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 investigate the expression of double-stranded DNA (dsDNA), citrulline histone 3 (CitH3), myeloperoxidase-DNA (MPO-DNA), IL-8 and IL-33 in plasma of patients with chronic obstructive pulmonary disease (COPD) and their clinical significance. Methods Forty patients with acute exacerbation COPD (AECOPD) who were hospitalized in The First Affiliated Hospital of Shihezi University School of Medicine from October 2020 to May 2021 were recruited in the AECOPD group, and recruited in the stable COPD group when they entered the stable stage. In the same period, forty healthy individuals were recruited in the control group. General informations including pulmonary function and peripheral blood were collected from each subject. Plasma levels of CitH3, MPO-DNA, interleukin (IL)-8 and IL-33 were measured by enzyme linked immunosorbent assay and plasma levels of dsDNA were measured by PicoGreen fluorescent dye quantitative analysis. Results The levels of dsDNA, CitH3, MPO-DNA, IL-8 and IL-33 in the AECOPD group were higher than those in the stable group and the control group, with statistical significance (P<0.05), and the levels of dsDNA, CitH3, MPO-DNA and IL-33 in the stable group were higher than those in the control group, with statistical significance (P<0.05) . The levels of CitH3, MPO-DNA, IL-33 and IL-8 in the AECOPD group were positively correlated with COPD assessment test (CAT) score. MPO-DNA and IL-8 were positively correlated with CAT score, MPO-DNA was negatively correlated with FEV1%pred, CitH3 was negatively correlated with FEV1/FVC. The levels of IL-8 and dsDNA, CitH3 were positively correlated with the levels of MPO-DNA in the AECOPD group, and positively correlated with the levels of IL-8 and dsDNA in the stable group, but not with CitH3 and MPO-DNA. The levels of IL-33 and IL-8, dsDNA, CitH3, MPO-DNA were positively correlated in the AECOPD group, but not in the stable group. Conclusions The levels of neutrophil extracellular traps (NETs), IL-8 and IL-33 in plasma of COPD patients were increased, and the levels of NETs were correlated with pulmonary function, CAT score, IL-33 and IL-8. NETs may be involved in the development of COPD.
Objective
To investigate the clinical value of plasma copeptin in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD).
Methods
Ninety patients with AECOPD admitted between October 2013 and November 2015 were recruited as an AECOPD group, and 40 healthy subjects underwent physical examination simultaneously were recruited as a control group. According to patient history and severity, the AECOPD patients were divided into 3 groups: grade Ⅰ group (25 cases), grade Ⅱ group (45 cases) and grade Ⅲ group (20 cases). Plasma copeptin level was measured by enzyme-linked immunosorbent assay (ELISA). The changes of copeptin, the total counts of white blood cells (WBC), and C-reactive protein (CRP) of the AECOPD patients were compared before and after treatment. Then the correlations between plasma levels of copeptin and severity of AECOPD were evaluated.
Results
The plasma level of copeptin in the AECOPD group was higher than that in the control group [(16.4±5.2) pmol/L vs. (5.7±2.8) pmol/L, P<0.05), and gradually increased with the severity of AECOPD. For the AECOPD patients both before and after treatment, the copeptin concentrations were positive correlated with the plasma CRP concentrations and the total counts of WBC in blood (both P<0.05).
Conclusions
The plasma levels of copeptin gradually increase with the severity of AECOPD. The changes of plasma copeptin may be as an indicator for the severity of AECOPD.
ObjectiveTo investigate the risk factors associated with failure of weaning from invasive mechanical ventilation in gerontal patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD).
MethodsA retrospective study was conducted on 76 patients aged 65 years and older with AECOPD who received invasive mechanical ventilation and met the weaning criteria from July 2012 to June 2014. The subjects who passed the spontaneously breathing trial (SBT) and did not need mechanical ventilation within 48 h were enrolled into a weaning success group. The subjects who did not pass the SBT or needed mechanical ventilation again within 48 h were enrolled into a weaning failure group. The risk factors associated with failure of weaning were studied by univariate and multivariate Logistic regression analysis.
ResultsThere were 53 subjects in the weaning success group and 23 in the weaning failure group. The incidences of sepsis, multiple organ dysfunction syndrome (MODS), fungal infection, hypoproteinemia, duration for mechanical ventilation > 14 d, the prevalences of aeropleura, cardiac failure, diabetes, coronary heart disease and hepatic insufficiency were higher in the weaning failure group than those in the weaning success group (P < 0.05). Logistic analysis revealed that MODS (OR=8.070), duration for mechanical ventilation > 14 d (OR=17.760), cardiac failure (OR=4.597) and diabetes (OR=13.937) were risk factors of weaning failure (P < 0.05).
