Ambient air pollution exposures and risk of drug-resistant tuberculosis.

BACKGROUND: Few epidemiological studies have explored the effects of air pollution on the risk of drug-resistant tuberculosis (DR-TB). OBJECTIVE: To investigate the short and long term residential concentrations of ambient air pollutants (particulate matter <10 µm in diameter (PM10) and particulate matter≤2.5 µm in diameter (PM2.5), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and carbon monoxide (CO)) in relation to the risk of DR-TB in a typical air pollution city, Jinan city, China. METHODS: A total of 752 new culture-confirmed TB cases reported in TB prevention and control institutions of Jinan from January 1, 2014 to December 31, 2015 were included. Average individual-level concentrations of air pollution for 5 different exposure windows, vary from 90 days to 720 days to diagnosis were estimated using measurements from monitor closest to the patient home addresses. Logistic regression model adjusted for potential confounders was employed to evaluate correlation between air pollution and DR-TB risk at different five exposure windows individually. RESULTS: There were substantially increased mono-drug resistance and poly-drug resistance risks for ambient PM2.5, PM10, O3, and CO exposures. High exposure to PM2.5, PM10, and CO was also significantly associated with increased incidence of multi-drug resistance (MDR) both in the single- and multi-pollutants regression models. The dominant positive associations for PM2.5was observed at 540 days exposure, for O3 was observed at 180 days exposure, and for PM10 and CO was observed from 90 days to 540 days exposures. CONCLUSIONS: Our finding suggest that exposure to ambient air pollution (PM2.5, PM10, O3, and CO) are associated with increased risk of DR-TB. We provided epidemiological evidence of association between pollution exposure and mono-, poly- and multi-drug resistance.

Effect of gefitinib on mucus hypersecretion in chronic obstructive pulmonary disease / 中华老年医学杂志

Objective To investigate the effect of gefitinib on mucus hypersecretion by inhibiting epidermal growth factor receptor (EGFR) activity in chronic obstructive pulmonary disease (COPD).Methods Human airway epithelail cell lines 16HBE cells were exposed to cigarette smoke extraction (CSE) to establish the COPD model.EGFR activity was inhibited by tyrosine kinase inhibitor gefitinib.The mRNA expressions of EGFR and MUC5AC were detected by real-time PCR.EGFR,p-EGFR and MUC5AC protein levels were determined by Western blot and ELISA.Results EGFR mRNA level was increased by 12.7％ in CSE and 8.6％ in gefitinib group,but had no significant differences among CSE,gefitinib group and control group (all P＞ 0.05).MUC5AC mRNA levels were enhanced by 141.7％,26.4％ in CSE group and gefitinib group respectively,and there were significant differences among CSE,gefitinib group and control group (all P＜0.05).EGFR protein levels were (600.34±64.58) μg/mg,(632.58±72.94) μg/mg,(584.57±67.39) μg/mg,in control,CSE and gefitinib groups,respectively,and there were no significant differences between groups (all P＞0.05).p-EGFR protein levels were (338.62±45.28) μg/mg,(679.43±78.23) μg/mg,(292.74±59.17) μg/mg in control,CSE and gefitinib groups,respectively.MUC5AC protein levels were(72.80±6.25)μg/mg,(187.00±±10.26)μg/mg,(92.57±8.32)μg/mg in control,CSE and gefitinib groups respectively.Compared with control group,p-EGFR and MUC5AC protein levels were increased significantly in CSE group (both P＜0.05),and had no significant differences in p EGFR and MUC5AC protein levels between control group and gefitinib group.Conclusions CSE may lead to mucus hypersecretion through activating the EGFR-mediated signaling pathways.Gefitinib may inhibit mucus hypersecretion by inhibiting EGFR tyrosine kinanse activity.EGFR may serve as a potential target for COPD.

miR-125b-1 gene mutation in lung cancer: relation with the clinic opathological parameters and prognosis of patients / 中国医师杂志

Objective To investigate the role of miR-125b-1 gene in oncogenesis and progression of human lung cancer. Methods PCR-SSCP was used to detect miR-125b-1 gene mutation in 121 specimens from primary site of lung cancer tissues and 22 samples of nor- real adjacent lung tissues. Results There were 40 cases of miR-125b-1 gene mutation, and gene mutation was positively correlated to the status of lymph node metastasis ( r,=0.285, P＜0.01 ) and clinical stage metastasis( r, =0. 241, P ＜0. 01 ), but no relationship between miR-125b-1 mutation and other clinical features was found. The postoperative survival time in patients with miR-125b-1 gene mutation was significantly longer than those with low expression ( P＜0.05). Conclusion There exist miR-125b-1 gene mutation in lung cancer, miR- 125b-1 gene mutation probably plays a crucial role in lung carcinogenesis.

Inhibitory effect of ground dragon on the expression of ?-SMA and FN in the lung tissue of mouse with asthma / 中国病理生理杂志

AIM:To investigate the inhibitory effect of ground dragon on the expression of ?-SMA and FN in the lung tissue with asthma.METHODS:The BALB/c mice were divided into four groups:control group(group A,n=20),asthmatic model group(group B,n=20),large-dose ground dragon treatment group(group C,n=20)and low-dose ground dragon treatment group(group D,n=20).To establish a mouse model of chronic asthma,we sensitized the mouse with 0.02% ovalbumin(OVA)by intraperitoneal injection,and stimulated the mice with 1% OVA by atomization.The treatment groups were given ground dragon before stimulation every time.After the last time of stimulation,the mice were subjected to laboratory tests.Inflammatory cells in bronchoalveolar lavage fluid were counted.Total level of IgE in serum was detected by ELISA.FN mRNA and ?-SMA mRNA in the lung tissue were measured by RT-PCR and AlphaImager 2200 semi-quantitation analysis system.Expressions of FN and ?-SMA were measured by the method of two-step immunohistochemistry and leica QWIN V3 analysis system.RESULTS:(1)Compared with those in group A,the expressions of ?-SMA and FN in group B were significantly increased(P0.05).(2)Compared with those in group A,the expression levels of ?-SMA mRNA and FN mRNA in group B had a great increase(P0.05).CONCLUSION:The ground dragon inhibits ?-SMA and FN expression in the lung tissue of mice with chronic asthma,indicating that ground dragon may inhibit airway remodeling in asthma through the inhibition of ?-SMA and FN expressions.