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    Bone mineral metabolism changes in epileptic children receiving valproic acid
    (Wiley, 2004) Öner, N; Kaya, M; Karasalihoglu, S; Karaca, H; Çeltik, C; Tütüncüler, F
    Objective: The aim of this study was to evaluate bone mineral density (BMD) in epileptic children receiving valproic acid (VPA) and to determine differences between osteopenic and non-osteopenic children. Methods: Thirty-three epileptic children, receiving VPA for at least 6 months, were compared with 33 healthy children for BMD. BMD was measured by dual-energy X-ray absorptiometry at lumbar vertebrae, femoral neck and greater trochanter. Serum calcium, phosphorus, alkaline phosphates, osteocalcin and VPA levels were also determined. Results: Patient's osteocalcin levels were significantly higher (P = 0.02) and femur and trochanter BMD values were significantly lower (P = 0.04 and P = 0.03, respectively). Duration of VPA therapy was significantly longer and doses of VPA were significantly higher in seven osteopenic patients compared with 26 non-osteopenic patients. Osteopenic patients (4.6 +/- 2.4 years) were younger than non-osteopenic patients (7.8 +/- 3.2 years) (P = 0.01). Conclusion: Long-term and high dose VPA therapy may cause osteopenia, primarily in younger epileptic children. These patients should be followed closely by BMD measurements.
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    Clinical utility of dorsal sural nerve conduction studies in healthy and diabetic children
    (Elsevier Ireland Ltd, 2004) Turgut, N; Karasalihoglu, S; Kücükugurluoglu, Y; Balci, K; Ekuklu, G; Tütüncüler, F
    Objective: Monitoring of the dorsal sural sensory nerve action potential (SNAP) is a sensitive method for detection of peripheral neuropathies. We tried to determine the normal dorsal sural nerve conduction values of the childhood population and assessed the clinical utility of this method in diabetic children who have no clinical sign of peripheral neuropathy. Methods: In the study, 36 healthy and 27 diabetic children were included. In all subjects peripheral motor and sensory nerve studies were performed on the upper and lower limbs including dorsal sural nerve conduction studies. Results: The dorsal sural SNAP mean amplitude was 8.24 +/- 3.08 muV, mean latency was 2.47 +/- 0.48 ms, mean sensory conduction velocity was 41.63 +/- 5.43 m/s in healthy children. Dorsal sural SNAPs were absent bilaterally in one diabetic patient. In the other 26 diabetic patients, the mean dorsal sural nerve distal latency was longer (2.93 +/- 0.63 ms, P = 0.004), mean SCV was slower than in healthy subjects (36.68 +/- 7.66 m/s, P = 0.005). However, dorsal sural nerve amplitude was not different between the groups. A dorsal sural nerve latency of more than 2.9 ms had a sensitivity of 50% and a specificity of 75%. A dorsal sural nerve velocity of less than 36 m/s had a sensitivity of 54% and a specificity of 92%. Conclusions: We designated the reference values of the dorsal sural nerve in healthy children. In addition, our findings suggest that dorsal sural nerve conduction studies may have value to determine neuropathy in the early stages in children with diabetes. Significance: The dorsal sural nerve conduction studies in diabetic children may have value to determine the neuropathy in its early stages. (C) 2003 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
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    The protective role of melatonin in experimental hypoxic brain damage
    (Blackwell Publishing, 2005) Tütüncüler, F; Eskiocak, S; Basaran, ÜN; Ekuklu, G; Ayvaz, S; Vatansever, Ü
    Background: It is known that oxygen-derived free radicals play an important role in the pathogenesis of brain injury. Melatonin is a powerful scavenger of the oxygen free radicals. In this study, the protective effect of melatonin against the damage inflicted by reactive oxygen species during brain hypoxia was investigated in newborn rats using biochemical parameters. Methods: For biochemical analyses, the levels of lipid peroxidation product (malondialdehyde ([MDA]), levels of reduced glutathione (GSH) and the activities of superoxide dismutase (SOD) and catalase (CAT) were estimated. Results: After the third day of brain hypoxia, the brain levels of MDA increased. Pretreatment of animals with melatonin abolished the rise in MDA induced by hypoxia. GSH concentration did not increase by pretreatment with melatonin. Additonally, the activities of two antioxidative enzymes (SOD and CAT) decreased after the experimental period with melatonin only preventing the change of CAT. The activity of SOD was not influenced by melatonin administration as expected. Conclusion: In this experimental study, exogenously administered melatonin effectively protected against brain injury by oxidative stress. This protective effect of melatonin may be due to its direct scavenger activity and activation of CAT. Thus, melatonin may potentially be useful in the treatment of neurodegenerative conditions that may involve free radical production, such as perinatal hypoxia.