Objective To explore a practicable method for analyzing the cost losses of residents' health impact induced by environmental pollution and evaluate the cost losses of local residents' health impact in arsenic contaminative area. Methods The data on residents' health were obtained in an arsenic polluted area as the basis analysis of economic loss. Additionally, the data on the sizes of local population, GDP, the annual personal income, the annual prevalence of acute diseases, absence due to sickness and patients' nursing care, the annual prevalence of chronic diseases in 1985. Local residents' age specific death rates and sizes of population in 1985-1995 were collected also. 3 mumerable indexes were screened for estimating the cost losses of residents' a health impact in arsenic contaminative area based on the data mentioned above and combined with abridged life table. Results Based on the calculated GDP and personal average income in 1995, the cost losses of residents due to arsenic pollution consisted of 3 sections: the first included GDP losses of 50.52 yuan/(person-year) and personal income loss of 43.71 yuan/(person-year) attributed to the reduced life expretancy of the residents living in arsenic-polluted area. The second was an excess of the annual medical expenditure of 56.30 yuan/(person-year) for residents living in arsenic-polluted area compared with that of control group. The third included GDP loss of 74.14 yuan/(person-year) and income loss of 64.23 yuan/(person' year) attributed to the health life days of residents in arsenic-polluted area during the period of number of working years. The total economic loss of 3 section mentioned above make the total GDP reduction of about 180.96 yuan/(person-year) and average income loss of about 164.27 yuan/(person-year) including excessive medical costs. Conclusion The analytical method could be applied to the estimation of economic loss of environmental pollution-attributable health impact.

Objective To evaluate the clinical value bronchofiberscope and perfusion in the treatment of multi- drug resistant pulmonary tuberculosis (MDR-TB).Methods Forty-two cases were treated by injecting amikacin (0.4 g), ofloxacin (0.4 g), after cleaning up exudation through bronchofiberscope and catheter intervention combined with chemotherapy therapy, while 37 controls were treated by chemotherapy only.Results By the end of 9 months, the sputum tubercle bacillus conversion rate, radiographical improvement rate were 92.9% and 90.5% respectively in the treated groups,while all these indications were higher than those of control group 62.2% and 59.5% (P

Objective To explore and compare the mechanism of high-fructose and high-fat diet induced triglyceride excessive accumulation in mice liver and its relationship with endoplasmic reticulum (ER) stress.Methods 45 Adult male C57BL/J6 mice,weight arranged from 25 gram to 30 gram were randomly divided into control group,high-fructose group and high-fat group,15 mice in each group.Common food was fed in control group,high-fructose food was fed in high-fructose group,high-fat food was fed in high-fat group,and the everyday calories consumption in 3 groups was almost equal.Intraperitoneal glucose tolerance test (ipGTT) was performed after feeding for 8 weeks.After mice were sacrificed,triglyceride content,lipogenic enzymes and ER stress markers expression in liver tissues of each group were measured.Results After feeding with different food for 8 weeks,the fat content of epididymis in high-fructose group and high-fat group both was (2.0±0.1) g/100 g (body weight),which was significantly higher than that of control group (1.2 ± 0.1) g/100 g (body weight),P＜0.01).After ipGTT test,the area under curve of blood glucose in high-fructose group and high-fat group was significantly higher than that in control group (P＜0.01).Compared with control group,triglyceride contents of liver tissues in high-fructose group and high-fat group were significantly increased,of those triglyceride contents in high-fructose group increased more obviously,and triglyceride contents in high-fructose group was significantly higher than that of high-fat group (P＜0.01).Compared with control group,the expression of acylCoA carboxylase (ACC),fatty acid synthase (FAS) and stearoyl-CoA desaturase 1 (SCD-1) increased in high-fructose group (P＜0.01),while decreased in high-fat group (P＜0.05) ; meanwhile,the expression of phosphorylated pancreatic ER kinase (p-PERK),inositol requiring enzyme 1 (p-IRE-1/t-IRE-1)and glucose-regulated protein 78 (GRP78) was up-regulated in both high-fructose group and high-fat group (all P＜0.01).Conclusion Both high-fructose diet and high-fat diet can induce fatty liver through different mechanisms.High-frucose diet promotes endogenous lipogenesis while high-fat diet inhibits endogenous lipogenesis.Both dietary factors can induce ER stress,which indicate that ER stress is associated with pathogenesis and development of food factors induced fatty liver.