsillar hypertrophy and chronic tonsillitis
(2019) Hetemoglu, Elif Koclu; Babakurban, Seda Turkoglu; Terzi, Yunus Kasim; Sahin, Feride Iffet; Erbek, Selim Sermed; 0000-0001-5612-9696; 0000-0001-7308-9673; 30554983; B-4372-2018; AAC-7232-2020
Objective: Fractalkine, member of chemokine family, is involved in many inflammatory processes in the human body. The aim of this study is to compare expression levels of fractalkine ligand and its receptor in chronic tonsillitis and hypertrophic tonsil samples. Methods: The study was conducted at Baskent University Departments of Otorhinolaryngology and Medical Genetics. It is designed as a prospective, non-randomized, controlled clinical study. Total 97 samples, obtained from adenotonsillectomy due to chronic tonsillitis or tonsillar hypertrophy, were participated in the study. Fractalkine and its receptor expression levels were determined and comparison was made between the tissue groups. c.839C > T (T280 M) polymorphism of fractalkine receptor was analyzed, then relationship between polymorphism and the expression level of fractalkine receptor was investigated. Results: Fractalkine receptor expression was significantly higher in the hypertrophic tonsil group than chronic tonsillitis group (p < 0.05). Conclusion: Fractalkine, member of chemokine family, and its receptor may play role in preventing chronic-recurrent tonsillitis. (C) 2019 Elsevier B.V. All rights reserved.
Effect of Hereditary Hemochromatosis Gene H63D and C282Y Mutations on Iron Overload in Sickle Cell Disease Patients
(2016) Terzi, Yunus Kasim; Balci, Tugce Bulakbasi; Boga, Can; Koc, Zafer; Celik, Zerrin Yilmaz; Ozdogu, Hakan; Karakus, Sema; Sahin, Feride Iffet; 27095682
Objective: Hemochromatosis is an autosomal recessive disease that is one of the most important reasons for iron overload. Sickle cell disease is a hemoglobinopathy that occurs as a result of a homozygous mutation in the hemoglobin gene. Erythrocyte transfusion is frequently used in the treatment of this disease. Iron overload as a result of transfusion is important in the mortality and morbidity of sickle cell anemia patients as well as in other hemoglobinopathies. In this study, the effect of hemochromatosis gene (HFE) p.H63D and p.C282Y mutations on transfusion-related cardiac and liver iron overload in sickle cell disease patients who carry homozygous hemoglobin S mutation has been investigated. Materials and Methods: This is a prospective single-center cross-sectional study in patients with homozygous hemoglobin S mutation between the years 2008 and 2013. The patients were divided into two groups. The first group (group A, n=31) was receiving chelation therapy and the second group (group B, n=13) was not. Direct and indirect iron loads were analyzed by magnetic resonance imaging and biochemically, respectively. HFE gene mutations were analyzed by polymerase chain reaction-restriction fragment length polymorphism method. Statistical analyses were performed by independent samples t-test. Results: p.H63D mutation was detected in 10 (32.3%) patients in group A and in only 1 patient (7.7%) in group B. When the 2 groups were compared for iron overload, iron deposition in the liver was significantly higher in group B (p=0.046). In addition, in group A, iron deposition was significantly higher in HFE mutation carriers compared to patients without the mutation (p=0.05). Conclusion: Results of this study showed that HFE gene mutations are important in iron deposition in the liver in patients with sickle cell disease.
