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Basic and clinical research into chronic obstructive pulmonary disease in China

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Chinese Medical Journal 2010年第4期123卷 491-497页

作者： LI Yuan-yuan liu xian-sheng XU Yong-jian Department of Respiratory Medicine Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430030 China

Chronic obstructive pulmonary disease （COPD）, one of the most common public health problemsworldwide, is the fourth leading cause of death in the world. In China, respiratory diseases （of which COPD is a major component） are the third leading cause of death in rural areas and the fourth leading cause of death in urban area, accounting for 1 million deaths and over 5 million disabilities each year. COPD ranks first among the burdens in China.1 Hence, medical workers and governments at different levels pay close attention to this disease~ The Respiratory Group under the Chinese Medical Association published the Guidelines for Diagnosis and Management of COPD in 2002^2 and the revised version in 2007^3. This publication serves as a milestone of the development of basic and clinical investigation in China. The guidelines are likely to affect the way for the treatment of COPD in addition to reflect the current knowledge about the underlying causes of COPD and recommend the proper diagnosis and management of COPD.

关键词： pulmonary disease, chronic obstructive prevalence risk factors etiology therapy China

CD8＋ Tc-lymphocytes immunodeviation in peripheral blood and airway from patients of chronic obstructive pulmonary disease and changes after short-term smoking cessation

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Chinese Medical Journal 2013年第19期 3608-3615页

作者： YU Mu-qing liu xian-sheng WANG Jian-miao XU Yong-jian Department of Respiratory and Critical Care Medicine TongjiHospital of Yongji Medical College Huazhong University of Scienceand Technology Wuhan Hubei 430030 China

Background Cigarette smoke induces an acute but persisting inflammation in peripheral blood and airway in chronic obstructive pulmonary disease （COPD）,and CD8＋ Tc-lymphocytes are considered as a key role in this *** aimed to investigate the Tc-lymphocytes immunodeviation in system and local airway of COPD patients and changes of the immunodeviation after short-term smoking *** Peripheral blood （PB） and bronchoalveolar lavage fluid （BALF） were collected from 42 patients （14 COPD patients,16 smokers with normal lung function and 12 nonsmokers）,while PB and induced sputum （IS） were obtained from other 19 patients （10 quitting smokers and 9 continuing smokers） at baseline and follow-up respectively of 4-week smoking *** of CD8＋ Tc-lymphocytes （%CD3＋） and Tc1/Tc2 ratios were measured by flow *** Percentages of CD8＋ Tc-lymphocytes were higher in COPD patients than those in smokers and nonsmokers in both PB and ***1/Tc2 ratio in PB and in BALF from COPD patients was greater than that from smokers and nonsmokers and negatively correlated with FEV1%*** comparing the ratios between PB and BALF,significantly positive correlation was found in COPD ***,after 4-week smoking cessation,percentages of CD8＋ Tc-lymphocytes in PB and IS in quitting smokers were decreased compared to that in baseline and continuing smokers,whereas Tc1/Tc2 ratios were not *** CD8＋ Tc1-trend immunodeviation profiles occurred in both system and local airway of COPD *** exceptional immunodeviation could not be relieved by short-term smoking cessation.

关键词： pulmonary disease, chronic obstructive smoke CD8-positive T-lymphocytes smoking cessation

Quantitative differentiation of dendritic cells in lung tissues of smokers with and without chronic obstructive pulmonary disease

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Chinese Medical Journal 2010年第12期123卷 1500-1504页

作者： SU Yan-wei XU Yong-jian liu xian-sheng Department of Respiratory Medicine Tongji Hospital affiliated to Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430030 China

