- Prediction of the risk of skin cancer caused by UVB radiation exposure using a method of meta-analysis.
-
D C Shin, J T Lee, J Y Yang
-
Korean J Prev Med. 1998;31(1):91-103.
-
-
-
Abstract
PDF
- Under experimental conditions, UVB radiation, a type of ultra violet radiation, has shown to relate with the occurrence of skin erythema (sun-burn) in human and skin cancer in experimental animal. Cumulative exposure to UVB is also believed to be at least partly responsible for the "aging" process of the skin in human. It has also been observed to have an effect of altering DNA (deoxyribonucleic acid). UVB radiation is both an initiator and a promotor of non-melanoma skin cancer. Meta-analysis is a new discipline that critically reviews and statistically combines the results of previous researches. A recent review of meta-analysis in the field of public health emphasized its growing importance. Using a meta-analysis in this study, we explored more reliable dose-response relationships between UVB radiation and skin cancer incidence. We estimated skin cancer incidence using measured UVB radiation dose at a local area of Seoul (Shin chon-dong). The studies showing the dose-response relationships between UVB radiation and non-melanoma skin cancer incidence were searched and selected for a meta-analysis. The data for 7 reported epidemiological studies of three counties (USA, England, Australia) were pooled to estimated the risk. We estimated rate of incidence change of skin cancer using pooled data by meta-analysis method, and exponential and power models. Using either model, the regression coefficients for UVB did not differ significantly by gender and age. In each analysis of variance, non-melanoma skin cancer incidence after removing the gender and age and UVB effects was significant (p>0.01). The coefficients for UVB dose were estimated 2.07x10-6 by the exponential model and 2.49 by the power model. At a local area of Seoul (Shin chon-dong), BAF value were estimated 1.90 and 2.51 by the exponential and power model, respectively. The estimated BAF value were increased statistical power than that of primary studies that using a meta-analysis method.
-
Summary
- Interaction of Sodium Selenite on Neurotoxicity Induced by Methylmercuric Chloride.
-
J S Park, H M Lee, Y Chung, D C Shin, J H Roh, Y H Moon
-
Korean J Prev Med. 1992;25(1):13-25.
-
-
-
Abstract
PDF
- This study was conducted to investigate the mechanism of protective effect by sodium selenite in Methylmercuric chloride neurotoxicity, increasing intracellular Ca2+ concentration of the neuron. Methylmercuric chloride of 3 mg/kg of body weight was administered simultaneously with sodium selenite of 5 mg/kg and pretreatment of sodium selenite via intraperitoneal injection to rats. Also, effect of methylmercuric chloride(25 micrometer, 50 micrometer, 100 micrometer) and sodirum selenite(200 micrometer) on free intrasynaptosomal Ca2+ concentration were studied using the fluorescent Ca2+ indicator fura2 in vitro. After the treatment, at 6, 24, and 48 hours later, mercury in the cerebral cortex, liver and kidney tissues, succinic dehydrogenase activities, adenosin-5'-triphosphate concentration, acetylcholinesterase activities, and intracellular Ca2+ concentration in the cerebral cortex were determined in vivo. Cerebral synaptosomes of rats were incubated with methylmercuric chloride and sodium selenite in Hepes buffer for 10 minutes and free intrasynaptosomal Ca2+ concentration were measured with fura2 in vitro.The results were summarized as follows; 1. The combined administration of CH3HgCl and Na2SeO3 and pretreatment of Na2SeO3 according to time significantly more increased in the cerebral cortex and decreased in the liver, kidney mercury concentrations compared to the administration of CH3HgCl only. 2. The combined administration of CH3HgCl and Na2SeO3 and pretreatment of Na2SeO3 increased more succinic dehydrogense and acetylcholinesterase activities compared to the administration of CH3HgCl only. Particularly pretreatment of Na2SeO3 significantly more compared to the administration of CH3HgCl only. The concentration of adenosine-5'-triphosphate in Na2SeO3 treatment groups revealed a favourable effect compared to the administration of CH3HgCl only. 3. Intracellular Ca2+ concentration in administration of CH3HgCl only was increased significantly more than control group in all test hours but was increased significantly more at 48 hous only after treatment in combined administration of CH3HgCl and Na2SeO3 and pretreatment of Na2SeO3 according to time interval more decreased significantly intracellular Ca2+ concentration compared to the administration of CH3HgCl only. 4. Free intrasynaptosomal Ca2+ concentration in the combined administration of CH3HgCl and Na2SeO3 was decreased (24%-40%) significantly more than the administration of CH3HgCl only. From the above results, the specific dosage of Na2SeO3 decreased increment of intracellular Ca2+ concentration induced by administration of CH3HgCl. These findings suggest the protective mechanism of Na2SeO3 on the neurotoxicity of CH3HgCl.
-
Summary
|