Enhancement of Vascular Endothelial Growth Factor's Angiogenic Capacity by the Therapeutic Modulation of Notch Signalling Improves Tram Flap Survival in Rats Submitted to Nicotine
(2017) Abbas, Ozan Luay; Terzi, Yunus Kasim; Ozatik, Orhan; Ozatik, Fikriye Yasemin; Turna, Gamze; Nar, Rukiye; Musmul, Ahmet; 0000-0001-5612-9696; 0000-0002-4662-6493; 0000-0002-8422-2975; 28277073; B-4372-2018; GXA-2381-2022; HOH-8201-2023
Background: Smoke of cigarettes, and specifically nicotine, has been shown to diminish pedicled transverse rectus abdominis musculocutaneous (TRAM) flap survival. Considering that Notch signalling through its ligand Delta-like 4 (Dll4) functions as anti-angiogenic factor by inhibiting the pro-angiogenic effects of vascular endothelial growth factor (VEGF), it is hypothesised that inhibition of the Notch would promote angiogenesis and increase TRAM flap survival in rats submitted to nicotine. Methods: Twenty rats were treated with nicotine for 28 days preoperatively. Thereafter, a pedicled TRAM flap was created in all animals. The Notch inhibitor N-[N-(3,5-difluorophenacetyl)-1-alanyl]-S-phenylglycine-t-butyl-ester was administered in animals of the treatment group. Animals in the control group were given the same amount of solvent. Five days after the surgery, viable flap areas were determined. Skin samples were evaluated for VEGF and Dll4 mRNA levels. Immunohistochemical analysis was used for the assessment of endothelial Dll4 expression. Vascular density was determined histologically. Plasma levels of VEGF and Dll4 were measured. Results: A significant improvement in TRAM flap surviving area was observed in the treatment group (53.5014.25%) compared with the controls (32.20 +/- 9.15%). Immunohistochemical analysis revealed a significant increase in the number of Dll4 stained vessels in animals of the treatment group (9.2 +/- 1.6) in comparison with the controls (5.7 +/- 1.9). VEGF mRNA levels (0.22 +/- 0.08) in the treatment group were significantly lower than those in the control group (0.36 +/- 0.09). Conclusion: Notch inhibition significantly improved TRAM flap survival in animals exposed to nicotine by promoting VEGF-induced angiogenesis.
Epigallocatechin 3-gallate applications on HT-29 and MCF-7 cell lines and evaluation of tumor suppressor gene methylation
(2015) Terzi, Yunus Kasim; Kaya, Ozge Ozer; Iseri, Ozlem Darcansoy; Celik, Zerrin; Sahin, Feride Iffet
Epigallocatechin 3-gallate (EGCG) is an antitumor molecule and shows this activity by binding to the active center of a methyltransferase enzyme (DNMT1). The methylation of DNA sequences of tumor suppressor and DNA repair genes is observed in different stages of carcinogenesis. In this study, we analyzed the effect of EGCG on the methylation status of 25 tumor suppressor genes in cancer cell lines HT-29 and MCF-7. HT-29 and MCF-7 cells were incubated with 10 mu M, 20 mu M, and 50 mu M and 1 mu M, 5 mu M, and 10 mu M EGCG for 48 h, respectively. We found promoter hypermethylation of (1) CDH13, GATA5, and RAR beta genes in MCF-7 cell line and (2) RAR beta, ESR1, PAX6, WT1, CADM1, CHFR, CDH13, and GATA5 genes in HT-29 cell line. However, (3) after EGCG application, no changes in methylation status were detected in our samples. Our results suggest that methylation status of tumor suppressor genes did not change with different EGCG doses.
Fractalkine (CX3CL1) and its receptor (CX3CR1) in children with hypertrophic adenoid and chronic otitis media with effusion
(2020) Inan, Serhat; Babakurban, Seda Turkoglu; Erbek, Selim Sermed; Terzi, Yunus Kasim; Sahin, Feride Iffet; 0000-0001-7308-9673; 0000-0001-5067-4044; 0000-0003-4825-3499; 0000-0001-5612-9696; 0000-0001-8821-4481; AAC-7232-2020; AAI-8856-2021; AAJ-1407-2021; B-7604-2019; B-4372-2018
Background: Adenoid hypertrophy (AH) is one of the possible causes of chronic inflammation in the middle ear. It has been suggested that CX3CL1 and its specific receptor (CX3CR1) could be related with the pathogenesis of some inflammatory diseases. The aim of the present study was to evaluate the role of CX3CL1 and CX3CR1 in the pathogenesis of AH with chronic otitis media with effusion (COME) in children. Materials and methods: Adenoid tissue samples were obtained from 91 pediatric patients and divided into two groups: adenoidectomy only for AH (n: 47) and adenoidectomy in conjunction with ventilation tube insertion for AH + COME (n: 44). Expression levels of CX3CL1 and CX3CR1 genes were compared. Results: Expression levels of CX3CL1 and CX3CR1 in hypertrophic adenoid tissue were not significantly different between the AH + COME and All only groups. Although no significant difference was detected in the expression of CX3CL1 in the adenoid samples, the expression of CX3CR1 was higher in children older than 48 months. Conclusions: When allergy, atopy and chronic adenoiditis does not exist to obstructive adenoid hypertrophy, inflammatory fractalkine chemokine expression levels in adenoid tissue was not observed to be increased in children with COME.
