ABSTRACT
The number of smokers in Chinese rural areas is more than 200 million, which is twice that in cities. It is very significant to carry out tobacco control interventions in rural areas. We performed this community intervention study to evaluate the efficacy of village-based health education of tobacco control on the male current smoking rate in rural areas. The population of this study was the males above 15 years old from 6 villages in rural areas. The villages were randomly assigned to intervention group or control group (3 villages in each group). Self-designed smoking questionnaire was applied. The intervention group received the village-based health education of tobacco control for one year. The primary outcome measurement was the male current smoking rate. In the baseline investigation, completed surveys were returned by 814 male residents from the control group and 831 male residents from the intervention group. The male current smoking rate in the control group and the intervention group was 61.2% and 58.5%, respectively, before intervention. There was no significant difference between these two groups (P>0.05). After one-year intervention, the current smoking rate in the intervention group (51.2%) was significantly lower than that in the control group (62.8%) (P<0.001). Our study suggested that the village-based health education of tobacco control was effective in lowering the male current smoking rate in rural areas, which could be a suitable and feasible way for tobacco control in the Chinese rural areas.
ABSTRACT
The number of smokers in Chinese rural areas is more than 200 million, which is twice that in cities. It is very significant to carry out tobacco control interventions in rural areas. We performed this community intervention study to evaluate the efficacy of village-based health education of tobacco control on the male current smoking rate in rural areas. The population of this study was the males above 15 years old from 6 villages in rural areas. The villages were randomly assigned to intervention group or control group (3 villages in each group). Self-designed smoking questionnaire was applied. The intervention group received the village-based health education of tobacco control for one year. The primary outcome measurement was the male current smoking rate. In the baseline investigation, completed surveys were returned by 814 male residents from the control group and 831 male residents from the intervention group. The male current smoking rate in the control group and the intervention group was 61.2% and 58.5%, respectively, before intervention. There was no significant difference between these two groups (P>0.05). After one-year intervention, the current smoking rate in the intervention group (51.2%) was significantly lower than that in the control group (62.8%) (P<0.001). Our study suggested that the village-based health education of tobacco control was effective in lowering the male current smoking rate in rural areas, which could be a suitable and feasible way for tobacco control in the Chinese rural areas.
Subject(s)
Adolescent , Adult , Humans , Male , Middle Aged , Case-Control Studies , China , Delivery of Health Care , Methods , Health Education , Methods , Rural Population , Smoking Prevention , Tobacco Use CessationABSTRACT
Cigarette smoke is associated with the development of several diseases, such as chronic obstructive pulmonary disease (COPD). The purpose of this study was to investigate genotoxicity and heat shock protein 70 (Hsp70) in human airway smooth muscle cells (HASMCs) exposed to cigarette smoke extract (CSE). HASMCs was exposed to CSE with different doses for 24 h. The level of 8-hydroxydeoxyguanosine (8-OHdG) was determined by using HPLC-ECD, the DNA damage was analyzed by using comet assay, and apoptosis was examined by using Annexin-FITC/PI staining. The production of Hsp70 after CSE stimulation was tested. Results indicated that CSE significantly increased the level of 8-OHdG, DNA damage and cell apoptosis, and reduced the production of Hsp70. In particular, levels of Hsp70 were inversely correlated with 8-OHdG, DNA damage and cell apoptosis. It was concluded that cigarette smoke induced genotoxicity and decreased the production of cell protective protein Hsp70, which may contribute to the development of some airway diseases.
