Browsing by Author "Sahin, Feride"
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Item Association Between Heat Shock Protein-72 Gene Polymorphism and Chronic Renal Failure in Children(2014) Gulleroglu, Kaan; Baskin, Esra; Kantar, Asli; Sahin, Feride; https://orcid.org/0000-0003-1434-3824; https://orcid.org/0000-0003-4361-8508; https://orcid.org/0000-0001-7308-9673; F-3294-2013; B-5785-2018; AAC-7232-2020Item The Clinical Characteristics and Prognosis of Exon 2 Mutations in Familial Mediterranean Fever(2023) Avci, Begum; Parmaksiz, Gonul; Sahin, Feride; Noyan, Aytul; 0000-0001-7308-9673; AAC-7232-2020Objective: It is unclear whether exon 2 mutations are variations or mutations that causes the disease. This study aimed to evaluate the clinical features and prognosis exon 2 mutations in Familial Mediterranean Fever. Methods: The clinical features, disease severity and prognosis of all patients with at least one exon 2 mutations were evaluated retrospectively. These data were compared separately for homozygous (Group 1), heterozygous (Group 2), compound heterozygous (Group 3), and complex alleles (Group 4), and the data were compared by grouping patients into those with and without exon 10 mutations. Results: There were a total of 119 patients with exon 2 mutations, including 11.7% in Group 1, 36.1% in Group 2, 21.8% in Group 3, and 30.2% in Group 4 were similar in terms of demographic data, clinical characteristics, and disease course. When compared patients with exon 10 mutations (+) to those with exon 10 mutations (-), the exon 10 mutations (+) group had a higher presence of chest pain (100%, p = 0.02) and a significantly higher mean Pras severity score (6.66 +/- 1.87, 6.01 +/- 1.40; p=0.02). Additionally, a higher number of patients with exon 10 mutation (-) achieved remission with treatment (76 (67.9%), 36 (32.1%); p = 0.03). Conclusion: Exon 2 mutations have a milder course and higher remission rates but they should be considered as Familial Mediterranean Fever disease because of their similar clinical presentation and response to colchicine treatment with exon 10 mutations. Early treatment and close follow- up should be performed.Item Evaluation of High Mobility Group Box 1 Protein As an Inflammation Marker in Patients with Familial Mediterranean Fever(2018) Ozturk, Betul; Baskin, Esra; Gulleroglu, Kaan; Sahin, Feride; Bayraktar, Nilufer; 0000-0003-4361-8508; 0000-0003-4361-8508; 0000-0003-1434-3824; 0000-0001-7308-9673; 0000-0002-7886-3688; HNQ-4875-2023; B-5785-2018; F-3294-2013; AAC-7232-2020; Y-8758-2018Item Fractalkine Receptor Gene Polymorphisms and Chronic Renal Disease(2014) Gulleroglu, Kaan; Baskin, Esra; Kantar, Asli; Sahin, Feride; https://orcid.org/0000-0003-1434-3824; https://orcid.org/0000-0003-4361-8508; AAJ-8833-2021; B-5785-2018Item The importance of BMP4 gene defects in renal transplant patients with cakut(2019) Baskin, Esra; Sahin, Vildan; Terzi, Yunus Kazim; Gulleroglu, Kaan; Uslu, Nihal; Akdur, Aydincan; Moray, Gokhan; Sahin, Feride; Haberal, Mehmet; 0000-0003-4361-8508; ABC-5258-2020; B-5785-2018Item No Interaction Between Childhood Maltreatment and Serotonin Transporter Gene in Recurrent Major Depressive Disorder: A Clinical Sample(2019) Ozcurumez, Gamze; Yurdakul, Hasan Talha; Terzi, Yunus; Direk, Nese; Essizoglu, Altan; Sahin, Feride; 0000-0001-5612-9696; 31223242; B-4372-2018Introduction: There is inconsistent evidence of interaction between childhood adversities and a serotonin transporter promoter polymorphism (5- HTTLPR) in depression. It is hypothesized that genetic sensitivity to stress could be more specific to recurrent major depressive disorder (MDD). The aim of the study is to replicate a recent study which provided preliminary evidence of interaction between severity of childhood maltreatment and the 5-HTTLPR polymorphism in recurrent MDD. Methods: Participants included a well-characterized clinical sample of 70 recurrent MDD cases and 67 never psychiatrically ill controls, aged 18 years or over. Socio-demographic and clinical information form, Composite International Diagnostic Interview (CIDI), Childhood Trauma Questionnaire (CTQ), Beck Depression Inventory (BDI) were applied to both groups, along with genotyping. Results: There was no interaction between childhood maltreatment and the 5-HTTLPR in relation to recurrent MDD. All forms of childhood maltreatment were reported as more severe by cases than controls, and there was an independent association between maltreatment and recurrent MDD. Conclusion: The path forward to detect genetic risk loci for depression remains challenging. Taking childhood maltreatment history into account could lead to a richer understanding of differences in biological correlates, genetic underpinnings, and outcomes.