Fractalkine Receptor Polymorphism and Chronic Tonsillitis
(2014) Babakurban, Seda Turkoglu; Erbek, Selim S.; Terzi, Yunus Kasim; Arslan, Fatih; Sahin, Feride I.; https://orcid.org/0000-0001-5067-4044; https://orcid.org/0000-0003-4825-3499; https://orcid.org/0000-0001-5612-9696; https://orcid.org/0000-0001-7308-9673; 24496565; AAI-8856-2021; B-7604-2019; B-4372-2018; AAC-7232-2020
The objective of this study is to examine whether there is an association of fractalkine gene receptor polymorphisms with chronic tonsillitis. This is a cross-sectional study in the setting of a tertiary referral center. The study group included 79 patients with chronic tonsillitis and 76 controls without history of chronic tonsillitis. Genotypes were identified by restriction fragment length polymorphism analyses after polymerase chain reaction. c.745G > A (V249I) single nucleotide polymorphism and the frequencies of the G and A alleles did not differ in the patient and control groups (p = 0.363; p = 0.743, respectively). c.839C > T (T280M) single nucleotide polymorphism was found to be higher in controls than in the patients with chronic tonsillitis (p < 0.001). Consistent with this result, T allele frequency was higher in controls than in the patients with chronic tonsillitis (p < 0.001). In this study, we suggested that fractalkine gene receptor c.839C > T (T280M) single nucleotide polymorphism could be associated with a reduced risk of chronic tonsillitis.
Frequency of IL-1B Gene Polymorphisms in Patients with Gastroesophageal Cancer in the Hakkari Region
(2023) Yaman, Derya; Akad Dincer, Selin; Karaka, Yusuf; Unsoy, Gozde; Terzi, Yunus Kasim; Sahin, Feride Iffet
Objective: Gastric cancer is a complex malignant tumor associated with chronic inflammation. In the present study, we aimed to investigate the frequency of interleukin 18 (IL-18) gene polymorphisms affecting gene expression in patients with gastroesophageal cancer (GC) diagnosed in the Hakkari region. Methods: Blood samples of 17 patients with GC (group 1) and 59 healthy controls (group 2) were enrolled in the study. The single-nucleotide polymorphisms (SNPs) rs1143627 c.-118C>T, rs16944 c.-598C>T, and rs1143634 c.315C>T polymorphisms in the IL-18 gene were studied among groups via polymerase chain reaction and restriction fragment length polymorphism. Results were analyzed by descriptive statistics and the x(2) test. The association between SNPs and GC risk was evaluated by odd ratios (ORs) and 95% confidence intervals. Results: The frequencies of the three genotypes in the SNP rs1143627, rs16944, and rs1143634 were similar between the groups, and C>T transition was not found to be significant [(p=0.69, OR: 1.16 95%, confidence interval (CI): 0.54-2.51; p= 0.16, OR: 0.58 95%, CI: 0.26-1.25; p=0.7, OR: 0.83 95%, CI: 0.32-2.11, respectively]. Conclusion: Our results did not reveal any significant association between IL-18 gene SNPs and gastroesophageal cancer in the Hakkari region.
