Ultrasound is a safe, non-invasive technique that provides a more precise and objective method of determining thyroid volume than inspection and palpation, particularly in areas of mild endemicity, and generally whenever goiters are small. Thyroid volume is also correlated with age, weight, height and body surface area (BSA) in non-iodine-deficient areas. Different authors prefer different parameters to assess thyroid gland volumes. In this study, thyroid volumes were determined using ultrasound in 605 school children aged 6-11 yr who had been living for at least 5 years in Antalya. The correlation between age, BSA, height, weight, BMI and thyroid volume was sought in this mild to moderate iodine-deficient area. Somatic development of our children was in the normal range. Thyroid volume was significantly correlated with age (r=0.41, p<0.001), height (r=0.33, p<0.001), weight (r=0.30, p<0.001), BSA (r=0.33, p<0.001), and BMI (r=0.13, p<0.001). The most significant correlation was found to be with age. The application of the International Council for Control of Iodine Deficiency Disorders (ICCIDD) and the World Health Organization (WHO) thyroid volume references to our subjects resulted in prevalence estimates of enlarged thyroid of 31% based on BSA and of 34% based on age. In conclusion, when thyroid volumes are to be compared with reference values, assessment of thyroid volumes based on age is the most reliable method, in the event of normal somatic development.
ABSTRACT.Purpose: The aim of the study was to investigate the effects of vitamin E on stress-induced changes in visual evoked potentials (VEPs) and lipid peroxidation. Methods: Eight experimental groups of 10 rats per group were formed. These consisted of the control group (C); the group treated with vitamin E (E); groups exposed to cold stress (CS), immobilization stress (IS) and both cold and immobilization stress (CIS), and groups exposed to equivalent stresses and treated with vitamin E (CSE, ISE, CISE). Vitamin E was injected intramuscularly in a dose of 30 mg/kg/day. Results: Following chronic stress (15 days), plasma corticosterone concentrations in all experimental groups were significantly increased over those in C group. Vitamin E significantly decreased corticosterone levels in all stress groups compared with their respective control groups. Brain nitrite levels were significantly more elevated in all stress groups than in the C group. Vitamin E reduced retina and brain nitrite levels in all stress and E groups compared with their respective control groups. Vitamin E decreased glutathione peroxidase (GSH-Px) activity in retina and brain tissues in the CSE group, but increased it in the ISE group compared with their respective control groups. Lipid peroxidation was increased in brain and retina tissues in all stress groups as indicated by the significant increase in thiobarbituric acid-reactive substance (TBARS) levels with respect to the C group. Vitamin E produced a significant decrease in brain and retina TBARS levels in all stress groups with respect to their corresponding control groups. The mean latencies of P 1 , N 1 , P 2 , N 2 and P 3 components were significantly prolonged in all stress groups compared with the C group. Conclusion: Vitamin E returned the VEP latencies in the stress groups to control values. Our findings clearly indicated that vitamin E has the potential to prevent VEP changes caused by stress.
The effect of sulfur dioxide (SO(2)) on somatosensory-evoked potentials (SEPs), thiobarbituric acid reactive substances (TBARS), and the activities of Cu,Zn-superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were investigated in young (3 months), middle-age (12 months), and old (24 months) Swiss male albino rats. Ten ppm SO(2) was administrated to the animals of SO(2) groups in an exposure chamber for 1 h/day x 7 days/week x 6 while control groups were exposed to filtered air in the same condition. SO(2) exposure caused increased levels of brain Cu,Zn-SOD activity and decreased levels of brain GSH-Px activity in all experimental groups with respect to their corresponding control groups. Brain CAT activities were unaltered. Brain TBARS levels of all SO(2)-exposed groups were significantly increased in comparison with their respective control groups. The mean latencies of P(1), P(2), and N(2) components in the older group were either significantly different from the young or from the middle-age groups. The mean latency of the N(1) component in the older group and that of P(1) and N(1) in the middle-age group were significantly increased compared with the young group. SO(2) exposure caused the prolongation of all components in the young group, whereas it affected only the P(2) component in the middle-age group, but it did not result in any latency change in the older group in comparison with their corresponding control groups.http://link.springer-ny. com/link/service/journals/00244/bibs/37n4p554.html++ +HEA
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