Objective To analyze outcome of pulmonary tuberculosis(TB) patients in different household in Shenzhen in 2008, and provide scientific basis for development of TB control strategy. Methods The data from monthly,quarterly,annual report as well as the TB report card and other related information were collected and analyzed. Results A total of 4 826 active pulmonary tuberculosis patients were found in 2008, in which 86.0% were mobile population;2 349 cases of new smear positive pulmonary tuberculosis patients were found;Mobile population cure rate of new smear positive(75.0%) was significantly lower than that of household population(P＜0.01). Mobile population moving out or loss rate of new smear positive(13.5%) was significantly higher than that of household population(P＜0.01). Conclusion Mobile population cure rate of new smear positive was lower and moving out or loss rate of new smear positive(13.5%) was higher. Mobile population TB control in Shenzhen was the key and difficult.

Objective To understand the situation of drug resistance( DR) and multi-drug resistance( MDRTB) tuberculosis in Shenzhen and provide scientific evidence for TB control in Shenzhen. Methods According to drug resistance TB guidelines issued by WHO/IUALD, all new smear positive cases and.new registered retreatment smear positive cases in 2005 and 2009 were included in the surveillance. A total of 1856 strains of mycobacterium tuberculosis were isolated and drug susceptibility test were performed with the proportional method. Results In 2005, the overall DR rate was 18. 3% , 17. 2% and 31. 3% for initial and acquired DR respectively, overall MDR rate was 4. 74% ,3.25% and 21.9% respectively for initial and acquired MDR. In 2009, the overall DR rate was 17.4% , 16% and 39. 3%for initial and acquired DR respectively,overall MDR rate was 3.8% ,3.02% and 16.4% respectively for initial and acquired MDR. In 2005,2009, the rates of acquired DR and acquired MDR were significantly higher than the rates of initial DR and initial MDR. Conclusion The incidence of TB drug resistance in Shenzhen was high and merits attention.

BACKGROUND: The study aims to correlate osteogenesis with autophagy during the mineralization induction of MC3T3-e1 through exploring the expression of runt-related transcription factor 2 (RUNX2)/lysosomal-associated transmembrane protein 5 (LAMPT5). METHODS: The induction of mineralization in MC3T3-e1 was followed by detecting the expressions of osteogenesisrelated indexes such as RUNX2, alkaline phosphatase (ALP), osteocalcin (OCN), and LAPTM5 using RT-qPCR and Western blot from 0 to 14 days. Transmission electron microscope was utilised in visualizing the alterations of autophagosomes, which was followed by immunofluorescence detecting the subcellular localization of autophagy-related index sequestosome 1 (P62) and microtubule-associated protein 1 light 3 (LC3) protein and scrutinising the expression of P62 mRNA and P62 and LC3 proteins. RESULTS: Induction of MC3T3-e1 mineralization demonstrated an increased expression of osteogenesis-related indicators such as RUNX2, ALP, OCN, and LAPTM5 (p < 0.05), as evident from the results of RT-qPCR and Western blot. Meanwhile, the expression of autophagosomes increased one day after mineralization induction and then experienced a gradual decline, and enhanced expression of LC3 protein was noted on days 1–2 of mineralization induction but was then followed by a corresponding reduce. In contrast, a continuous increase was reported in the expression of P62 mRNA and protein, respectively (p < 0.05). Up- and down-regulating RUNX2/LAPTM5 expression alone confirmed the aforementioned results. CONCLUSION It was therefore proposed that RUNX2 may be responsible for an early increase and then a gradual decrease in LAPTM5-mediated autophagy through the regulation of its high expression. Meanwhile, increased LAPTM5 expression in osteogenic mineralization presumed that RUNX2/LAPTM5 promoted autophagy and osteogenic expression, which may play a bridging role in the regulation of autophagy and osteogenesis.