The purpose of this study was to investigate the changes of protein kinase Ca （PKCα） and cyclin D1 expressions in pulmonary arteries from＇smokers with normal lung function and smokers with mild to moderate chronic...The purpose of this study was to investigate the changes of protein kinase Ca （PKCα） and cyclin D1 expressions in pulmonary arteries from＇smokers with normal lung function and smokers with mild to moderate chronic obstructive pulmonary disease （COPD）. The peripheral lung tissues were obtained from 10 non-smokers with normal lung function （non-smoker group）, 14 smokers with normal lung function （smoker group）, 11 smokers with mild to moderate COPD （COPD group）. The morphological changes of pulmonary arteries were observed by HE-staining. The expressions of ct-smooth muscle actin （α-SMA）, proliferating cell nuclear antigen （PCNA）, PKCα and cyclin D1 proteins in pulmonary artery smooth muscle cells （PASMCs） were immunohistochemically determined. The percentages of PCNA-positive cells were taken as the smooth muscle cells proliferation index （PI）. The mRNA expressions of PKCα and cyclin D l in PASMCs were evaluated by real-time fluorescence PCR. Morphometrical analysis showed that the ratio of pulmonary artery wall area to total area （WA%） in smoker group and COPD group was significantly greater than that in non-smoker group （P〈0.01）. The PASMCs proliferation index in smoker group and COPD group was significantly higher than that in nonsmoker group （P〈0.01）. The protein levels of PKCct and cyclin D1 inPASMCs were significantly increased in smoker group and COPD group as compared with non-smoker group （P〈0.01）. The mRNA expressions of PKCα and cyclin D1 in PASMCs were significantly elevated in smoker group and COPD group as compared with non-smoker group （P〈0.01）. Significant correlations were found between PKCα protein and WA% or PI （P〈0.01）. Correlations between cyclin D1 protein and WA% or PI also existed （P〈0.01）. The expression of PKCa was positively correlated with the expression of cyclin D 1 at both protein and mRNA levels （P〈0.01）. In conclusion, increased expressions of PKCα and cyclin D1 might be involved in the pathogenesis of abnormal proliferation of PASMCs in smokers with normal lung function and smokers with mild to moderate COPD.展开更多
Objective: To observe the relationship of deep slow respiratory pattern and respiratory impedance(RI) in patients with chronic obstructive pulmonary disease (COPD). Methods: RI under normal respiration and during deep...Objective: To observe the relationship of deep slow respiratory pattern and respiratory impedance(RI) in patients with chronic obstructive pulmonary disease (COPD). Methods: RI under normal respiration and during deep slow respira tion was measured one after the other with impulse oscillometry for 8 patients with COPD and for 9 healthy volunteers as control. Results: When r espiration was changed from normal pattern to the deep slow pattern, the tida l volume increased and respiratory frequency significantly decreased in both gro ups , the total respiratory impedance (Z respir) showed a decreasing trend in COPD group, but with no obvious change in the control group. No chang e in the resonant frequency (fres) was found in both groups, and the respiratory viscous resistance obviously decreased in the COPD group(R5: P =0.0168 ; R20: P =0.0498; R5—R20: P =0.0388),though in the control group it was unchanged. Conclusion: IOS detection could reflect the response he terogeneity of different compartments of respiratory system during tidal breathi ng. During deep slow respiration, the viscous resistance in both central airw ay and peripheral airway was decreased in patients with COPD. RI measurement by impulse oscillometry may be a convenient pathophysiological method for studying the application of breathing exercise in patients with COPD.展开更多
Objective:To describe a patient with presarcopenia and chronic cough secondary to chronic obstructive pulmonary disease(COPD)successfully treated with supplements and physical exercise.Case report:A 75-year-old female...Objective:To describe a patient with presarcopenia and chronic cough secondary to chronic obstructive pulmonary disease(COPD)successfully treated with supplements and physical exercise.Case report:A 75-year-old female patient with a positive past medical history of systemic hypertension,dyslipidemia,heart arrhythmia,and smoking during 20 years evolved with chronic cough due to a chronic obstructive pulmonary disease diagnosed ten years ago.She came to our private clinic due to low weight,low energy.Her weight was 44.8 kg,her height 1.57 m,body mass index of 18.18 kg/m^(2).Laboratory tests showed SDHEA 76.3,vitamin D of 15.6 ng/ml(nr:>30 ng/ml),C-reactive protein(CRP)of 55 mg/ml.Computed tomography showed bronchiectasis.She had an skeletal muscle mass index of 5.0 kg/m^(2)(nr:>5.5 kg/m^(2))by