Objective To understand the causes and the ratio of cause constituents in children with chronic cough in Beijing. Methods Patients with chronic cough treated at respiratory clinic of the Children' s Hospital Affiliated to Capital Institute of Pediatrics from May 2009 to April 2011 were included in this study. Etiologic diagnostic procedure suggested for children by the Subspecialty Group of Respiratory Diseases,the Society of Pediatrics,Chinese Medical Association in 2008 was implemented to manage the patients. After three - month follow - up,the etiological data was analyzed. Results Totally 213 patients with chronic cough aged 1. 1 to 14. 0 years old were enrolled,inclu-ding 40 cases(18. 8% )aged≤3 years old,134 cases(62. 9% )aged ﹥ 3 to 6 years old,and 39 cases(18. 3% ) aged ﹥ 6 years old. The majority of patients with positive allergen tests were sensitized to inhaled allergens. One child had positive result in 24 - hour esophageal pH monitoring,but his cough didn't respond well to the specific treatment for gastroesophageal reflux,so he wasn't diagnosed as gastroesophageal reflux cough. The 4 leading causes of the 213 pa-tients with chronic cough were cough variant asthma(CVA)in 92 cases(43. 2% ),CVA associated with upper airway cough syndrome(UACS)in 57 cases(26. 8% ),UACS in 28 cases(13. 2% ),respiratory infection and post - infec-tion cough(PIC)in 26 cases(12. 2% ),while other causes were found in 8 cases(3. 7% ),and unknown etiology in 2 cases(0. 9% ). The incidence of CVA ranked top 1 in all the 3 age groups,followed by PIC in ≤3 years old group, while CVA associated with UACS in the other 2 age groups. Conclusions CVA,CVA associated with UACS,UACS and PIC were the 4 leading causes for children with chronic cough in Beijing. Children in different age groups had dif-ferent constituents ratio of causes of chronic cough.

the effect of maintaining integrity of epithelial cells by increasing occludin protein expression,and the effect is related with the up-regulation of occludin mRNA.

Objective To detect the changes of number and function of endothelial progenitor cells (EPCs) in gld.apoE-/-C57BL/6 mice,and to investigate whether premature atherosclerosis of gld.apoE-/-C57BL/6 mice was mediated by the dysfunction of these EPCs.Methods EPCs were isolated from peripheral blood and bone marrow of four types of C57BL/6 female mice:gld+/+apoE+/+,gld,apoE-/-and gld.apoE-/-.The percentage of EPCs was analyzed by FACS as CD11b-Sca-1+CD309+ cells.The attached cells were stained with DiI labeled acetylated low-density lipoprotein (DiI-ac-LDL) and FITC-labeled Ulex Europaeus agglutinin 1 (FITC-UEA-1) double staining to determine their phagocytic function.The adherent function of EPCs was determined by calculating the number of re-cultured EPCs.The capacity of EPCs to form the cavity structure was detected by calculating the number of the formed vascular-like structure.Results The percentage of circulating EPCs was significantly decreased in the gld.apoE-/-group (0.012±0.002)％ compared to the gld+/+ apoE+/+ group [(0.039±0.005)％,P＜0.01],the gld group [(0.025±0.001)％,P＜0.05],and the apoE-/-group [(0.028±0.002)％,P＜0.01].The percentage of bone marrow derived EPCs was decreased in the gld.apoE-/-group (0.12±0.01)％ compared to the gld+/+apoE+/+ group [(0.42±0.05)％,P＜0.05].The percentage of DiI-acLDL and FITC-UEA-1 double positive cells was decreased in the gld.apoE-/-group [(59.2±2.1)％] compared to the gld+/+apoE+/+ group [(87.5±3.0)％,P＜0.01],and the gld group [(84.2±6.0)％,P＜0.01] ; the adherent function of EPCs was impaired in the gld.apoE-/-group [(50.0±5.3)％] compared to the gld+/+ apoE+/+ group [(86.0±7.3)％,P＜0.01],the gld group [(73.0±1.0)％,P＜0.01],and the apoE-/-group [(65.0±4.0)％,P＜0.05] respectively.The capacity of EPCs to form the cavity structure was decreased in the gld.apoE-/-group (4.0±0.3) compared to the gld+/+apoE+/+ group (12.0±1.4,P＜0.01).Conclusion The number of EPCs is decreased in the gld apoE-/-C57BL/6 mice,the adhesion,phagocytosis and angiogenic function of EPCs in the bone marrow are impaired,which may be one of the causes of lupus with atherosclerosis.