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    Association of ambulatory arterial stiffness index with sEPCR in newly diagnosed hypertensive patients
    (Taylor & Francis Ltd, 2015) Yilmaz, Hakki; Cakmak, Muzaffer; Inan, Osman; Darcin, Tahir; Aktas, Aynur; Gurel, Ozgul Malcok; Bilgic, Mukadder Ayse
    Aim: Increased arterial stiffness is strongly associated with cardiovascular diseases, while thrombotic events are more common than hemorrhagic events in hypertensive patients. Markers of a hypercoagulable state may also predict future cardiovascular events in hypertensive patients. Here, we speculated that increased arterial stiffness might lead to the development of a hypercoagulable state that can play a role in the thrombotic complications of hypertension. Soluble endothelial protein C receptor (sEPCR) is one such marker of hypercoagulation. The ambulatory arterial stiffness index (AASI) could be accepted as a non-invasive measure of arterial stiffness. The aim of this study was to investigate association of AASI with levels of sEPCR in newly diagnosed hypertensive patients. Materials and methods: The study included 263 newly diagnosed essential hypertensive patients and 55 healthy normotensive controls. All subjects underwent 24 h ambulatory blood pressure monitoring (ABPM); the AASI was derived from ABPM tracings. Plasma sEPCR was measured by ELISA. Results: Hypertensive patients (n=263) had higher AASI, C-reactive protein (CRP) and sEPCR versus the normotensive healthy group (n=55). Univariate analysis showed that AASI was positively associated with age (r=0.212, p< 0.001) body mass index (r=0.412, p<0.001), pulse pressure (r=0.350, p<0.001), plasma sEPCR (r=0.894, p<0.001), 24-h heart rate (r=0.176, p=0.001) and inversely related to high-density lipoprotein (HDL) (r=-0.293, p<0.001). Multivariate analyses revealed that sEPCR and HDL are independently correlated to AASI. Conclusion: We suggest that increased AASI is associated with elevated sEPCR. It might be responsible for subsequent thrombotic events in newly diagnosed hypertensive patients.
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    Circulating irisin levels reflect visceral adiposity in non-diabetic patients undergoing hemodialysis
    (Taylor & Francis Ltd, 2016) Yilmaz, Hakki; Cakmak, Muzaffer; Darcin, Tahir; Inan, Osman; Sahiner, Enes; Demir, Canan; Aktas, Aynur
    Background: Recent evidence suggests that increased visceral adiposity is a strong independent risk factor for cardiovascular death and all-cause mortality in hemodialysis (HD) patients. Irisin, which is a novel myokine, can play critical roles in diabetes and adiposity. The purpose of our study was to investigate whether serum irisin levels are associated with body mass index, waist circumference (WC), and total fat mass in non-diabetic patients undergoing maintenance HD.Methods: This cross-sectional study included 108 non-diabetic HD patients and 40 age- and sex-matched apparently healthy subjects. Serum irisin concentrations were determined using an enzyme-linked immunosorbent assay. Body fat composition (TBF-410 Tanita Body Composition Analyzer) was measured and calculated.Results: Serum irisin levels did not differ between HD patients and the healthy controls (523.50 +/- 229.32 vs. 511.28 +/- 259.74, p=0.782). Serum irisin levels were associated with age (r=0.314; p=0.006), HOMA-IR (r=0.472; p=0.003), WC (r=0.862; p<0.001), and total fat mass (r=0.614; p<0.001). In multivariate regression analysis, WC (=1.240, p<0.001) and total fat mass (=0.792, p=0.015) were the variables that were significantly associated with irisin concentrations (R-2=0.684, p<0.001) after adjusting for confounding factors (age and HOMA-IR). Conclusions: These results suggest that serum irisin levels are related to visceral adiposity in non-diabetic HD patients.