ABSTRACT
In order to study whether cysteine-rich 61 protein (cyr61) is involved in the pathogenesis of asthma and its relation to airway inflammation, the effect of dexamethasone (Dxm) on the expression of cyr61 in the lung tissues of asthmatic mice was investigated. Forty BALB/c mice were divided into asthma group (n=15), control group (n=10) and Dxm group (n=15). The asthma group was sensitized and challenged by ovalbumin (OVA). The mice in Dxm group were intraperitoneally administered with Dxm after OVA challenge. The expression of cyr61 in the lung tissues was detected by using immunohistochemistry, and that of eotaxin protein in the bronchoalveolar lavage fluid (BALF) by using enzyme-linked immunosorbent assay (ELISA). The number of inflammatory cells in BALF was also analyzed. The results showed that the cyr61 expression was highest in asthma group (P<0.05), followed by Dxm group (P<0.05) and control group. The cyr61 had a positive correlation with the total nucleated cells (r=0.867, P<0.05), especially eosinophils (r=0.856, P<0.05), and eotaxin level (r=0.983, P<0.05) in the BALF. Our findings suggested that cyr61 is expressed in airway epithelial cells and has a positive correlation with eotaxin and number of airway infiltrating eosinophils.
ABSTRACT
In order to study whether cysteine-rich 61 protein (cyr61) is involved in the pathogenesis of asthma and its relation to airway inflammation, the effect of dexamethasone (Dxm) on the expression of cyr61 in the lung tissues of asthmatic mice was investigated. Forty BALB/c mice were divided into asthma group (n=15), control group (n=10) and Dxm group (n=15). The asthma group was sensitized and challenged by ovalbumin (OVA). The mice in Dxm group were intraperitoneally administered with Dxm after OVA challenge. The expression of cyr61 in the lung tissues was detected by using immunohistochemistry, and that of eotaxin protein in the bronchoalveolar lavage fluid (BALF) by using enzyme-linked immunosorbent assay (ELISA). The number of inflammatory cells in BALF was also analyzed. The results showed that the cyr61 expression was highest in asthma group (P<0.05), followed by Dxm group (P<0.05) and control group. The cyr61 had a positive correlation with the total nucleated cells (r=0.867, P<0.05), especially eosinophils (r=0.856, P<0.05), and eotaxin level (r=0.983, P<0.05) in the BALF. Our findings suggested that cyr61 is expressed in airway epithelial cells and has a positive correlation with eotaxin and number of airway infiltrating eosinophils.
Subject(s)
Animals , Female , Mice , Anti-Inflammatory Agents , Pharmacology , Asthma , Drug Therapy , Metabolism , Bronchoalveolar Lavage Fluid , Chemistry , Cell Biology , Chemokines, CC , Metabolism , Cysteine-Rich Protein 61 , Dexamethasone , Pharmacology , Enzyme-Linked Immunosorbent Assay , Epithelial Cells , Metabolism , Pathology , Immunohistochemistry , Injections, Intraperitoneal , Leukocyte Count , Lung , Metabolism , Pathology , Mice, Inbred BALB C , Neutrophils , Pathology , OvalbuminABSTRACT
Cigarette smoke is associated with the development of several diseases, such as chronic obstructive pulmonary disease (COPD). The purpose of this study was to investigate genotoxicity and heat shock protein 70 (Hsp70) in human airway smooth muscle cells (HASMCs) exposed to cigarette smoke extract (CSE). HASMCs was exposed to CSE with different doses for 24 h. The level of 8-hydroxydeoxyguanosine (8-OHdG) was determined by using HPLC-ECD, the DNA damage was analyzed by using comet assay, and apoptosis was examined by using Annexin-FITC/PI staining. The production of Hsp70 after CSE stimulation was tested. Results indicated that CSE significantly increased the level of 8-OHdG, DNA damage and cell apoptosis, and reduced the production of Hsp70. In particular, levels of Hsp70 were inversely correlated with 8-OHdG, DNA damage and cell apoptosis. It was concluded that cigarette smoke induced genotoxicity and decreased the production of cell protective protein Hsp70, which may contribute to the development of some airway diseases.