DXA.A diagnosis of presarcopenia was determined based on DXA evaluation with low muscle mass but normal gait speed handgrip strength.We suggested to the patient to increase physical exercise and prescribed a supplement formula.After five months,she returned asymptomatic,without cough,marked improvement of fatigue,increased energy levels,and weight increased to 50 kg,BMI of 20.28 kg/m^(2).Laboratory tests showed SDHEA to 140,vitamin D3 to 64.5 ng/ml,reduced CRP reduced to 5 mg/dl,and amlodipine was excluded due to better blood pressure control.Currently,two years later,the patient continues without cough and has dyspnea only with high efforts,without fatigue,and her weight is 52 kg and BMI 21.1 kg/m^(2).She also reduced her conventional treatment for COPD,using only a bronchodilator on-demand,without topical corticoids.Conclusions:This case illustrates an interesting case of a patient with presarcopenia and chronic cough,refractory to conventional approach,successfully treated with a combination of nutraceuticals and physical exercises.展开更多
Increased levels of surfactant protein D (SP-D) and lipid-laden foamy macrophages (FMs) are frequently found under oxidative stress conditions and/or in patients with chronic obstructive pulmonary disease (COPD) who a...Increased levels of surfactant protein D (SP-D) and lipid-laden foamy macrophages (FMs) are frequently found under oxidative stress conditions and/or in patients with chronic obstructive pulmonary disease (COPD) who are also chronically exposed to cigarette smoke (CS). However, the roles and molecular mechanisms of SP-D and FMs in COPD have not yet been determined. In this study, increased levels of SP-D were found in the bronchoalveolar lavage fluid (BALF) and sera of ozone- and CS-exposed mice. Furthermore, SP-D-knockout mice showed increased lipid-laden FMs and airway inflammation caused by ozone and CS exposure, similar to that exhibited by our study cohort of chronic smokers and COPD patients. We also showed that an exogenous recombinant fragment of human SP-D (rfhSP-D) prevented the formation of oxidized low-density lipoprotein (oxLDL)-induced FMs in vitro and reversed the airway inflammation and emphysematous changes caused by oxidative stress and CS exposure in vivo. SP-D upregulated bone marrow-derived macrophage (BMDM) expression of genes involved in countering the oxidative stress and lipid metabolism perturbations induced by CS and oxLDL. Our study demonstrates the crucial roles of SP-D in the lipid homeostasis of dysfunctional alveolar macrophages caused by ozone and CS exposure in experimental mouse emphysema, which may provide a novel opportunity for the clinical application of SP-D in patients with COPD.展开更多
基金supported by a grant from the National Natural Sciences Foundation of China (No. 30871128)
文摘The purpose of this study was to investigate the changes of protein kinase Ca （PKCα） and cyclin D1 expressions in pulmonary arteries from＇smokers with normal lung function and smokers with mild to moderate chronic obstructive pulmonary disease （COPD）. The peripheral lung tissues were obtained from 10 non-smokers with normal lung function （non-smoker group）, 14 smokers with normal lung function （smoker group）, 11 smokers with mild to moderate COPD （COPD group）. The morphological changes of pulmonary arteries were observed by HE-staining. The expressions of ct-smooth muscle actin （α-SMA）, proliferating cell nuclear antigen （PCNA）, PKCα and cyclin D1 proteins in pulmonary artery smooth muscle cells （PASMCs） were immunohistochemically determined. The percentages of PCNA-positive cells were taken as the smooth muscle cells proliferation index （PI）. The mRNA expressions of PKCα and cyclin D l in PASMCs were evaluated by real-time fluorescence PCR. Morphometrical analysis showed that the ratio of pulmonary artery wall area to total area （WA%） in smoker group and COPD group was significantly greater than that in non-smoker group （P〈0.01）. The PASMCs proliferation index in smoker group and COPD group was significantly higher than that in nonsmoker group （P〈0.01）. The protein levels of PKCct and cyclin D1 inPASMCs were significantly increased in smoker group and COPD group as compared with non-smoker group （P〈0.01）. The mRNA expressions of PKCα and cyclin D1 in PASMCs were significantly elevated in smoker group and COPD group as compared with non-smoker group （P〈0.01）. Significant correlations were found between PKCα protein and WA% or PI （P〈0.01）. Correlations between cyclin D1 protein and WA% or PI also existed （P〈0.01）. The expression of PKCa was positively correlated with the expression of cyclin D 1 at both protein and mRNA levels （P〈0.01）. In conclusion, increased expressions of PKCα and cyclin D1 might be involved in the pathogenesis of abnormal proliferation of PASMCs in smokers with normal lung function and smokers with mild to moderate COPD.
