Recently, many researchers paid more attentions to the association between air pollution and chronic obstructive pulmonary disease (COPD). Haze, a severe form of outdoor air pollution, affected most parts of northern and eastern China in the past winter. In China, studies have been performed to evaluate the impact of outdoor air pollution and biomass smoke exposure on COPD; and most studies have focused on the role of air pollution in acutely triggering symptoms and exacerbations. Few studies have examined the role of air pollution in inducing pathophysiological changes that characterise COPD. Evidence showed that outdoor air pollution affects lung function in both children and adults and triggers exacerbations of COPD symptoms. Hence outdoor air pollution may be considered a risk factor for COPD mortality. However, evidence to date has been suggestive (not conclusive) that chronic exposure to outdoor air pollution increases the prevalence and incidence of COPD. Cross-sectional studies showed biomass smoke exposure is a risk factor for COPD. A long-term retrospective study and a long-term prospective cohort study showed that biomass smoke exposure reductions were associated with a reduced decline in forced expiratory volume in 1 second (FEV1) and with a decreased risk of COPD. To fully understand the effect of air pollution on COPD, we recommend future studies with longer follow-up periods, more standardized definitions of COPD and more refined and source-specific exposure assessments.
Objective To investigate the relationship of pulmonary surfactant protein D( SP-D) with chronic obstructive pulmonary disease ( COPD) by measuring SP-D level in serum and lung tissue of rats with COPD.Methods The rat COPD model was established by passive smoking as well as intratracheal instillation of lipopolysaccharide ( LPS) . Thirty male SD rats were randomly divided into a control group, a LPS group, and a COPD group( n =10 in each group) . The pathologic changes of lung tissue and airway were observed under light microscope by HE staining. Emphysema changes were evaluated by mean linear intercept ( MLI) of lung and mean alveolar number ( MAN) . The level of SP-D in serum was measured by enzymelinked immunosorbent assay ( ELISA) . The expression of SP-D in lung tissue was detected by Western-blot and immunohistochemistry.Results The MLI obviously increased, and MAN obviously decreased in the COPD group compared with the control group ( Plt;0.05) . There was no significant difference in the MLI and MAN between the LPS group and the control group ( Pgt;0.05) . The serum SP-D level was ( 49.59 ±2.81) ng/mL and ( 53.21±4.17) ng/mL in the LPS group and the COPD group, which was significantly higher than that in the control group [ ( 42.14±2.52) ng/mL] ( Plt;0.05) . The expression of SP-D in lung tissue was 0.56±0.01 and 0.63±0.01 in the LPS group and the COPD group, which was also obviously ber than that in the control group ( 0.39 ±0.01) ( Plt;0.05) .Meanwhile the SP-D levels in serumand lung tissue were higher in the COPD group than those in the LPS group ( Plt;0.05) . The levels of SP-D between serum and lung tissue were positively correlated in all three groups ( r=0.93, 0.94 and 0.93, respectively, Plt;0.01) .Conclusion Both the SP-D level in serum and in lung tissue increase significantly in COPD rats and correlate well each other, which suggests that SP-D may serve as a biomarker of COPD.
Objective To explore the role of macrophage-stimulating protein ( MSP) and receptor tyrosine kinase RON in the airway inflammation of chronic obstructive pulmonary disease( COPD) , and investigate its possible mechanism. Methods The rat COPDmodel was established by exposing the rats to cigarette smoke daily for three months. Rat alveolar macrophages ( AMs) were isolated in vivo and cultured,and then challenged with different concentrations of MSP for 24 hours. The concentrations of MSP in broncho-alveolar lavage fluid ( BALF) and serum, and the levels of IL-1β, TNF-α, IL-8, and IL-10 in the supernatants were measured by ELISA. The expression of RONmRNA in lung tissue was assessed by reverse transcription-polymerase chain reaction. The levels of RON protein in the lung tissue and AMs cultured in vitro were observed by immunohistochemistry. The activity of superoxide dismutase ( SOD) and malondialdehyde ( MDA) content in the culture solution were measured with chromatometry method. Results Compared with the control group, the concentrations of MSP in serum and BALF of the COPD rats were significantly higher ( P lt;0. 01) . The levels of RONmRNA and RON protein in the COPD rats were also upregulated significantly ( P lt; 0. 01) . MSP evoked the AMs isolated from the normal and COPD rats to generate more content of MDA and caused a reduction in activity of SOD. In addition, MSP stimulated TNF-α, IL-8, IL-1βand IL-10 release fromAMs of the normal and COPD rats dose-dependently. The levels of TNF-α, IL-8, and IL-1βwere higher, while the level of IL-10 and the SOD activity were lower in AMs of the COPD group than those of the control group in the same dose of MSP ( P lt;0. 01) . The more significant increase in the levels of TNF-α, IL-8, IL-1β, and the more notable decrease in the activity of SOD was found in the COPD group compared with the control group. But the degree of increasing MDA and IL-10 in the AMs of the COPD group was lower than that in the control group. Linear correlation analysis showed that the MSP concentration and the RON protein level in the COPD rats were positively associated with the total cellcounts and AM counts in BALF, and were related to the indexes for pulmonary emphysema. Conclusions There is a close correlation between the MSP and receptor tyrosine kinase RON with the airway inflammation of COPD. The mechanism might be that MSP promote the macrophages release inflammatory factors and increase the production of oxygen free radicals.