A highly efficient and faithful MDS patient-derived xenotransplantation model for pre-clinical studies
(2019) Song, Yuanbin; Rongvaux, Anthony; Taylor, Ashley; Jiang, Tingting; Tabaldi, Toma; Balasubramanian, Kunthavai; Bagale, Arun; Terzi, Yunus Kasim; Gbyli, Rana; Wang, Xiaman; Fu, Xiaoying; Gao, Yimeng; Zhao, Jun; Podoltsev, Nikolai; Xu, Mina; Neparidze, Natalia; Wong, Elice; Torres, Richard; Bruscia, Emanuela M.; Kluger, Yuval; Manz, Markus G.; Flavell, Richard A.; Halene, Stephanie; 0000-0001-5612-9696; 30664659; B-4372-2018
Comprehensive preclinical studies of Myelodysplastic Syndromes (MDS) have been elusive due to limited ability of MDS stem cells to engraft current immunodeficient murine hosts. Here we report a MDS patient-derived xenotransplantation model in cytokine-humanized immunodeficient "MISTRG" mice that provides efficient and faithful disease representation across all MDS subtypes. MISTRG MDS patient-derived xenografts (PDX) reproduce patients' dysplastic morphology with multi-lineage representation, including erythro- and megakaryopoiesis. MISTRG MDS-PDX replicate the original sample's genetic complexity and can be propagated via serial transplantation. MISTRG MDS-PDX demonstrate the cytotoxic and differentiation potential of targeted therapeutics providing superior readouts of drug mechanism of action and therapeutic efficacy. Physiologic humanization of the hematopoietic stem cell niche proves critical to MDS stem cell propagation and function in vivo. The MISTRG MDS-PDX model opens novel avenues of research and long-awaited opportunities in MDS research.
Immune and inflammatory genes possibly involved in the pathogenesis of severe COVID-19
(2021) Beksac, Burcu; Dincer, Selin Akad; Avdullahi, Egzon; Yaman, Derya; Terzi, Yunus Kasim; Babakurban, Seda Turkoglu; Celik, Zerrin Yilmaz; Tasci, Canturk; Sahin, Feride Iffet
The Influence of Sex on Brain Development Genetics and the Possible Relationship with Sex-Dependent Differences in Psychiatric Disorders
(2021) Bagcaz, Arda; Terzi, Yunus Kasim; Sahin, Feride Iffet; 0000-0001-5947-0179; 0000-0001-7308-9673; AAK-2321-2021; AAC-7232-2020
There are sex-dependent differences in the prevalence, age of onset, and course of psychiatric disorders and cognitive abilities. Although it has been assumed that the direct effect of gonadal hormones in sensitive periods leads to sexually dimorphic brain development, current evidence suggests that another possible factor may be sex-specific regulations at the gene level. Understanding the sex differences at the gene level can be promising to identify the mechanisms that predispose or trigger psychiatric disorders, and may provide new prevention or treatment strategies. This paper aims to review the findings on the mechanisms that affect the sex-specific differences in brain development at the gene level and to discuss the relationship of these findings with different cognitive characteristics of the sexes and psychiatric disorders.