Background Chronic obstructive pulmonary disease （COPD） is thought to be an inflammatory immune response disease. In most cases, the disease is caused by cigarette smoke, but it has been demonstrated that only 10% to 20% of smokers will definitely suffer from COPD. Dendritic cells （DCs） are considered to be the promoter of immune ***, the underlying mechanisms involved are still unrevealed. In this study, we aimed to investigate the quantitative differentiation of pulmonary DC in smokers with or without COPD to explore the possible role of DCs in smokers suffering *** Peripheral lung specimens from non-smokers without airflow obstruction （control group, n=7）, smokers without airflow obstruction （smoker group, n=7） and patients with COPD （COPD group, n=7） were investigated to detect the quantity of S-100 and CD1a positive cells by immunohistochemical or immunofluorescent *** In smokers with COPD, the number of S-100＋ DCs was higher than in the controls and smokers without COPD （P 〈0.01 and P 〈0.05） and there was a higher number of S-100＋ DCs in smokers with COPD than in smokers without COPD, but without a significant difference （P 〉0.05）. An inverse correlation was found between the number of DCs and forced expiratory volume in the first second （FEV1）% pred （r=-0.75, P 〈0.05）, which was also found between the number of DCs and FEV1/forced vital capacity （FVC）（r=-0.72, P 〈0.05）. The mean number of CD1a＋ DCs, increased from non-smokers to non-COPD smokers to COPD patients, with significant differences between each group （P 〈0.01）.Conclusions The quantity of DCs significantly increased in smokers with COPD compared with non-smokers or smokers without COPD. The results suggest that DCs may play an important role in the pathogenesis of smoking-induced COPD, and the upregulation of DCs may be a potential maker to identify the smokers who have more liability to suffer from COPD.

关键词： dendritic cells smoking chronic obstructive pulmonary disease

A Negative Thermal Expansion Material of ZrMgMo_(3)O_(12)

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Chinese Physics Letters 2013年第12期30卷 100-103页

作者： SONG Wen-Bo LIANG Er-Jun liu xian-sheng LI Zhi-Yuan YUAN Bao-He WANG Jun-Qiao School of Physical Science&Engineering and Key Laboratory of Materials Physics of Ministry of Education of China Zhengzhou UniversityZhengzhou 450052 North China University of Water Resources and Electric Power Zhengzhou 450011

A material with the formula ZrMgMo_(3)O_(12) having negative thermal expansion is presented and *** is shown that ZrMgMo_(3)O_(12) crystallizes in an orthorhombic symmetry with space group Pnma(62)or Pna21(33)and exhibits negative thermal expansion in a large temperature range(αl=-3.8×10^(-6) K^(-1) from 300 K to 1000 K by x-ray diffraction andαl=-3.73×10^(-6) K^(-1) from 295 K to 775 K by dilatometer).ZrMgMo_(3)O_(12) remains the orthorhombic structure without phase transition or decomposition at least from 123 K to 1200 K and is not *** properties make it an excellent material with negative thermal expansion for a variety of applications.

关键词： expansion thermal

Cigarette smoke extract promotes human pulmonary artery smooth muscle cells proliferation through protein kinase C alpha-dependent induction of cyclin D1

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Chinese Medical Journal 2010年第24期123卷 3663-3670页

作者： xianG Min XU Yong-jian liu xian-sheng ZENG Da-xiong Department of Respiratory Medicine Tongji Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430030 Chin Department of Respiratory Medicine Tongji Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430030 China

Background Exposure to cigarette smoke stimulates the proliferation of human pulmonary artery smooth muscle cells （HPASMCs） in vivo and in vitro. However, the molecular mechanism remains unclear. This study aimed at investigating the role of signaling pathways involving protein kinase C alpha （PKCα） and cyclin D1 in the cigarette smoke extract （CSE）-induced HPASMCs *** Synchronized HPASMCs were treated with different concentrations of CSE. Cell proliferation was evaluated by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyttetrazolium bromide （MTT） assay and cell counting. Cell cycle was analyzed by flow cytometry with propidium iodide staining. Activation of PKCα was measured by detecting the expression of PKCαprotein in the cytosolic and membrane fractions using Western blotting analysis. Small interfering RNA （siRNA） was used to knockdown PKCα and cyclin D1. The cyclin D1 mRNA was assessed by real-time RT-PCR. The PKCα and cyclin D1protein levels were detected by Western *** Low concentrations of CSE （1%-10%） stimulated proliferation of HPASMCs, with its maximal effect at 5%.CSE （5%） led to PKCα activation. Inhibition of PKCα activity using G（o） 6976 or siRNA-mediated knockdown of PKCα significantly attenuated CSE-induced cell proliferation and G1/S transition. Cyclin D1, one of key regulators of G1/S transition, was found to be upregulated by 5% CSE at both the mRNA and protein levels. CSE-stimulated cellproliferation and G1/S transition was abolished by cyclin D1 siRNA. Moreover, G（o） 6976 or PKCα siRNA significantlysuppressed CSE-induced upregulation of cyclin D1 at both the mRNA and protein *** PKCα-cyclin D1 pathway at least partially mediates the CSE-induced proliferation in HPASMCs.