Objective To determine if supervised hospital-based exercise can maintain the benefits of functional exercise ability and quality of life gained from a pulmonary rehabilitation program in COPD.Methods A prospective and randomized study was carried out. Following completion of an eight-week pulmonary rehabilitation program in hospital, 43 COPD patients were recruited and randomized into either a supervised group ( supervised, every 10 days, hospital-based exercise, 22 cases ) or a control group ( unsupervised home exercise,21 cases) and followed for 12 months. Measurements were taken at baseline and 12 months later. Exercise measurements include six-minute walk test( 6MWT) and pulmonary function test. Quality of life was measured using the Chronic Respiratory Questionnaire ( CRQ) . Results After 12 months of different exercise program,6MWT in the supervised group was significantly longer than that in the unsupervised group[ ( 532. 0 ±168. 4) m vs ( 485. 0 ±151. 6) m, P lt; 0. 05] . There was no significant difference in pulmonary function between the two groups. The quality of life of the supervised group was higher than that of the unsupervised group( 114. 6 ±20. 8 vs 105. 6 ±21. 7, P lt;0. 05) . Conclusions After the completion of pulmonary rehabilitation program, a supervised, every 10 days, hospital-based following exercise program can maintain better functional exercise capacity and quality of life compared to home exercise in COPD patients.
Objective The risk factors of noninvasive positive pressure ventilation (NPPV) in the treatment of acute exacerbation of chronic obstructive pulmonary disease (AECOPD) combined with failure of respiratory failure were identified by meta-analysis, so as to provide a basis for early clinical prevention and treatment failure and early intervention. Methods PubMed, The Cochrane Library, EMbase, China National Knowledge Infrastructure, Wanfang, VIP and CBM Data were searched to collect studies about risk factors about failure of noninvasive positive pressure ventilation in AECOPD and respiratory failure published from January 2000 to January 2021. Two researchers independently conducted literature screening, literature data extraction and quality assessment. Meta-analysis was performed on the final literature obtained using RevMan 5.3 software. Results Totally 19 studies involving 3418 patients were recruited. The statistically significant risk factors included Acute Physiology and Chronic Health Evaluation (APACHEⅡ) score, pre-treatment PCO2, pre-treatment pH, Glasgow Coma Scale (GCS), respiratory rate (RR) before treatment, body mass index (BMI), age, C-reactive protein (CRP), renal insufficiency, sputum disturbance, aspiration of vomit. Conclusions High APACHE-Ⅱ score, high PCO2 before treatment, low pH value before treatment, low GCS score, high RR before treatment, low BMI, advanced age, low albumin, high CRP, renal insufficiency, sputum disturbance, and vomit aspiration were the risk factors for failure of respiratory failure in patients with COPD treated by NIPPV. Failure of non-invasive positive pressure ventilation in COPD patients with respiratory failure is affected by a variety of risk factors, and early identification and control of risk factors is particularly important to reduce the rate of treatment failure.
Objective To explore the regulation of peroxisome proliferator-activated receptor γ coactivator 1α( PGC-1α) and NF-E2-related factor 2( Nrf2) on expression of γ-glutamylcysteine synthetase ( γ-GCS) , and their roles in chronic obstructive pulmonary disease( COPD) . Methods Twenty-four SD rats were randomly divided into a COPD group and a normal control group. COPD model was established by intratracheal instillation of lipopolysaccharide ( LPS) and daily exposure to cigarette smog in the COPD group. The lung function was measured and the pathological changes were observed. The protein and mRNA expressions of PGC-1α, Nrf2, and γ-GCS in lung tissue were measured by immunohistochemistry, Western blot, in site hybridization ( ISH) , and reverse transcription-polymerase chain reaction ( RT-PCR ) ,respectively. Results In the COPD group, the pulmonary function ( FEV0. 3, FEV0. 3 /FVC, PEF) damage and lung pathological changes were conformed as morphological characteristics of COPD. The mRNA of PGC-1α and Nrf2 expressed in lung tissues of two group rats in the region consistent with γ-GCS mRNA. The protein and mRNA expressions of PGC-1αand γ-GCS were markedly increased in the COPD group( all P lt;0. 05) ,and the protein expression of Nrf2 was obviously up-regulated ( P lt; 0. 01) , while Nrf2 mRNA had no significant difference between the two groups( P gt;0. 05 ) . Linear correlation analysis showed that the level ofPGC-1αprotein was positively correlated with the levels of Nrf2 protein and mRNA ( r = 0. 775, 0. 515, all P lt; 0. 01) , and the levels of PGC-1αand Nrf2 protein were positively correlated with the levels of γ-GCS protein ( r = 0. 531, 0. 575, all P lt; 0. 01) and mRNA ( r = 0. 616, 0. 634, all P lt; 0. 01) . Conclusions PGC-1α, which may serve as a co-activator of Nrf2, can up-regulate the expression of γ-GCS gene cooperatively with Nrf2 through a common pathway, which might involve in the oxidative and antioxidative mechanism in the pathogenesis of COPD.