文摘Objective: To observe the relationship of deep slow respiratory pattern and respiratory impedance(RI) in patients with chronic obstructive pulmonary disease (COPD). Methods: RI under normal respiration and during deep slow respira tion was measured one after the other with impulse oscillometry for 8 patients with COPD and for 9 healthy volunteers as control. Results: When r espiration was changed from normal pattern to the deep slow pattern, the tida l volume increased and respiratory frequency significantly decreased in both gro ups , the total respiratory impedance (Z respir) showed a decreasing trend in COPD group, but with no obvious change in the control group. No chang e in the resonant frequency (fres) was found in both groups, and the respiratory viscous resistance obviously decreased in the COPD group(R5: P =0.0168 ; R20: P =0.0498; R5—R20: P =0.0388),though in the control group it was unchanged. Conclusion: IOS detection could reflect the response he terogeneity of different compartments of respiratory system during tidal breathi ng. During deep slow respiration, the viscous resistance in both central airw ay and peripheral airway was decreased in patients with COPD. RI measurement by impulse oscillometry may be a convenient pathophysiological method for studying the application of breathing exercise in patients with COPD.
文摘Objective:To describe a patient with presarcopenia and chronic cough secondary to chronic obstructive pulmonary disease(COPD)successfully treated with supplements and physical exercise.Case report:A 75-year-old female patient with a positive past medical history of systemic hypertension,dyslipidemia,heart arrhythmia,and smoking during 20 years evolved with chronic cough due to a chronic obstructive pulmonary disease diagnosed ten years ago.She came to our private clinic due to low weight,low energy.Her weight was 44.8 kg,her height 1.57 m,body mass index of 18.18 kg/m^(2).Laboratory tests showed SDHEA 76.3,vitamin D of 15.6 ng/ml(nr:>30 ng/ml),C-reactive protein(CRP)of 55 mg/ml.Computed tomography showed bronchiectasis.She had an skeletal muscle mass index of 5.0 kg/m^(2)(nr:>5.5 kg/m^(2))by DXA.A diagnosis of presarcopenia was determined based on DXA evaluation with low muscle mass but normal gait speed handgrip strength.We suggested to the patient to increase physical exercise and prescribed a supplement formula.After five months,she returned asymptomatic,without cough,marked improvement of fatigue,increased energy levels,and weight increased to 50 kg,BMI of 20.28 kg/m^(2).Laboratory tests showed SDHEA to 140,vitamin D3 to 64.5 ng/ml,reduced CRP reduced to 5 mg/dl,and amlodipine was excluded due to better blood pressure control.Currently,two years later,the patient continues without cough and has dyspnea only with high efforts,without fatigue,and her weight is 52 kg and BMI 21.1 kg/m^(2).She also reduced her conventional treatment for COPD,using only a bronchodilator on-demand,without topical corticoids.Conclusions:This case illustrates an interesting case of a patient with presarcopenia and chronic cough,refractory to conventional approach,successfully treated with a combination of nutraceuticals and physical exercises.
基金supported by the Ministry of Science and Technology(MOST)of Taiwan(grant numbers 103-2321-B-006-030 and 104-2321-B-006-008),funding received in part from the Headquarters of University Advancement at the National Cheng Kung University,which is sponsored by the Ministry of Education in Taiwan,and a research grant(1JA8)from the Center for Allergy,Immunology,and Microbiome(A.I.M.),China Medical University Hospital,Taichung,Taiwan.
文摘Increased levels of surfactant protein D (SP-D) and lipid-laden foamy macrophages (FMs) are frequently found under oxidative stress conditions and/or in patients with chronic obstructive pulmonary disease (COPD) who are also chronically exposed to cigarette smoke (CS). However, the roles and molecular mechanisms of SP-D and FMs in COPD have not yet been determined. In this study, increased levels of SP-D were found in the bronchoalveolar lavage fluid (BALF) and sera of ozone- and CS-exposed mice. Furthermore, SP-D-knockout mice showed increased lipid-laden FMs and airway inflammation caused by ozone and CS exposure, similar to that exhibited by our study cohort of chronic smokers and COPD patients. We also showed that an exogenous recombinant fragment of human SP-D (rfhSP-D) prevented the formation of oxidized low-density lipoprotein (oxLDL)-induced FMs in vitro and reversed the airway inflammation and emphysematous changes caused by oxidative stress and CS exposure in vivo. SP-D upregulated bone marrow-derived macrophage (BMDM) expression of genes involved in countering the oxidative stress and lipid metabolism perturbations induced by CS and oxLDL. Our study demonstrates the crucial roles of SP-D in the lipid homeostasis of dysfunctional alveolar macrophages caused by ozone and CS exposure in experimental mouse emphysema, which may provide a novel opportunity for the clinical application of SP-D in patients with COPD.