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    Role of interlekin-35 as a biomarker in patients with newly diagnosed hashimoto’s thyroiditis
    (Institute of Experimental Endocrinology macvetrev@fvm.ukim.edu.mk, 2016) Yilmaz, Hakki; Çakmak, Muzaffer; Ceydilek, Bilge; Demir, Canan; Aktas, Aynur
    Objective. Interleukin-35 (IL-35), an interleukin-12 (IL-12) cytokine family member, is shown to be a potent immunosuppressive and anti-inflammatory cytokine. Inducible regulatory T cells (Tregs) produce IL-35 that mediates the immune inhibitory function of Tregs. Growing evidence revealed that upregulation of IL-35 expression may play a critical role in the prevention of autoimmune diseases in various experimental autoimmunity models and vice versa. Hashimoto’s thyroiditis (HT) is considered to be a Treg cell-related autoimmune disease with loss of self-tolerance. Methods. One hundred-twenty eight subjects, newly diagnosed hypothyroid HT patients [56 overt (Group 1), 72 subclinical hypothyroid (Group 2)] and 38 healthy controls (Group 3) were enrolled in the study. The levels of serum IL-35 were determined by enzyme-linked immunosor-bent assay (ELISA). Results. Serum IL-35 levels were lower in the HT group when compared with subclinical HT group [304.5 (834.6) pg/ml vs. 636.1 (1542.0) pg/ml, p=0.004] and control cases [304.5 (834.6) pg/ml vs. 1064.7 (2526.8) pg/ml, p<0.001]. Serum IL-35 levels were inversely associated with thyroid stimulating hormone (TSH; rs=–0.396, p<0.001) and anti-thyroid peroxidase antibodies (TPOAb; rs=–0.571, p<0.001) in whole group. Serum IL-35 were negatively associated with TSH (rs=–0.264, p=0.003) and TPOAb (rs=–0.735, p<0.001) in patients with Hashimoto’s thyroiditis (Group 1 + Group 2). Conclusion. The results suggest that IL-35 may play a role in the pathogenesis of HT. © 2020 Elsevier B.V., All rights reserved.
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    Serum levels of endocan correlate with the presence and severity of pre-eclampsia
    (Taylor & Francis Inc, 2016) Cakmak, Muzaffer; Yilmaz, Hakki; Baglar, Esra; Darcin, Tahir; Inan, Osman; Aktas, Aynur; Celik, Huseyin Tugrul
    Background: Endocan, a cysteine-rich dermatan sulfate proteoglycan expressed by endothelial cells, is seemed to be a new biomarker for endothelial dysfunction. Pre-eclampsia (PE) is characterized by the new onset of hypertension, proteinuria after 20 weeks of gestation, placental vascular remodeling, systemic vascular inflammation and endothelial dysfunction. The aim of this study was to investigate the relationship of PE and its severity with serum endocan levels. Methods: A cross-sectional study was performed. Serum was collected from women with PE and normotensive controls. Serum endocan and tumor necrosis factor alpha (TNF-alpha) concentrations were measured by a specific enzyme linked immunosorbent assay. Results: Patients with PE had significantly higher median (interquartile range) endocan and mean TNF-alpha concentrations than controls [20.04 (12.26) ng/mL vs 15.55 (6.19) ng/mL, p < 0.001 for endocan; 26.49 +/- 12.14 pg/mL vs 14.62 +/- 5.61 pg/mL, p < 0.001 for TNF-alpha; respectively]. Serum endocan concentrations were positively correlated with systolic blood pressure (r = 0.618, p < 0.001), diastolic blood pressure (r = 0.608, p < 0.001), the amount of 24-h proteinuria (r = 0.786, p < 0.001) and TNF-alpha (r = 0.474, p < 0.001) in women with PE. In subgroup analysis, patients with severe PE had significantly higher endocan concentrations than those with mild PE. Receiver operating characteristic analysis of endocan was used to identify the patients with PE and also discriminating between mild and severe PE. Conclusion: Serum endocan concentrations were significantly elevated in women with PE versus normotensive controls, and concentrations seem to be associated with the severity of the disease.