ABSTRACT
<p><b>OBJECTIVE</b>To observe the role of myeloperoxidase(MPO)and eosinophilic cationic protein(ECP)in the airway inflammation and their correlation with clinical feature in asthma-COPD overlap (ACO) patients.</p><p><b>METHODS</b>Twenty patients with COPD, 20 with asthma, 20 with ACO and 20 control subjects underwent pulmonary function test for measurement of forced expiratory volume in 1 second (FEV), forced vital capacity (FVC), peak expiratory flow (PEF), and maximum midexpiratory flow (MMF). COPD assessment test (CAT) was used to evaluate the clinical symptoms of the patients with COPD and ACO. The asthma control test (ACT) was used to evaluate the asthma control in the patients with asthma and ACO. Induced sputum samples were collected from the subjects for analysis of neutrophil and eosinophil ratios, and enzyme-linked immunosorbent assay was used to determine the expression levels of MPO and ECP in the sputum.</p><p><b>RESULTS</b>No significant difference was observed in the CAT scores between ACO group and COPD group (> 0.05). Compared with the asthma group, the patients with ACO had significantly lower ACT scores and lower FEV, PEF and MMF ( < 0.05). The patients with ACO had significantly higher FVC and sputum eosinophil ratio than those with COPD ( < 0.05), and a higher sputum neutrophil ratio than those with asthma ( < 0.01). In ACO group, the MPO level in sputum was significantly higher than that in the asthma group ( < 0.05), while sputum ECP level was significantly higher than that in both the asthma group and COPD group ( < 0.05 or 0.01). In ACO group, sputum MPO level was positively correlated with sputum neutrophil ratio (=0.8358, < 0.01) but was not correlated with CAT score or FEV (> 0.05); sputum ECP level was positively correlated with sputum eosinophil ratio (=0.4666, < 0.05) and was inversely correlated with ACT score (=-0.4966, < 0.05) and FEV (=-0.4610, < 0.05).</p><p><b>CONCLUSIONS</b>Both neutrophilic and eosinophilic inflammations occur in the airway of patients with ACO, and their sputum ECP level is negatively correlated with asthma control and obstructive airflow limitation.</p>
ABSTRACT
Objective To evaluate the diagnostic value of astograph methacholine provocation test for bronchial asthma.Methods A total of 238 asthma patients and 499 non-asthma patients participated in the detection by astograph methacholine provocation test.Statistical methods were used to analyze the differences of astograph parameters and find the indicators of asthma diagnosis and the critical value.Results Dmin,Cmin and PD15 were much lower in the asthma group (P ＜ 0.01),compared with the the non-asthma group,when SGrs,SGrs/Grs cont were much higher (P ＜ 0.01).SGrs was relevant with Dmin,Cmin,PD15 in the asthma group (P =0.000;r =0.685,r =0.657,r =0.639) as well as the SGrs/Grs cont did (P =0.000,r =0.775;r =0.740,r =0.708).In ROC analysis,Dmin presented an AUC of 0.661,the cutoff value was 2.71 unit,with a sensitivity of 0.739 and specificity of 0.551.PD15 presented an AUC of 0.746,the cutoff value was 4.856 5 unit,with a sensitivity of 0.693 and specificity of 0.684.Conclusion Astograph methacholine provocation test shows good sensitivity and specificity in the diagnosis of asthma,particularly when Dmin ≤ 2.71 Unit or PD15 ≤ 4.8565 Unit as the cutoff value.
ABSTRACT
This study examined the effects of over-expression of leucine-rich repeats and immunoglobulin-like domains 3 (LRIG3) on the cell cycle and survival of human glioma cell line U87 and U251 and explored the possible mechanisms. The LRIG3 gene was transduced into U87 and U251 cells respectively by using lentivirus and the transduced cells were selected by puromycin. The changes in LRIG3 mRNA and protein levels were measured by RT-PCR and Western blotting. The apoptosis rate was detected by Annexin V-FITC/PI double labeling and the cell cycle was flow cytometrically analyzed. Compared with control cells, LRIG3 mRNA expression in U251 and U87 cells transduced with pLVX-DsRed-LRIG3-Monomer-N1 were increased by 77.6% and 129.7%, and LRIG3 protein expression was raised by 141.3% and 322.7%, respectively. Cell cycle analysis showed that LRIG3 over-expression increased the percentage of cells at G(0)/G(1) phase (P<0.01). Over-expressed LRIG3 could significantly promote the apoptosis of U87 and U251 cells (P<0.05). These findings suggest that the over-expression of LRIG3 could arrest the cell cycle in G(0)/G(1) phase, and promote apoptosis of U87 and U251 cells.