Objective To investigate the geographic distribution panem of patients with anorectal atresia/stenosis in China.in order to provide clue for research on its etiology.Methods Data were collected from Chinese Birth Defects Monitoring Network(CBDMN),which was a hospital-based congenital malformations registry system.From 2001 to 2005,all fetuses with more than 28 weeks of gestation and neonates up to 7 days of age,were monitored.Two-dimensional graphic cluster method was used to divide monitoring stations into difierent classes with the incidence rates of anorectal atresia/stenosis.Results The overall incidence of anorectal atresia/stenosis was 3.17 per 10000 during 2001 to 2005.The incidence was higher in Eastern than that in Mid or Western paas of China and tbe difierence was statistically significant(z=2.50,3.69;P=0.012,＜0.001).The monitoring stations were grouped into 6 classes.Class I was with Helongjiang,Jilin and Liaoling;Class Ⅱ was with Fujian,Guangdong,Hainan,Guangxi,and South Hunan and Jiangxi;ClassⅢwas with Beijing,Tianjin,Hebei,Shandong,and Noah Jiangsu and Anhui;Class Ⅳ was with Zhejiang,Shanghai,South Anhui and Jiangsu,Noah Hunan and Jiangxi,Hubei,Henan,Shanxi and Inner Mongolia,Class V was with Ningxia,Gansu and Qinghai;and Class Ⅳ was with Shaanxi,Sichuan,Chongqing,Yunnan,Guizhou.Xinjiang and Tibet.Conclusion Our findings discovered the geographic distribution patterns of patients with anorectal atresia/stenosis in China.It is important to further analyze the relevant environmental factors attached to it so a beRer regional monitoring system for anorectal atresia/stenosis can be operated.

Objective To investigate the effects of montelukast on atherescleresis and monocyte chemoattractant protein-1 expression in a hyperchulesterolemic rabbit modeL Methods Thirty four male New Zealand white rabbits were randomized into four groups including normal control group (n=6), placebo in normal control group were fed a high cholesterol diet for 12 weeks. Serum lipids were measured at 0, 8 and 12 weeks after intervention. The intima/media ratio, percentages of macrophages or smooth muscle cells in intima and the expression of MCP-1 mRNA were examined. Results Atheresclerosis was evidenced in placebo group and atorvastatin or montelukast treatment significantly reduced neointima (0.32±0.12 and 0.34±0.10 vs. 1.12±0.36,P<0.05) and macrophage content [(9.8±4.6) % and(11.2±3.7) % vs. (34.6±8.8)%,P<0.05], increased SMC content [(18.6±6.9)% and(19.2±8.6)% vs. (5.2±2.3) %, P<0.05] and inhibited expression of MCP-1 mRNA (0.42±0.08 and 0.40±0.06 vs. 2.36±0.48 ,P<0.01). Montelukast had similar anti-atherogenetic effects as atorvastatin but had no influence on plasma lipids. Conclusions Montelukast could attenuate atherosclerosis in this hyperchulesterolemic rabbit model which might be attributed to its anti-inflammatory effects.