Objective To analyze morbidity,mortality and epidemiological characteristics of epidemic encephalitis B (Japanese encephalitis) from 2002 to 2013 in Zunyi.Methods The descriptive and statistical analysis of the incidence and death of epidemic encephalitis B from 2002 to 2013 in Zunyi was carried out.Results The morbidity and mortality were on a downward trend of epidemic encephalitis B in Zunyi from 2002 to 2013;most of the death and incidence cases occurred in July and August from children living scattered and students under age 15;after immunization expansion,the incidence of encephalitis B showed significant differences between ages,occupations,and time points (P<0.05);in the regional distribution of epidemic encephalitis B,incidence and mortality had significant differences (P<0.05).Conclusion Promising results might be generally obtained after expansion of encephalitis B immunization.However,there is a tendency of shifting back in terms of onset age and month.Therefore,comprehensive prevention measures should be implemented according to the epidemiological features of epidemic encephalitis B.

Objective To explore the association between Q-1 and T1 locus polymorphism in ADAM33 gene and chronic obstructive pulmonary disease in Han population in northern Guizhou by detecting Q-1 and T1 locus polymorphism in ADAM33 gene in patients with COPD in the distribution of frequency ,provide a theoretical basis for the prevention and treatment of COPD. Methods Polymerase chain reaction and DNA sequencing tech-nology,electrophoresis separation method were applied to detect Q-1 and T1 locus polymorphism in ADAM33 gene. Results The genotype distribution of Q-1 and T1 locus in the case group and the control group of ADAM33 gene were in accordance with the Hardy-Weinberg equilibrium law and ADAM33 gene Q-1,T1 locus were C and T alleles. There was no significant difference in genotype and allele frequency distribution between the case group with control group,and COPD complicated with chronic respiratory failure(COPD)and hypoxemia(P > 0.05). T1(83 bp,112 bp)at a high probability of two heterozygous in the same samples(18/19),and is located in the encoding region. Conclusion No association was found between Q-1,T1 locus polymorphism in ADAM33 gene and chronic obstructive pulmonary disease in Han population in northern Guizhou.

Objective To investigate the effect of indoor coal PM2.5 on the airway inflammation and the pathological morphology alterations of lung tissue in asthmatic rats induced by ovalbumin(OVA). Methods Forty six?week?old male SD rats were randomly divided into four groups(Control,OVA,PM2.5,PM2.5+OVA). Normal saline,OVA(15μg/mL)and(or)PM2.5(2.5 mg/mL)were given to rats in the four groups through intratracheal instillation for four times (two weeks one time),respectively. Twenty?four hours after the last intratracheal instillation ,bronchoalveolar irrigation lavage fluid (BALF) was collected for determinations of serum interleukin 4(IL?4),interferon gamma (IFN?γ). The lung tissue was collected for HE staining and electron microscopy detection. Results HE staining showed less inflammatory cell infiltration was observed in the control group;In PM2.5 group and OVA group,there was medium quantity of inflammatory cell infiltration,In PM2.5+OVA group, severe inflammatory cell infiltration was observed. Electron microscopy showed no abnormal lung tissue in the control group,but organelles were gradually destroyed,endothelial cell edama,alveolar interval with a large number of fibersin were observed in PM2.5 group. The exfoliated cells,local typeⅡ cells with visible damage were found in OVA group. A large number of fibers were existed among the lung tissues and organelles were destroyed,thickness of basement membrane was non?uniform,and blood air barrier structure was not clear in PM2.5 + OVA group. Compared with PM2.5+OVA group,concentration of IL?4 in PM2.5,OVA and the control group was siganificantly different(P < 0.05). A negative correlation between IL?4 and IFN?γ was observed (r =-0.358,P < 0.05). Conclusion Indoor coal PM2.5 exacerbates the airway inflammatory cell infiltration and airway remodeling in OVA?induced asthmatic rats.