关键词： cell proliferation cell cycle protein kinase C cyclin D1

Cigarette smoke extract promotes proliferation of airway smooth muscle cells in asthmatic rats via regulating cyclin D1 expression

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Chinese Medical Journal 2010年第13期123卷 1709-1714页

作者： ZHANG Xiao-yu XU Yong-jian liu xian-sheng ZHANG Zhen-xiang Department of Respiratory Medicine Tongji Hospital Affiliated to Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430030 China Department of Respiratory Medicine Henan Provincial People's Hospital Zhengzhou Henan 450003 China

Background Increased proliferation of airway smooth muscle cells （ASMCs） are observed in asthmatic patients and smoking can accelerate proliferation of ASMCs in asthma. To elucidate the molecular mechanisms leading to these changes, we studied in vitro the effect of cigarette smoke extract （CSE） on the proliferation of ASMCs and the expression of cyclin D1, an important regulatory protein implicated in cell cycle. Methods ASMCs cultured from 8 asthmatic Brown Norway rats were studied. Cells between passage 3 and 6 were used in the study and were divided into control group, pcDNA3.1 group, pcDNA3.1-antisense cyclin D1 （ascyclin D1） group, CSE group, CSE＋pcDNA3.1 group and CSE＋pcDNA3.1-ascyclin D1 group based on the conditions for intervention. The proliferation of ASMCs was examined with cell cycle analysis, MTT colorimetric assay and proliferating cell nuclear antigen （PCNA） immunocytochemical staining. The expression of cyclin D1 was detected by reverse transcriptase-PCR （RT-PCR） and Western blotting. Results （1） The percentage of S＋G2M phase, absorbance value at 490 nm wavelength （A490） and the expression rate of PCNA protein in CSE group were （31.22±1.17）%, 0.782±0.221, （90.2±7.0）% respectively, which were significantly increased compared with those of control group （18.36±1.02）%, 0.521±0.109, and （54.1±3.5）%, respectively）（P 〈0.01）. After the transfection with antisense cyclin D1 plasmid for 30 hours, the percentage of S＋G2M phase, A490 and the expression rate of PCNA protein in ASMCs were much lower than in untreated cells （P 〈0.01）. （2） The ratios of A490 of cyclin D1 mRNA in CSE group was 0.288±0.034, which was significantly increased compared with that of control group （0.158±0.006）（P 〈0.01）. After the transfection with antisense cyclin D1 plasmid for 30 hours, the ratios of A49o of cyclin D1 mRNA in ASMCs was much lower than in untreated cells （P 〈0.01）. （3） The ratios of A490 of cyclin D1 protein expression in CSE group was 0.375±0.008, which was signifi

关键词： cigarette smoke extract asthma airway smooth muscle cells proliferation cyclin D1

Role of extracellular signal-regulated kinase in regulating expression of interleukin 13 in lymphocytes from an asthmatic rat model

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Chinese Medical Journal 2010年第13期123卷 1715-1719页

作者： LI Yuan-yuan liu xian-sheng liu Chang XU Yong-jian XIONG Wei-ning Department of Respiratory Medicine Tongji Hospital Tongii Medical College Huazhong University of Science and Technology Wuhan Hubei 430030 China