Subject(s)
Humans , Apoptosis , DNA Damage , Deoxyguanosine , Metabolism , HSP70 Heat-Shock Proteins , Genetics , Metabolism , Lung , Cell Biology , Myocytes, Smooth Muscle , Metabolism , Smoke , Nicotiana , Toxicity , Tumor Cells, CulturedABSTRACT
<p><b>BACKGROUND</b>Cigarette-smoke induced DNA damage can cause airway cell apoptosis and death, which may be associated with the development of chronic obstructive pulmonary disease (COPD). However, only 20% - 30% of smokers develop COPD, suggesting that different degrees of DNA repair produce different outcomes in smokers, i.e., part of them develop COPD. We investigated the association between polymorphisms in DNA repair genes hOGG1 (Ser326Cys) and XRCC1 (Arg399Gln), alone or in combination, and susceptibility of COPD.</p><p><b>METHODS</b>Altogether 201 COPD patients and 309 controls were recruited and frequency-matched on age and sex. hOGG1 and XRCC1 genotypes were determined by PCR-restriction fragment length polymorphism analysis.</p><p><b>RESULTS</b>The risk of COPD was not significantly different among individuals with Ser/Cys and Cys/Cys genotypes compared with those with hOGG1 Ser/Ser genotype. The risk of COPD was not significantly different among individuals with Gln/Gln genotype compared with those with XRCC1 Arg/Arg genotype, but it was significantly elevated among individuals with Arg/Gln genotype (adjusted odds ratios (OR) = 1.55, 95% confidence intervals (CI) 1.05 - 2.29, P = 0.029). Assessment of smoking status in current smokers compared with those with hOGG1 Ser/Ser genotype revealed that the risk of COPD was significantly elevated among individuals with Cys/Cys genotype (adjusted OR = 5.07, 95% CI 1.84 - 13.95, P = 0.002). Compared with those with XRCC1 Arg/Arg genotype, the risk of COPD was significantly elevated among individuals with Arg/Gln genotype (adjusted OR = 2.77, 95% CI 1.52 - 5.07, P = 0.001). Assessment of smoking exposure in light smokers compared with those with hOGG1 Ser/Ser genotype showed that the risk of COPD was significantly elevated among individuals with Cys/Cys genotype (adjusted OR = 4.02, 95% CI 1.05 - 16.80, P = 0.042). Compared with those with XRCC1 Arg/Arg genotype, the risk of COPD was significantly elevated among individuals with Gln/Gln genotype (adjusted OR = 4.48, 95% CI 1.35 - 14.90, P = 0.014). In heavy smokers compared with those with XRCC1 Arg/Arg genotype, the risk of COPD was significantly elevated among individuals with Arg/Gln genotype (adjusted OR = 2.55, 95% CI 1.42 - 4.58, P = 0.002). When hOGG1 Ser326Cys and XRCC1 Arg399Gln polymorphisms were evaluated together, compared with those with 0 - 1 of hOGG1 326Cys and XRCC1 399Gln alleles, the risk of COPD was significantly elevated among individuals with 3 - 4 of hOGG1 326Cys and XRCC1 399Gln alleles (adjusted OR = 3.18, 95% CI 1.86 - 5.43, P = 0.000). Assessment of smoking status and smoking exposure in current/light/heavy smokers showed that the risk of COPD was significantly elevated among individuals with 3 - 4 of hOGG1 326Cys and XRCC1 399Gln alleles (adjusted OR = 8.32, 95% CI 3.59 - 19.27, P = 0.000; OR = 5.46, 95% CI 2.06 - 14.42, P = 0.001; OR = 2.93, 95% CI 1.43 - 6.02, P = 0.003; respectively).</p><p><b>CONCLUSIONS</b>hOGG1 Ser326Cys and XRCC1 Arg399Gln polymorphisms are associated with the susceptibility to COPD. The risk of COPD is significantly elevated among current/light smokers with hOGG1 326Cys and XRCC1 399Gln.</p>
Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , DNA Glycosylases , Genetics , DNA-Binding Proteins , Genetics , Genetic Predisposition to Disease , Genetics , Genotype , Polymerase Chain Reaction , Polymorphism, Genetic , Polymorphism, Restriction Fragment Length , Pulmonary Disease, Chronic Obstructive , Genetics , X-ray Repair Cross Complementing Protein 1ABSTRACT
