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    Serum levels of soluble P-selectin are increased and associated with disease activity in patients with Behcet's syndrome
    (Hindawi Ltd, 2005) Turkoz, Y; Evereklioglu, C; Özkiris, A; Mistik, S; Borlu, M; Özerol, IH; Duygulu, F
    Behcet's syndrome (BS) is a relapsing, chronic, inflammatory disease characterized by endothelial dysfunction, atherothromboembogenesis, and leukocytoclastic vasculitis with complex immunologic molecular interactions. Generalized derangements of the lymphocyte and neutrophil Populations, activated monocytes, and increased PMNLs motility with upregulated cell surface Molecules such as ICAM-1, VCAM-1, and E-selectin, which are found on the endothelial cells, leukocytes, and platelets, have all been demonstrated during the Course of BS. Our aim is to investigate the association of serum concentrations of soluble P-selectin in patients with BS, and to evaluate whether disease activity has an effect on their blood levels. This multicenter study included 31 patients with BS (15 men and 16 women) and 20 age- and sex-matched health), control volunteers (11 men and nine women). Neutrophil count, erythrocyte sedimentation rate, and acute-phase reactants as well as soluble P-selectin levels were determined. The mean age and sex distributions were similar (P>.05) between BS patients (35 years) and control volunteers (36 years). Serum levels of soluble P-selectin in patients with BS (399 +/- 72 ng/mL) were significantly (P<.001) higher when compared with control subjects (164 +/- 40 ng/mL). In addition, active BS patients (453 37 ng/mL) had significantly (P<.001) elevated levels of soluble P-selectin than those in inactive period (341 +/- 52 ng/mL). This study clearly demonstrated that serum Soluble P-selectin levels are increased in BS patients when compared with control Subjects, Suggesting a modulator role for soluble P-selectin during the Course of platelet activation and therefore, atherothrombogenesis formation in BS, especially in active disease.
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    Tumour necrosis factor ?, lipid peroxidation and NO• are increased and associated with decreased free-radical scavenging enzymes in patients with Weill-Marchesani syndrome
    (Hindawi Ltd, 2004) Evereklioglu, C; Turkoz, Y; Calis, M; Duygulu, F; Karabulut, AB
    AIM: Weill-Marchesani syndrome (WMS) is a rare systemic disorder with both autosomal recessive and dominant inheritances. Accumulation of reactive oxygen species such as O-2(.-), H2O2 and OH. causes lipid peroxidation (LPO), whereas antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GSHPx)) mediate defence against oxidative stress. Excess tumour necrosis factor (TNF)-alpha and NO. react with O-2(.-) and cause further antioxidant depletion with an increase in mutation frequency by H2O2. This study investigated the levels of SOD, GSHPx, catalase (CAT), TNF-alpha, NO. and LPO in patients with WMS. Methods: A group of 10 WMS patients (four males, six females; age, 26.5 +/- 19.0 years) and 10 age-matched and sex-matched controls (five males, five females; age, 27.3 +/- 18.2 years) were included. Serum TNF-alpha levels were determined by a spectrophotometer technique using immulite chemiluminescent immunometric assay. Malondialdehyde (MDA) was determined in plasma; CAT in red blood cells (RBCs), and SOD and GSHPx in both plasma and RBCs. Total serum NO. levels were evaluated by Griess reaction. Results: Mean levels of TNF-alpha (8.3 +/- 0.6 pg/ml) in WMS patients were significantly (p < 0.001) higher than controls (4.3 +/- 0.2 pg/ml). Plasma MDA levels in patients and controls were 5.4 +/- 0.8 and 1.8 +/- 0.6 mu mol/l, respectively, and the difference was significant (p = 0.0002). SOD and GSHPx activities were significantly lower in both RBCs and plasma of WMS than in controls (RBC-SOD, 3981.9 +/- 626.6 versus 5261.6 +/- 523.0 U/g haemoglobin (Hb), p = 0.0005; plasma-SOD, 529.4 +/- 49.3 versus 713.4 +/- 55.7 U/g protein, p = 0.0002; RBC-GSHPx, 682.7 +/- 42.0 versus 756.5 +/- 47.6 U/g Hb, p = 0.0011; plasma-GSHPx, 107.3 +/- 15.0 versus 131.4 +/- 19.7 U/g protein, p = 0.0113). In addition, serum NO center dot (NO2- + NO3-) levels were also significantly (p = 0.0002) increased in WMS patients (54.4 +/- 5.7 versus 26.9 +/- 6.7 mumol/l). RBC-CAT levels were similar between groups (125.6 +/- 21.3 versus 131.0 +/- 21.5 k/g Hb, p = 0.8798). Conclusions: The elevated LPO, TNF-alpha and NO. with decreased antioxidant enzyme activities indicated impaired antioxidative defence mechanisms with an oxidative injury and cell toxicity in WMS patients. The use of multiple antioxidants and free radical scavengers might be helpful in this genetic disorder.
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    Urinary nitric oxide levels are increased and correlated with plasma concentrations in patients with Behcet's disease
    (Wiley, 2003) Evereklioglu, C; Özbek, E; Çekmen, M; Mehmet, N; Duygulu, F; Ozkiris, A; Çalip, M
    Nitric oxide ( NO) is a free radical and serves many functions within the kidney. Excess NO causes glomerular injury. Behcet's disease (BD) is a systemic immunoinflammatory vasculitis, affecting every organ in the body including the kidneys ( subclinic glomerulonephritis). We investigated the role of urinary total nitrite levels (end product of NO) in BD and evaluated whether urinary concentrations were correlated with its plasma levels or disease activity. Thirty-six consecutive Behcet's patients (19 men, 17 women; 35.9 years), and 20 age- and sex-matched healthy control volunteers (12 men, eight women; 33.2 years) were divided into an active (n = 16) and inactive ( n = 20) period. Urinary and serum NO levels (mumol/mg urinary creatinine) were higher in BD patients (4.1 +/- 0.3) than control subjects (1.7 +/- 0.2; P < 0.001). Serum NO levels in Behcet's patients and control subjects were 51.3 +/- 9.8 and 21.7 +/- 7.3 mu mol/ L, respectively (P < 0.001). Active patients had higher urinary NO excretion (4.9 +/- 0.3) than inactive patients (3.3 +/- 0.3; P < 0.01). Urinary NO levels were correlated with its serum levels (r(2) = 0.69, P < 0.001). Higher urinary NO levels found in BD may be produced by the kidney as a result of an inflammatory stimulation. As excess NO is toxic to the tissues, increased NO levels may play a role in mediating subclinic glomerular injury of such patients. However, we could not determine the exact site(s) of NO synthesis by the kidney, such as the glomeruli, blood vessels and/or the tubular cells. Whatever the source, urinary NO levels may be used as a new activity marker in the diagnosis and follow up of BD by serial measurements.