Investigation of Toll Like Receptor-7 Gene (TLR-7) Mutations in COVID-19 Patients
(2021) Dincer, Selin Akad; Beksac, Burcu; Avdullahi, Egzon; Yaman, Derya; Terzi, Yunus Kasim; Babakurban, Seda Turkoglu; Celik, Zerrin Yilmaz; Tasci, Canturk; Sahin, Feride Iffet
A newborn case diagnosed as isolated TBX1 deletion with 22q11 deletion syndrome
(2020) Turan, Ozden; Celik, Zerrin Yilmaz; Ince, Deniz Anuk; Terzi, Yunus Kasim; Ecevit, Ayse; 0000-0002-2232-8117; 0000-0002-7707-1881; 0000-0002-4369-2110; AAJ-4616-2021; AAJ-2333-2021; I-6746-2016
The Notch Signaling System Is Involved in the Regulation of Reparative Angiogenesis in the Zone of Stasis
(2017) Abbas, Ozan Luay; Ozatik, Orhan; Terzi, Yunus Kasim; Ozatik, Fikriye Yasemin; Nar, Rukiye; Turna, Gamze; https://orcid.org/0000-0001-5612-9696; 28319529; B-4372-2018
The Notch pathway ligand Delta-like 4 (Dll4) functions as an antiangiogenic factor, inhibiting vascular endothelial growth factor (VEGF)-induced angiogenesis. This function is documented in tumor and embryonic vasculature. However, its implication in burn wounds remains unexplored. Our objective was to explore the involvement of the Notch in the healing of zone of stasis burns. We hypothesized that anti-Dll4 therapy would prevent progressive necrosis in the stasis zone by promoting angiogenesis. Burns were created in 21 rats using the comb burn model. The Notch inhibitor N-[N-(3,5-difluorophenacetyl)1- alanyl]-S-phenylglycine-t-butyl-ester was administered in the treatment group. Controls were given the same amount of solvent. Seven days after the burn, skin samples were evaluated for VEGF and Dll4 gene expressions. Immunohistochemical analysis was used for the assessment of vascular density, endothelial Dll4 expression, and apoptosis count. Histologic grading of tissue damage was performed. Circulating levels of VEGF and Dll4 were determined. VEGF and Dll4 mRNA levels were found to be simultaneously induced after the burn. In the treatment group, a significant increase in the number of vessels was observed. However, gross evaluation documented an expansion of necrosis to the zone of stasis with marked activation of apoptosis. Histologic assessment showed that the resultant vascular overgrowth was accompanied by extensive edema and abundant infiltration of leukocytes. We provide evidence for the involvement of Notch in the regulation of angiogenesis in zone of stasis burns.
Odontogenic effects of two calcium silicate-based biomaterials in human dental pulp cells
(2018) Onay, Emel Olga; Yurtcu, Erkan; Terzi, Yunus Kasim; Ungor, Mete; Oguz, Yener; Sahin, Feride İffet; 30070078
Background. The goal of treating exposed pulp with an appropriate pulp capping material is to promote the dentinogenic potential of the pulpal cells. There have been recent attempts to develop more effective pulp-capping materials. Objectives. The aim of this study was to evaluate the effect of newly developed calcium silicate-based material on odontogenic differentiation of primary human dental pulp cells (HDPCs), in comparison with a contemporary calcium silicate-based material. Material and methods. Human dental pulp cells isolated from dental pulps were cultured in standard culture conditions in Dulbecco's Modified Eagle's Medium (DMEM) and then the effects of Micro-Mega mineral trioxide aggregate (MM-MTA) (Micro-Mega, Besancon, France) and ProRoot MTA (MTA) (Dentsply Sirona, Tulsa, USA) (positive control) were evaluated on HDPCs at 1, 7 and 14 days. Untreated cells were used as a negative control. Odontoblastic differentiation was assessed by alkaline phosphatase (ALP) activity. Runtrelated transcription factor 2 (RUNX2), alkaline phosphatase liver/bone/kidney (ALPL), bone morphogenetic protein 2 (BMP2), dentin sialophosphoprotein (DSPP), and Distal-less homeobox 3 (DLX3), as odontoblastic/ osteoblastic expression markers, were evaluated by semi-quantitative real-time polymerase chain reaction (RT-PCR) analysis. Calcium levels of culture media were also determined. Results. The MM-MTA group significantly increased the expression of BMP2 compared with that of the MTA group at 3 different time periods (p < 0.05). The up-regulation of ALPL between day 1 and 14 and the up-regulation of DSPP between day 7 and 14 were significant in both groups (p < 0.05). Micro-Mega MTA and MTA exhibited similar messenger RNA (mRNA) expression levels of ALPL, DSPP, RUNX2, DLX3, and ALP activities, as well as calcium levels. Conclusions. Based on the cell responses observed in this study, MM-MTA might be used efficiently in dental pulp therapy as a potential alternative to MTA.