This study is to investigate the expression of CyclinD1 in asthmatic rats and construct expression plasmids of sense and antisense CyclinD1 gene and transfect them to asthmatic airway smooth muscle cell to study the effects of CyclinD1 on the proliferation of airway smooth muscle cells in asthmatic rats. CyclinD1 cDNA was obtained by RT-PCR of total RNA extracted from the airway smooth muscle in asthmatic rats. The sequence was inserted into eukaryotic expression vector pcDNA3.1 (+) to recombinate the sense and antisense pcDNA3.1-CyclinD1 eukaryotic expression vector. The two recombinations and vector were then separately transfected into airway smooth muscle cell in asthmatic rats by using liposome. The expression level of CyclinD1 was certificated by Western blotting analysis. The proliferations of ASMCs isolated from asthmatic rats were examined with cell cycle analysis, MTT colorimetric assay and proliferating cell nuclear antigen (PCNA) immunocytochemical staining. Results showed (1) Compared with control group, the content of CyclinD1 was significantly increased; (2) It was comformed by restriction endonucleasa digestion and DNA sequence analysis that the expression plasmid of sense and antisense CyclinD1 were successfully recombinated. There was significant change of CyclinD1 expression between vector and sense CyclinD1 transfected cells, and the expression level of CyclinD1 in ASMC transfected with antisense CyclinD1 was lower than that in vector transfected cells (P <0.01); (3) In the asthmatic groups, compared with the vecter group, the percentage of S + G2M phase, absorbance A value of MTT and the expression rate of PCNA protein in ASMC transfected with pcDNA3. 1-CyclinD1 vector significantly increased. The values decreased remarkably in the pcDNA3,1-as CyclinD1 group. Statistical analysis revealed that there were significant differences in these indicators of cell proliferation in three groups (P <0.01). In the normal groups, statistical analysis revealed that there were significant differences in the percentage of S + G2M phase, a value of MTT and the expression rate of PCNA protein in three groups (P <0.01). Sense CyclinD1 eukaryotic expression vectors could have a positive effect on the proliferation of ASMC, however the antisence one have a negative effect, which implicated that CyclinD1 might contribute to the process of airway smooth muscle cell proliferation.
Subject(s)
Animals , Male , Rats , Asthma , Pathology , Cell Cycle , Cell Proliferation , Codon , Genetics , Pharmacology , Cyclin D1 , Genetics , DNA, Antisense , Genetics , Pharmacology , Disease Models, Animal , Gene Expression , Genetic Vectors , Genetics , Myocytes, Smooth Muscle , Pathology , Rats, Sprague-Dawley , Recombination, Genetic , Genetics , Respiratory System , Reverse Transcriptase Polymerase Chain Reaction , Transduction, Genetic , TransfectionABSTRACT
<p><b>BACKGROUND</b>Airway smooth muscle (ASM) is suspected to be a determining factor in the structural change of asthma. However, the role of protein kinase C alpha (PKCalpha) and cyclin D1 involved in the dysfunction of ASM leading to asthmatic symptoms is not clear. In this study, the central role of PKCalpha and cyclin D1 in ASM proliferation in asthmatic rats was explored.</p><p><b>METHODS</b>Thirty-six pathogen-free male Brown Norway (BN) rats were randomly divided into 2 groups: control groups (group N1, N2 and N3) and asthmatic groups (group A1, A2, and A3). Groups A1, A2 and A3 were challenged with ovalbumin (OA) for 2 weeks, 4 weeks and 8 weeks respectively. Control animals were exposed to an aerosolized sterile phosphate buffered saline (PBS). The ASM mass and nucleus numbers were studied to estimate the degree of airway remodeling by the hematoxylin-eosin staining method. PKCalpha and cyclin D1 expression in the ASM cells was detected by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. The relation between PKCalpha and cyclin D1 was assessed by linear regression analysis. PKC agonist phorbol 12-myristate 13-acetate (PMA), PKC inhibitor Ro31-8220 and an antisense oligonucleotide against cyclin D1 (ASOND) were used to treat ASM cells (ASMCs) obtained from the 2 weeks asthmatic rats. The cyclin D1 protein expression level was detected by Western blotting.