Objective To compare the therapeutic effect of percutaneous transhepatic cholangial drainage (PTCD) and operation drainage for the patients with inoperable malignant obstructive jaundice. Methods A total of 131 patients with inoperable malignant obstructive jaundice were treated in this hospital, in which 102 patients had PTCD by placement of metallic stent and (or) plastic tubes to remove obstruction of bile duct (interventional treatment group). Simultaneously 29 patients were selected for operation by intraexternal drainage (operation drainage group). The patients were followed up for comparison of the serum level of total bilirubin, postoperative complications, average length of hospitalization and average cost between the two groups. Results PTCD was successfully performed in all the patients of the interventional treatment group. There were no significant differences of 50% decrease period of average total bilirubin level or postoperative complications between the two groups (Pgt;0.05). The average length of hospitalization and average cost of interventional treatment group were less than those of operation drainage group (Plt;0.05). Conclusions Compare with operation drainage, interventional treatment can reduce average length of hospitalization and average cost, without increase of postoperative complications, which is a main chance of treatment for malignant obstructive jaundice.
Objective To determine the efficacy of forced expiratory volume in six seconds( FEV6 ) as an alternative for forced vital capacity( FVC) in the diagnosis for mild-moderate chronic obstructive pulmonary disease( COPD) .Methods A total of 402 mild-moderate COPD and 217 non-COPD patients’ spirometric examinations were retrospectively analyzed. The correlation between FEV6 and FVC, FEV1 /FVC and FEV1 /FEV6 was evaluated by the Spearman test. Considering FEV1 /FVC lt;70% as being the ‘golden standard’ for airway obstruction, a ROC curve was used to determine the best cut-off point for the FEV1 /FEV6 ratio in the diagnosis for COPD. Results The Spearman correlation test revealed the FEV1 and FEV6 , FEV1 /FEV6 and FEV1 /FVC ratios were highly correlated ( r = 0. 992, 0. 980, respectively, P = 0. 000) . Using FEV1 /FEV6 lt; 70% as the diagnosis standard, 12. 69% of the 402 patients could not be diagnosed as COPD. The FEV1 /FVC ratio of these patients was very close to 70% . The best cut-off point for the FEV1 /FEV6 ratio in the diagnosis of mild-moderate COPD was 72% while the sensitivity and specificity were 94. 7% and 92. 2% , respectively. Conclusions There is a b correlation between FEV1 /FVC and FEV1 /FEV6 . The FEV6 can be a valid alternative for FVC in the diagnosis for mild-moderate COPD, although it may result in false negative. The best cut-off point for the FEV1 /FEV6 ratio is 72% .
Objective The purpose of the current research was to analyze the relevant risk factors for short-term death in patients with chronic obstructive pulmonary disease (COPD) and heart failure (HF), and to build a predictive nomogram. Methods We conducted a retrospective analysis of clinical data from 1 323 COPD and HF comorbidity patients who were admitted to the Affiliated Hospital of Southwest Medical University from January 2018 to January 2022. Samples were divided into survival and death groups based on whether they died during the follow-up. General data and tested index of both groups were analyzed, and the discrepant index was analyzed by single factor and multiple factor Logistic regression analysis. R software was applied to create the nomogram by visualizing the results of the regression analysis. The accuracy of the results was verified by C index, calibration curve, and ROC curve. Results The results from the multiple factor Logistic regression analysis indicated that age (OR=1.085, 95%CI 1.048 to 1.125), duration of smoking (OR=1.247, 95%CI 1.114 to 1.400), duration of COPD (OR=1.078, 95%CI 1.042 to 1.116), comorbidity with respiratory failure (OR=5.564, 95%CI 3.372 to 9.329), level of NT-proBNP (OR=1.000, 95%CI 1.000 to 1.000), level of PCT (OR=1.153, 95%CI 1.083 to 1.237), and level of D-dimer (OR=1.205, 95%CI 1.099 to 1.336) were risk factors for short-term death of COPD and HF comorbidity patients. The level of ALB (OR=0.892, 95%CI 0.843 to 0.942) was a protective factor that was used to build the predictive nomogram with the C index of 0.874, the square under the working characteristics curve of the samples of 0.874, the specify of 82.5%, and the sensitivity of 75.0%. The calibration curve indicated good predictive ability of the model. Conclusion The nomogram diagram built by the current research indicated good predictability of short-term death in COPD and HF comorbidity patients.