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    Relationship among serum selenium levels, lipid peroxidation, and acute bronchiolitis in infancy
    (Humana Press Inc, 2004) Gurkan, F; Atamer, Y; Ece, A; Kocyigit, Y; Tuzun, H; Mete, M
    Thirty-four infants with acute bronchiolitis and 25 age-matched healthy controls were enrolled to investigate the possible relationship between serum malondialdehyde (MDA) and selenium (Se) levels and the occurrence and severity of acute bronchiolitis in children. Serum samples were taken for serum Se and MDA measurements, and the clinical score was assessed at admission. Blood was taken again from the children with bronchiolitis at 2 mo after discharge from the hospital. Mean serum MDA levels were significantly higher in patients with acute bronchiolitis than at the postbronchiolitis stage and the controls (4.2+/-2.5 nmol/L, 1.4+/-0.8 nmol/L, and 0.7+/-0.2 nmol/L, respectively [p<0.001]). Infants with bronchiolitis had lower mean serum Se levels at the acute stage than after 2 mo (31.7+/-28.9 mug/L versus 68.4+/-26.4 mug/L, p<0.05, respectively); both of which were significantly lower than the control group measurements (145.0+/-21.9 mug/L) (p<0.001). There was a negative correlation between serum MDA and Se levels in the patient group (r=-0.85, p<0.001). The age of the patient, child's immunization status, parental smoking habit, and family crowding index were not correlated with serum Se, MDA levels, or clinical score at admission. In conclusion, increased MDA levels and impaired Se status demonstrate the presence of possible relationship of these parameters with pathogenesis of acute bronchiolitis, and antioxidant supplementation with Se might be thought to supply a beneficial effect against bronchiolitis.
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    Serum leptin levels in asthmatic children treated with an inhaled corticosteroid
    (Amer Coll Allergy Asthma Immunology, 2004) Gurkan, F; Atamer, Y; Ece, A; Kocyigit, Y; Tuzun, H; Mete, N
    Background: Recent observations suggest the presence of an interaction between leptin and the inflammatory system; however, there is no adequate knowledge about the role of leptin in atopic states such as asthma. Objectives: To evaluate the potential role of leptin in relation to bronchial asthma and inhaled corticosteroid therapy. Methods: Twenty-three children with mild-to-moderate, newly diagnosed asthma enrolled in this 2-period trial. The control group consisted of 20 age- and sex-matched children. Serum leptin levels were measured in patients at initiation and after 4 weeks of budesonide treatment and were compared with control group measurements. Results: Asthmatic children had higher mean +/- SD serum leptin levels at admission (19.3 +/- 5.1 ng/mL) than after budesonide treatment (10.6 +/- 1.6 ng/mL) and vs control group measurements (9.8 +/- 1.6 ng/mL) (P < .001). There was a significant correlation between serum leptin levels before and after budesonide treatment (r = 0.68; P = .007). Mean +/- SD body mass indices in patients and controls were 16.7 +/- 2.1 and 16.9 +/- 2.6 kg/m(2), respectively. Serum leptin levels did not correlate with body mass indices before budesonide treatment in the study group (r = -0.13; P = .65) but correlated well after budesonide treatment (r = 0.58; P = .009) and in the control group (r = 0.65; P = .008). Conclusions: The role of leptin elevation in children with asthma might be a regulatory mechanism rather than being etiologic, but a question may be raised whether it is possible that leptin may contribute to poor patient outcomes. Further research, both basic and clinical, is essential to explain the exact mechanism.