</p><p><b>RESULTS</b>Compared with the control group, the PKCalpha and cyclin D1 mRNA levels were increased in the asthmatic group. Similar to RT-PCR results, immunohistochemistry analysis for PKCalpha and cyclin D1 expression revealed an increased production in ASMCs after allergen treatment for 2, 4 and 8 weeks compared with the respective control groups. No difference in expression of PKCalpha and cyclin D1 in ASM were found in the 2, 4 or 8 weeks asthmatic rats. There were significant positive correlations between PKCalpha and cyclin D1 expression, both transcriptionally (r = 0.944, P < 0.01) and translationally (r = 0.826, P < 0.01), in ASM. The content of cyclin D1 in asthmatic ASMCs increased after being stimulated by PMA, and decreased when induced by Ro31-8220. ASOND targeting for cyclin D1 lowered the expression of cyclin D1 induced by PMA.</p><p><b>CONCLUSIONS</b>Increased expression of PKCalpha and cyclin D1 in ASM along with smooth muscle structure changes might implicate PKCalpha and cyclin D1 participation in the proliferation of ASM and contribute to the pathogenesis of asthma after repeated allergen exposure in rats. The results suggested that cyclin D1 might be downstream of PKC signal transduction pathway.</p>
Subject(s)
Animals , Male , Rats , Asthma , Pathology , Cell Proliferation , Cyclin D1 , Genetics , Physiology , Lung , Pathology , Myocytes, Smooth Muscle , Pathology , Protein Kinase C-alpha , Genetics , Physiology , RNA, Messenger , Rats, Inbred BNABSTRACT
Objective To explore the expression of tissue inhibitor of metalloproteinases-2(TIMP-2) in peripheral blood lymphocytes in patients with chronic obstructive pulmonary diseases(COPD) and the association of smoking and TIMP-2 mRNA. Methods The expression of TIMP-2 mRNA in peripheral blood lymphocytes was measured by reverse transcription-polymerase chain reaction(RT-PCR) in 44 patients with COPD and 42 healthy smokers.The correlation analysis was then conducted between TIMP-2 mRNA expression and smoking index. Results The expression of TIMP-2 mRNA was 0.753?0.154 and 1.170?0.196,respectively,in patients with COPD and healthy smokers(P
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<p><b>OBJECTIVE</b>To investigate whether polymorphism in gene for surfactant protein A(SPA) has any bearing on individual susceptibility to the development of chronic obstructive pulmonary disease(COPD).</p><p><b>METHODS</b>The genotypes of 88 patients with COPD and 87 healthy smoking subjects as controls were tested with polymerase chain reaction followed by restriction fragment length polymorphism analysis for SPA gene.</p><p><b>RESULTS</b>In COPD group, the frequencies of +186 locus genotypes AA, AG and GG were 86.4%, 12.5% and 1.1%i respectively and in the control group, these were 66.7%, 27.6% and 5.7%; the frequencies of polymorphic genotypes or alleles showed statistically significant difference between the COPD group and the control group(P<0.05). The frequencies of polymorphic genotypes at +655 locus and +667 loci showed no significant difference between the COPD group and the control group in(P>0.05).</p><p><b>CONCLUSION</b>Genetic polymorphism in SPA is associated with the development of COPD in the Chinese Hans.</p>
Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Alleles , Gene Frequency , Genetic Predisposition to Disease , Genetics , Genotype , Polymerase Chain Reaction , Polymorphism, Genetic , Pulmonary Disease, Chronic Obstructive , Genetics , Pulmonary Surfactant-Associated Protein A , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To determine whether 2 polymorphism sites of the high-affinity IgE receptor beta (Fc epsilon RI beta) gene were associated with allergic asthma in Han nationality of Hubei province in China.</p><p><b>METHODS</b>DNA and clinical data were obtained from allergic asthma patients and were compared with those from a group of healthy control subjects. The subjects were genotyped for the -109C/T and a coding variant Glu237Gly in Fc epsilon RI beta gene by polymerase chain reaction-restriction fragment length polymorphism.</p><p><b>RESULTS</b>(1) The genotype frequencies were 0.403 for -109T/T, 0.491 for -109T/C and 0.106 for -109C/C in allergic asthma patients in a Chinese population. No significant difference in the distribution of -109C/T polymorphism was found between allergic asthma patients and healthy control subjects; however, a homozygosity for the -109T allele was associated with increased total plasma IgE levels in patients with allergic asthma (F=7.523, P<0.01). (2) The frequency of Gly237Gly genotype was 0.051 in patient group, and 0.020 in control group. The allele frequencies of Gly237 in the patients and control were 0.236 and 0.136 respectively. There was a significant association between Gly/Gly genotype and allergic asthma. Among allergic asthma patients Gly237Gly was significantly associated with high IgE.</p><p><b>CONCLUSION</b>These data suggested that the Gly237Gly genotype of the Fc epsilon RI beta gene conferred genetic susceptibility to allergic asthma in Chinese, which affected the total plasma IgE levels in the allergic asthma patients. And a homozygosity for the -109T allele was associated with increased total plasma IgE.</p>
Subject(s)
Adolescent , Adult , Aged , Child , Child, Preschool , Female , Humans , Male , Middle Aged , Young Adult , Asian People , Genetics , Asthma , Blood , Genetics , China , Gene Frequency , Genetic Predisposition to Disease , Genetics , Genotype , Immunoglobulin E , Blood , Polymerase Chain Reaction , Polymorphism, Genetic , Polymorphism, Restriction Fragment Length , Promoter Regions, Genetic , Genetics , Receptors, IgE , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To investigate the polymorphism of interleukin-10 (IL-10) gene promoters in Chinese Han people, and to disclose whether such polymorphism is associated with susceptibility to chronic obstructive pulmonary disease (COPD).</p><p><b>METHODS</b>After the process of extracting genomic DNA from blood of 94 health smokers and 88 COPD smokers by use of phenol-chloroform-isoamyl alcohol, three single nucleotide polymorphism (SNP) sites in IL-10 gene promoter marked as -1082G/A,-819C/T,-592C/A were determined by polymerase chain reaction/restriction fragment length polymorphism analysis.</p><p><b>RESULTS</b>Eleven different promoter genotypes were detected from all of the 182 smokers, and AA*TT*AA, AA*TC*AC, AA*TC*AA genotypes accounted for about 80% of genotypes in the research subjects. Two previously unreported haplotypes of IL-10 gene promoter (ATC and ACA) were found in Chinese Han people by analyzing the promoter genotypes. -1082G/A and -592C/A SNP sites polymorphisms were not associated with susceptibility to COPD, whereas the genotypes of -819C/T SNP site were associated with susceptibility to COPD in Chinese Han people. In respect to the alleles frequencies of the three SNP sites respectively, the Chinese Hans were similar to Japanese, but different from whites.</p><p><b>CONCLUSION</b>Polymorphism of IL-10 -819C/T SNP site is associated with susceptibility to COPD in Chinese Han people; at least five haplotypes of IL-10 gene promoter (ATA, ACC, GCC, ATC and ACA) exist in Chinese Han people.</p>