ConclusionMODS, duration for mechanical ventilation > 14 d, cardiac failure and diabetes were associated with the failure of weaning from invasive mechanical ventilation in gerontal patients with AECOPD.
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 assess the effects of physiotherapy on pulmonary function in COPD patients with lung cancer after lobectomy or pneumonectomy.
Methods
Fifty-five COPD patients with lung cancer undergoing lobectomy or pneumonectomy from January 2005 to May 2014 were recruited in the study. They were divided into group A received comprehensive physiotherapy before surgery and group B without comprehensive physiotherapy before surgery. The changes of lung function and tolerance were compared before physiotherapy (T1 time point) and after physiotherapy (T2 time point) in the group A, and between two groups before lung resection (T2 time point) and after lung resection (T3 time point).
Results
In group A, the forced expiratory volume in one second (FEV1), vital capacity (VC), peak expiratory flow at 50% of vital capacity (FEF50) and FEF25 increased significantly respectively by 16.96%, 14.75%, 20.69% and 13.79% compared with those before physiotherapy. Meanwhile, six-minutes walking distance (6MWD) achieved a significant improvement. After resection of lung, FEV1 and VC appeared to reduce, and pulmonary small airway function, tolerance, and clinical features deteriorated significantly. The differences between T2 and T1 in FEV1, FEF50 and FEF25 in the patients with FEV1%pred ≥80% and 50%-80% were similar with those in the patients with FEV1%pred<50%. The differences between T2 and T3 in FEF50 and FEF25 in the patients with FEV1%pred≥80% and 50%-80% were higher than those with FEV1%pred<50%. For the patients with lobectomy, FEV1 and VC in the group B were lower than those in the group A (FEV1: 10.24% vs. 22.44%; VC: 10.13% vs. 20.87%). For the patients with pulmonary resection, FEV1 and VC had little differences (FEV1: 36.33% vs. 36.78%; VC: 37.23% vs. 38.98%).
Conclusion
Physiotherapy is very important for the preoperative treatment and postoperative nursing of COPD patients with primary lung cancer.
Objective
To summarize the association between CYP1A1 rs4646903 polymorphisms and COPD risk.
Methods
Systematic literature search was conducted (up to January 2016) in five online databases, ie. PubMed, Embase, China National Knowledge Infrastructure (CNKI), VIP database, and WanFang databases. The strength of association was calculated by odds ratio (OR) and corresponding 95% confidence interval (CI).
Results
Six case-control studies with 1 050 cases and 1 202 controls were included. This study suggested a significant association between the CYP1A1 rs4646903 polymorphism and COPD risk (CC vs. TT: OR=1.63, 95%CI 1.17-2.27, P=0.004; CC vs. TC+TT: OR=1.62, 95%CI 1.19-2.20, P=0.002). However, there was no significant difference between allele model (C vs. T, OR=1.20, 95%CI 0.95-1.51, P=0.118) and dominant model (CC+TC vs. TT, OR=1.19, 95%CI 0.82-1.72, P=0.366).
Conclusions
The CYP1A1 rs4646903 polymorphisms might alter the susceptibility of COPD. More well-designed studies with larger sample size are warranted.
Objective
To investigate drug usage and costs of chronic obstructive pulmonary disease (COPD) inpatients in Karamay Central Hospital in 2014 and to provide evidence and reference for evidence-based pharmacy study on COPD.
Methods
The information of drug use and expenditure of COPD inpatients were collected from the hospital information system (HIS). We analyzed the data including frequency, proportion and cumulative proportion by Excel 2007 software.
Results
A total of 194 inpatients with COPD/AECOPD were included in Karamay Central Hospital in 2014, the average age was 74.28±7.81 years old. Fifty-three drugs were used for COPD treatment; the total frequency were 1 798 times and per capita cost was 7 419.78 yuan. The top three used drugs were budesonide suspension, montelukast tablets and methylprednisolone injection. In total expenditure, the cost of piperacillin-tazobactam, imipenem/cilastatin and moxifloxacin injection ranked top three.
Conclusion
The top 3 used drugs are budesonide suspension, montelukast tablets and methylprednisolone injection for COPD inpatients in Karamay Central Hospital in 2014, while the top 3 total expenditure drugs are piperacillin-tazobactam, imipenem/cilastatin and moxifloxacin injection.
