Browsing by Author "Terzi, Yunus K."

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FCN2 c.772G > T Polymorphism Is Associated With Chronic Adenoiditis And/Or Tonsillitis, But Not-4 A > G and-602 G > A
(2016) Erkan, Alper N.; Oz, Isilay; Terzi, Yunus K.; Aydin, Erdinc; Ozkale, Murat; Babakurban, Seda Turkoglu; Koycu, Alper; Sahin, Feride Iffet; 0000-0003-0625-1057; 0000-0001-5612-9696; 0000-0001-7138-1400; 0000-0003-1290-3509; 0000-0002-7380-4566; 0000-0001-5067-4044; 0000-0001-7308-9673; 0000-0001-6864-7378; 27368434; A-7806-2016; B-4372-2018; H-1063-2019; AAF-3650-2021; AAJ-1452-2021; AAI-8856-2021; AAC-7232-2020; AAJ-2379-2021
Objective: Ficolins are complement activating peptides that play a role in the initial host defense against infectious pathogens. In the present study, we investigated the relationship between single nucleotide polymorphisms (SNPs) in the ficolin 2 gene (FCN2) and chronic adenotonsillitis in pediatric cases. Study Design: Case-control study. Methods: A total of 101 pediatric patients diagnosed with chronic adenotonsillitis and 100 healthy children were enrolled in the study. Genotypes of FCN2 promoter SNPs -602 G>A and -4 A>G, and the exonic SNP c.772G>T were determined by light SNP assay after realtime PCR analysis using genomic DNA samples obtained from peripheral blood samples of all participants. Results: Of the 101 chronic tonsillitis patients, 38 were girls and 63 were boys; the mean age was 5.2 +/- 2.3 years. The c.772G>T SNP frequency was significantly higher in chronic adenotonsillitis cases compared to the control group (p = 0.00); however, no significant difference was determined at positions -602 G>A or -4 A>G (p > 0.05). Conclusions: The FCN2 c.772G>T genotype appears to be associated with predisposition to chronic adenotonsillitis in the pediatric age group. This nucleotide change is likely to influence the level of gene expression and contribute to the development of disease. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
The Impact of Iron Overload in Acute Leukemia: Chronic Inflammation, But Not the Presence of Nontransferrin Bound Iron is a Determinant of Oxidative Stress
(2017) Olcay, Lale; Serteser, Mustafa; Kolay, Murat; Balci, Havva F.; Yildirim, Ulku M.; Tekgunduz, Sibel A.; Hazirolan, Tuncay; Terzi, Yunus K.; https://orcid.org/0000-0002-5684-0581; https://orcid.org/0000-0001-5612-9696; 28731917; AAK-3548-2021; B-4372-2018
In the literature, studies on the oxidant effects of nontransferrin bound iron [NTBI (eLPI assay)] during chemotherapy of acute lymphoblastic leukemia and acute myeloblastic leukemia are lacking. We established NTBI and oxidative stress determinants (OSD), iron parameters, high-sensitive C-reactive protein (hs-CRP) levels, liver tests, cumulative chemotherapeutic doses, and transfused blood in 36 children with acute leukemia throughout chemotherapy. These parameters were determined at the beginning and end of chemotherapy blocks (11 time points) and in 20 healthy children using enzyme-linked immunosorbent assay, and colorimetric and fluorometric enzymatic methods. In acute lymphoblastic leukemia, NTBI, OSD, and hs-CRP were higher than controls at 4/11, 7/11, and 9/11 time points (P<0.05). At 3 time points, NTBI and OSD concurrently increased. Ferritin, soluble transferrin receptor, serum iron, and transferrin saturation were higher than in controls at 5 to 11/11 time points (P<0.05). Those with NTBI had higher iron parameters than those without NTBI (P<0.05), but showed similar OSD, hs-CRP, liver enzymes, cumulative chemotherapeutics, and transfused blood (P>0.05). OSD did not correlate with NTBI, but correlated with hs-CRP. In conclusion, NTBI is a poor predictor of OSD in acute leukemia possibly because of the heterogeneity of NTBI and chronic inflammation. Further studies are needed to delineate the pathophysiology of these diseases.
