Search

Chronic obstructive pulmonary disease is a common, frequent and high mortality chronic disease of the respiratory system, while infection is the main cause of acute exacerbation of COPD；In recent years, serum amyloid A and heparin-binding protein have received increasing attention in the field of respiratory diseases as newer indicators of infection because of their rapid response, sensitivity and specificity；This article will summarize the research progress of HBP and SAA in acute exacerbation of chronic obstructive pulmonary disease combined with pulmonary infections, and provide a reference for clinical diagnosis and assessment of prognosis. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Kunming Medical University / Kunming Yike Daxue Xuebao is the property of Kunming Medical Journal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective　To investigate the correlation of pulmonary function indexes and bronchial wall thickness measured as computed with high resolution computed tomography in patients with chronic obstructive pulmonary diseases. Methods　Eighty COPD patients were assigned to four groups based on the new COPD Global Initiative Classification, meanwhile，fifty normal people with physical examination in the hospital were selected as controls simultaneously. All subjects underwent chest HRCT scanning to measure the bronchial wall thickness at the bilateral apical bronchial opening，and the correlation between the bronchial wall thickness and lung function was studied. Results　Bronbronchial wall thickness was significantly increased in COPD patients compared with normal population，and the difference was statistically significant （ P < 0.05）. From the mild group to the very severe group， the bilateral bronchial wall thickness gradually increased，FEV1，FVC，FEV1/FVC gradually decreased，with statistically significant differences （ P < 0.05） . Correlation analysis： bilateral bronchial wall thickness was significantly inversely associated with each index of lung function （ P < 0.05）. Conclusions　HRCT can be used to measure bronchial wall thickness and evaluate the degree of bronchial wall remodeling in COPD patients. With the deepening of the disease grade，the thickness of the bronchial wall of COPD patients gradually increased. There is a significant correlation between lung function indexes and bronchial wall thickness，that is，the thickening of bronchial wall，the decline of lung function indexes and the deterioration of lung function. HRCT measurement of bronchial wall thickness in COPD patients has clinical significance for the evaluation of the severity of the disease. [ABSTRACT FROM AUTHOR]

Objective The correlation between pulmonary artery diameter measured by high resolution computedtomography （HRCT） and pulmonary artery pressure measured by echocardiography in patients with chronic obstructive pulmonary disease （COPD） was investigated to find a new method to assess pulmonary artery pressure and to add a new method to the clinical assessment of the disease. Methods Seventy-seven patients with stable chronic obstructive pulmonary disease who were seen in Kunming First People’ s Hospital from May 2018 to May 2020 were set as the test group, and 50 healthy individuals who underwent health checkups in same period were selected as the control group, all of whom underwent chest HRCT to measure right pulmonary artery diameter, left pulmonary artery diameter, and main pulmonary artery diameter, and also underwent cardiac ultrasound to measure right ventricular diameter, pulmonary artery pressure, and main pulmonary artery diameter. The data collected were analyzed for correlation. Results The data of left and right pulmonary artery diameter and main pulmonary artery diameter measured by HRCT in the COPD group were larger than those in the normal group （P < 0.05）, and there were differences in the data of right pulmonary artery diameter and main pulmonary artery diameter between the COPD groups （P < 0.05）, but not in the left pulmonary artery diameter （P > 0.05）; the right intraventricular diameter and pulmonary artery pressure measured by echocardiography were different between the COPD groups （P < 0.05）. The right intraventricular diameter, pulmonary artery pressure, and main pulmonary artery diameter were significantly correlated with the left and right pulmonary artery diameters and main pulmonary artery diameter by Pearson linear correlation analysis （P < 0.05）, and all were positively correlated. Conclusio There is a significant correlation between the values of pulmonary artery pressure and the values of pulmonary artery diameter in patients with COPD. HRCT measurement of pulmonary artery trunk diameter and right pulmonary artery diameter can be used as a method to assess pulmonary artery pressure. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Kunming Medical University / Kunming Yike Daxue Xuebao is the property of Kunming Medical Journal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Kunming Medical University / Kunming Yike Daxue Xuebao is the property of Kunming Medical Journal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Kunming Medical University / Kunming Yike Daxue Xuebao is the property of Kunming Medical Journal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the inhibitory effect of erythromycin on the TNE-α release of human macrophages stimulated by cigarette smoke and its possible mechanism. Methods The human monocytic cell line U937 cells were differentiated into human macrophages by Phorbol esters (PMA). The cigarette smoke extract (CSE) (0.1, 1 , 2.5% ) and erythromycin (EM) (0. 1 , 1 , 10 μg/mE) were used to deal with the macrophages at different time points (24. 48, and 72 h) , respectively, and we chose the time and concentrations with the least effect on proliferation activity of macrophages. The 1 μg/mL CSE, 1% EM and 24-hour treatment time were selected for the experiment. The differentiated L’937 cells were randomly divided into four groups; die control group (with no intervention) , CSE group ( 1% CSE stimulation for 24 h) , CSE + EM group ( pre-incubation with 1 μg/ml EM for 24 h before 1% CSE stimulation for 24 h) , and TSA group (TSA stimulation for 24 h). The TNF-α level in the culture supernatants was measured by ELISA; Western blotting was used to measure the expression of the histone deacetvlase-1 ( HDAC1) and NE-kB protein. Results The level of TNE-α in die culture supernatants of the control group, CSE group, and CSE + EM group were (274. 96 ± 182. 39) , (744. 46 ± 638.38), and (646.57 ±603.53) pg/mL, respectively (all P <0.05). Compared with the control group, the expressionof HDAC1 protein in the CSE group, EM + CSE group, and TSA group decreased, and the expression of NF-κB protein increased (all P <0. 05). Compared with the CSE group, die expression of HD AC 1 protein increased, and die expression of NE-κB protein decreased in the EM + CSE group ( both P < 0. 05 ). Compared with the EM + CSE group, the expression of HDAC1 protein in the TSA group decreased, and the expression of NE-kB protein increased (both P <0. 05). Conclusions EM inhibits die release of TNE-α ol human macrophages induced by cigarette smoke. The mechanism is that EM may restore the expression of HDAC1 and inhibit the expression of NE-kB, which decreases the release of TNE-α and thus alleviates the inflammatory response. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Kunming Medical University / Kunming Yike Daxue Xuebao is the property of Kunming Medical Journal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Kunming Medical University / Kunming Yike Daxue Xuebao is the property of Kunming Medical Journal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Kunming Medical University / Kunming Yike Daxue Xuebao is the property of Kunming Medical Journal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)