Objective To establish a machine learning-based risk prediction model of combined chronic obstructive pulmonary disease (COPD) with lung cancer, so as to explore the high risk factors for COPD patients with lung cancer and to lay the foundation for early detection of lung cancer risk in COPD patients. Methods A total of 154 patients from the Second Hospital of Dalian Medical University from 2010 to 2021 were retrospectively analyzed, including 99 patients in the COPD group and 55 patients in the COPD with lung cancer group. the chest high resolution computed tomography (HRCT) scans and pulmonary function test of each patient were acquired. The main analyses were as follow: (1) to valid the statistically differences of the basic information (such as age, body mass index, smoking index), laboratory test results, pulmonary function parameters and quantitative parameters of chest HRCT between the two groups; (2) to analyze the indicators of high risk factors for lung cancer in COPD patients using univariate and binary logistic regression (LR) methods; and (3) to establish the machine learning model (such as LR and Gaussian process) for COPD with lung cancer patients. Results Based on the statistical analysis and LR methods, decreased BMI, increased whole lung emphysema index, increased whole lung mean density, and increased percentage activity of exertional spirometry and prothrombin time were risk factors for COPD with lung cancer patients. Based on the machine learning prediction model for COPD with lung cancer patients, the area under the receiver operating characteristic curve for LR and Gaussian process were obtained as 0.88 using the soluble fragments of prothrombin time percentage activity, whole lung emphysema index, whole lung mean density, and forced vital capacity combined with neuron-specific enolase and cytokeratin 19 as features. Conclusion The prediction model of COPD with lung cancer patients using a machine learning approach can be used for early detection of lung cancer risk in COPD patients.
Objective To investigate the intervention effect of 3-phosphoinositede dependent protein kinase-1 (PDK1) inhibitor on prostaglandin E2 (PGE2) in smoking-induced chronic obstructive pulmonary disease (COPD) mice. Methods Fifty C57BL/6 male mice were randomly divided into normal control group, smoking group, smoking +low dose PDK1 inhibitor group, smoking + medium dose PDK1 inhibitor group and high dose PDK1 inhibitor group with 10 mice in each group. The mice in the normal control group inhaled phosphate-buffered saline twice a day for 12 weeks, and the mice in the smoking group were fumigated twice a day, 5 days per week for 12 weeks, and the other three groups were given intraperitoneal injection of low-dose PDK1 inhibitor OSU-03012 (0.25 mg/kg), medium-dose PDK1 inhibitor (0.5 mg/kg) and high-dose PDK1 inhibitor (1.0 mg/kg) respectively before smoking. After smoking, lung function was tested, the bronchoalveolar lavage fluid (BALF) of each mouse was taken for cell count, the PGE2 in serum and BALF of mice was determined by enzyme linked immunosorbent assay, and the lung tissue of mice was sectioned with paraffin and stained by hematoxylin-eosin (HE), and pathological changes were observed under microscope. Results Compared with the control group, FEV100/FVC and FEV200/FVC of the mice in each smoking group were significantly decreased (P<0.05); The number of cells in BALF of smoking group was significantly higher than that of normal control group (P<0.05). There was no significant difference in the total number of BALF cells, the proportion of neutrophils and macrophages between the smoking + low-dose PDK1 inhibitor group and the smoking group. However, the total number of BALF cells and the proportion of neutrophils in the smoking + medium dose PDK1 inhibitor group and the high dose PDK1 inhibitor group gradually decreased, while the proportion of macrophages gradually increased, compared with the normal control group, the PGE2 concentrations of serum and BALF in the smoking group and the smoking + PDK1 inhibitor group were significantly higher than those in the control group. Compared with the smoking group, the PGE2 concentrations of serum and BALF in the middle and high dose PDK1 inhibitor groups were significantly lower than those in the smoking group. HE staining of lung tissue showed that there were a large number of inflammatory cell infiltration, alveolar cavity dilatation, alveolar wall rupture and fusion, alveolar formation, significant decrease in the number of alveoli and other pathological changes in the smoking group, which were consistent with the pathological changes of COPD. The inflammatory cell infiltration, mucus obstruction and alveolar dilatation were slightly alleviated in the smoking + low-dose PDK1 inhibitor group, while the inflammatory cell infiltration, alveolar wall thinning and alveolar dilatation were improved in both the medium-dose inhibitor group and the high-dose inhibitor group, and the improvement was more obvious in the high-dose inhibitor group. Conclusion The lung function of the smoked COPD mouse decreases, the airway inflammation is obvious, and the secretion of PGE2 is also increased, while the use of PDK1 inhibitor could reduce the secretion of PGE2, reduce airway inflammation and pathological changes, and improve lung function in a dose-dependent manner.