Inhibition of the Notch Pathway Promotes Flap Survival by Inducing Functional Neoangiogenesis
(2015) Abbas, Ozan Luay; Borman, Huseyin; Terzi, Yunus K.; Terzi, Aysen; Bayraktar, Nilufer; Ozkan, Burak; Yazici, Ayse C.; 0000-0002-7886-3688; 0000-0003-3093-8369; 0000-0002-1225-1320; 0000-0002-3132-242X; 0000-0001-5612-9696; 25180956; Y-8758-2018; AAI-5063-2020; F-7546-2013; AAS-6810-2021; B-4372-2018
Objective The Notch pathway seems to function as an antiangiogenic factor, negatively regulating the sprouting effect of vascular endothelial growth factor (VEGF). This function is well defined in embryonic and tumor vasculature. However, little is known about its function in ischemia-induced angiogenesis. In the first part of this study, we investigated the role of Notch in reparative angiogenesis after ischemia. In the second part, we hypothesized that anti-Notch therapy will result in increased angiogenic sprouting. We analyzed the effect of Notch inhibition in the induction of angiogenic sprouting. Methods In the first part, we investigated the effect of ischemia on the Notch ligand delta-like ligand 4 (DLL4). Twenty rats were divided equally into 2 groups. In the surgery group, dorsal skin flap was used as model of ischemia. In the control group, no surgical procedure was performed. DLL4 and VEGF gene expressions were assessed. Immunohistochemical staining was used for detection of DLL4 in tissue materials. Plasma levels of VEGF and DLL4 were measured. In the second part, we investigated the effect of Notch inhibition using a gamma-secretase inhibitor (GSI) on inducing neoangiogenesis. Twenty rats were assigned to 2 equal groups. In all animals, dorsal skin flap was raised and sutured back into its bed. Animals in the GSI-treated group received GSI intravenously after surgery for 3 days. Saline was administered in the control group. Necrotic area measurements, microangiography, and histologic evaluations were performed to compare groups. Results In the first part, VEGF and DLL expressions increased in ischemic tissues (P < 0.01). Immunohistochemical analysis revealed that DLL4 expression was upregulated in capillary endothelial cells after ischemia. Plasma levels for VEGF and DLL4 were higher in the animals that underwent surgery (P < 0.01). In the second part, GSI treatment resulted in higher flap survival rates (P < 0.05). Microscopic analysis exhibited increase in the number of microvascular structures after GSI treatment (P < 0.05). Microangiographic evaluation showed that neovascularization increased in the GSI-applied flaps. Conclusions We present an evidence for the importance of the Notch pathway in the regulation of ischemia-induced angiogenesis. Notch inhibition promotes flap survival by creating a neovasculature that has an increase in vascular density.
Lack of Association of Matrix Metalloproteinase-9 Promoter Gene Polymorphism in Obstructive Sleep Apnea Syndrome
(2015) Yalcinkaya, Mustafa; Erbek, Selim S.; Babakurban, Seda Turkoglu; Kupeli, Elif; Bozbas, Serife; Terzi, Yunus K.; Sahin, Feride Iffet; 0000-0001-5612-9696; 0000-0001-5067-4044; 0000-0003-4825-3499; 0000-0002-5826-1997; 0000-0001-7308-9673; 0000-0002-7230-202X; 26169999; B-4372-2018; AAI-8856-2021; B-7604-2019; AAB-5345-2021; AAC-7232-2020; AAI-8064-2021
Purpose: Obstructive sleep apnea syndrome (OSAS) is a public health problem. There is an effort to establish the genetic contributions to the development of OSAS. One is matrix metalloproteinases, extracellular matrix degrading enzymes related to systemic inflammation. However, the impact of matrix metalloproteinase-9 (MMP-9) genotypes on the development of OSAS is unknown. Our aim was to determine whether MMP-9 single nucleotide polymorphism (SNP) (MMP-9 -1562C > T) is related to susceptibility to OSAS. Material and methods: A total of 106 patients with a history of sleep apnea and 88 controls without a history of sleep apnea were enrolled in this study. Genotypes were determined by restriction fragment length polymorphism analyses after polymerase chain reaction. Results: Genotypes and allele frequencies of the MMP-9 -1562C > T SNP was not statistically different between the patient and control groups (p > 0.05). There was a statistical association between apnea -hypopnea index (AHI) and body mass index (BMI), and also between AHI and neck circumference (p < 0.001). There was no association among the genotypes and AHI, neck circumference, or BMI (p > 0.05). Conclusions: We found no association between MMP-9 -1562C > T SNP and OSAS. Studies to investigate the role of other polymorphisms and expression of MMP-9 gene will provide more information. (C) 2015 European Association for Cranio-Maxillo-Facial Surgery. Published by Elsevier Ltd. All rights reserved.
The Notch Pathway Is A Critical Regulator of Angiogenesis in A Skin Model of Ischemia
(2015) Abbas, Ozan L.; Borman, Huseyin; Terzi, Yunus K.; Terzi, Aysen; Bayraktar, Nilufer; Yazici, Ayse C.; 0000-0002-1225-1320; 0000-0002-7886-3688; 0000-0001-5612-9696; 0000-0002-3132-242X; 25834117; F-7546-2013; Y-8758-2018; B-4372-2018; AAS-6810-2021
The Notch pathway is definitely required for normal vascular development. Although the contribution of Notch in postnatal angiogenesis is the focus of intense investigation, the implication of Notch in reparative neovascularization in the skin remains unexplored. In this study, we investigated Notch changes using a skin model of ischemia. Thirty Sprague-Dawley rats were divided into two groups. In the surgery group (n = 24), a caudally based dorsal skin flap was raised and sutured back into its initial position. In the control group, no surgical procedure was performed. Tissue biopsies were obtained at different time intervals. Tissue specimens were assessed for Delta-like ligand 4 (DLL4) and vascular endothelial growth factor (VEGF) gene expression by real-time polymerase chain reaction (PCR). Immunohistochemical staining was used for detection of DLL4 in tissue materials. Quantitative assessment of skin flap microvasculature was made. Compared with normoperfused tissue, VEGF and DLL4 expressions increased significantly (p < 0.01). Immunohistochemical analysis revealed weak and patchy expression of DLL4 in microvascular endothelial cells of normoperfused tissues. Conversely, DLL4 expression was upregulated in capillary endothelial cells after ischemia. In conclusion, in this study we have shown that the Notch ligand DLL4 is upregulated in skin tissue after ischemia. A deeper understanding of these fundamental principles will aid in the development of new avenues for the treatment of blood vessel-related skin pathologies.