Background The extracellular signal-regulated kinase （ERK） is widely expressed in mammal cells and involved in airway proliferation and remodeling in asthma. In this study, we intend to explore the role of ERK in the expression of the Th2 cytokine, interleukin 13 （IL-13） in lymphocytes in asthma. Methods Forty Sprague-Dawley rats were randomly divided into two groups： normal control and asthmatic groups. Peripheral blood lymphocytes were isolated and purified from the blood of each rat and divided into five groups： control, asthmatic lymphocytes, asthmatic cells stimulated with ERK activator epidermal growth factor （EGF）, or with ERK inhibitor PD98059, or with EGF and PD98059 together. The expression of phosphorylated-ERK （p-ERK） was observed by immunocytochemical staining, the expression of ERK mRNA was determined by reverse transcriptase-PCR, IL-13 protein in supernatants was measured by ELISA. Results （1） The ERK mRNA level and the percentage of cells with p-ERK in lymphocytes from asthmatic rats were significantly higher than those in normal controls, and were significantly increased by EGF administration. This effect of EGF was significantly inhibited by PD98059 pretreatment. （2） IL-13 protein in supernatants of asthmatic lymphocytes was higher than that produced by normal control lymphocytes, and was significantly increased by EGF treatment. This EGF effect was partly blocked by PD98059 pretreatment. （3） There was a significant positive correlation between the percentage of cells with p-ERK in peripheral blood lymphocytes and IL-13 protein in supernatants of lymphocytes from asthmatic rats. Conclusions In asthma the ERK expression and activation levels were increased, as was the protein level of IL-13. The ERK signaling pathway may be involved in the increased expression of the Th2 cytokine IL-13 in asthma.

关键词： asthma interleukin 13 lymphocytes extraceUular signal-regulated MAP kinases

Expression of Nitric Oxide Synthase Isoenzyme in Lung Tissue of Smokers with and without Chronic Obstructive Pulmonary Disease

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Chinese Medical Journal 2015年第12期128卷 1584-1589页

作者： Wen-Ting Jiang xian-sheng liu Yong-Jian Xu Wang Ni Shi-Xin Chen Department of Respiratory Medicine Tongji Hospital Affiliated to Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430030 China

Background：It has been demonstrated that only 10%-20% cigarette smokers finally suffer chronic obstructive pulmonary disease （COPD）.The underlying mechanism of development remains uncertain so *** oxide （NO） has been found to be closely associated with the pathogenesis of COPD,the alteration of NO synthase （NOS） expression need to be *** study aimed to investigate the alterations of NOS isoforms expressions between smokers with and without COPD,which might be helpful for identifying the susceptibility of smokers developing into ***：Peripheral lung tissues were obtained from 10 nonsmoker control subjects,15 non-COPD smokers,and 15 smokers with *** NOS （nNOS）,inducible NOS （iNOS）,and endothelial NOS （eNOS） mRNA and protein levels were measured in each sample by using real-time polymerase chain reaction and Westem ***：INOS mRNA was significantly increased in patients with COPD compared with nonsmokers and smokers with normal lung function （P 〈 0.001,P =0.001,respectively）.iNOS protein was also higher in COPD patients than nonsmokers and smokers with normal lung function （P 〈 0.01 and P =0.01,respectively）.However,expressions ofnNOS and eNOS did not differ among nonsmokers,smokers with and without ***,there was a negative correlation between iNOS protein level and lung function parameters forced expiratory volume in 1 s （FEV1）（% predicted）（r =-0.549,P =0.001） and FEV1/forced vital capacity （%,r =-0.535,P =0.001）.Conclusions：The expression of iNOS significantly increased in smokers with COPD compared with that in nonsmokers or smokers without *** results suggest that iNOS might be involved in the pathogenesis of COPD,and may be a potential marker to identify the smokers who have more liability to suffer COPD.

关键词： Chronic Obstructive Pulmonary Disease Nitric Oxide Synthase Smoking

Dynamic DNA methylation associated with histone modifications regulates hormone-induced stem cell formation during shoot regeneration in Arabidopsis

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Dynamic DNA methylation associated with histone modification...