Objectives: This study Development of a healthy college life, and effective for smoking cessation programs for education is to utilize as a basis for. Methods: The study employs frequency analysis, cross-analysis and correlation analysis through SPSS Win 17.0 on 296 (84.6% of total participants) from the entire participants of 350. The significance test is delivered with ${\chi}^2$-test. Results: 1) The participants consist of 47.7% (147) males and 52.3% (161) females. 78.2% (241) has experience of smoking cessation program at high school. 61.7% (190) has parents who are smoking. 40.9% (126) answers that they are currently smoking while 59.1% (182) answers that they are not. 2) When asked about their perception on quitting smoking, 81.2% (250) says that non-smokers are distressed by others' smoking. 74.0% (228) has unpleasant experience with cigarette smoke. 3) The analysis of the relation between smoking cessation program at high school and smoking shows that 63.8% of the ones who have experience of the program are non-smokers while 68.7% of those with no experience of the program are smokers. 4) Among those who have tried to quit smoking, 73.9% have experience of smoking cessation program at high school. 31.8% of these participants also reveal their interest in the cessation program. 5) In the analysis of the correlation between smoking habits, the experience of smoking cessation program at high school is closely related to non-smoking while current smoking habit is highly related to the strong interest in participation of cessation program. Also, the more interest they have in participating, the stronger needs they feel for smoking prevention program at college. Conclusion: Therefore, the last phase of education-related courses at the University of educated and credits granted through open non-smoking pledge, non-smoking club, non-smoking camps, training programs, such as smoking in non-smoking education and programs for students interested in openness and participation must be done will.
Kim, You-Sun;Kim, Ji-Young;Huh, Jin Won;Lee, Sei Won;Choi, Soo Jin;Oh, Yeon-Mok
Tuberculosis and Respiratory Diseases
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제78권3호
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pp.239-245
/
2015
Background: Chronic obstructive pulmonary disease is characterized by emphysema, chronic bronchitis, and small airway remodeling. The alveolar destruction associated with emphysema cannot be repaired by current clinical practices. Stem cell therapy has been successfully used in animal models of cigarette smoke- and elastase-induced emphysema. However, the optimal dose of mesenchymal stem cells (MSCs) for the most effective therapy has not yet been determined. It is vital to determine the optimal dose of MSCs for clinical application in emphysema cases. Methods: In the present study, we evaluated the therapeutic effects of various doses of MSCs on elastase-induced emphysema in mice. When 3 different doses of MSCs were intravenously injected into mice treated with elastase, only $5{\times}10^4$ MSCs showed a significant effect on the emphysematous mouse lung. We also identified action mechanisms of MSCs based on apoptosis, lung regeneration, and protease/antiprotease imbalance. Results: The MSCs were not related with caspase-3/7 dependent apoptosis. But activity of matrix metalloproteinase 9 increased by emphysematous lung was decreased by intravenously injected MSCs. Vascular endothelial growth factor were also increased in lung from MSC injected mice, as compared to un-injected mice. Conclusion: This is the first study on the optimal dose of MSCs as a therapeutic candidate. This data may provide important basic data for determining dosage in clinical application of MSCs in emphysema patients.
Background: Smoking is a risk factor for idiopathic pulmonary fibrosis (IPF), but the mechanism of the association remains obscure. There is evidence demonstrating that plasminogen activator inhibitor-1 (PAI-1) is involved in the progression of pulmonary fibrosis. This study was to determine whether the administration of small interfering RNA (siRNA) targeting PAI-1 or PAI-1 inhibitor to the cigarette smoking extract (CSE)-exposed rat alveolar type II epithelial cells (ATII cells) limits the epithelial-mesenchymal transition (EMT). Methods: ATII cells were isolated from lung of SD-rat using percoll gradient method and cultured with 5% CSE. The EMT was determined from the ATII cells by measuring the real-time RT PCR and western blotting after the PAI-1 siRNA transfection to the cells and after administration of tiplaxtinin, an inhibitor of PAI-1. The effect of PAI-1 inhibitor was also evaluated in the bleomycin-induced rats. Results: PAI-1 was overexpressed in the smoking exposed ATII cells and was directly associated with EMT. The EMT from the ATII cells was suppressed by PAI-1 siRNA transfection or administration of tiplaxtinin. Signaling pathways for EMT by smoking extract were through the phosphorylation of SMAD2 and ERK1/2, and finally Snail expression. Tiplaxtinin also suppressed the pulmonary fibrosis and PAI-1 expression in the bleomycin-induced rats. Conclusion: Our data shows that CSE induces rat ATII cells to undergo EMT by PAI-1 via SMAD2-ERK1/2-Snail activation. This suppression of EMT by PAI-1 siRNA transfection or PAI-1 inhibitor in primary type II alveolar epithelial cells might be involved in the attenuation of bleomycin-induced pulmonary fibrosis in rats.
Lee, Jeon-Soo;Lee, Joo Young;Lee, Mi Young;Hwang, Daniel H.;Youn, Hyung Sun
Molecules and Cells
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제25권2호
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pp.253-257
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2008
Acrolein is a highly electrophilic ${\alpha},{\beta}$-unsaturated aldehyde present in a number of environmental sources, especially cigarette smoke. It reacts strongly with the thiol groups of cysteine residues by Michael addition and has been reported to inhibit nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) activation by lipopolysaccharide (LPS). The mechanism by which it inhibits $NF-{\kappa}B$ is not clear. Toll-like receptors (TLRs) play a key role in sensing microbial components and inducing innate immune responses, and LPS-induced dimerization of TLR4 is required for activation of downstream signaling pathways. Thus, dimerization of TLR4 may be one of the first events involved in activating TLR4-mediated signaling pathways. Stimulation of TLR4 by LPS activates both myeloid differential factor 88 (MyD88)- and TIR domain-containing adapter inducing $IFN{\beta}$ (TRIF)-dependent signaling pathways leading to activation of $NF-{\kappa}B$ and IFN-regulatory factor 3 (IRF3). Acrolein inhibited $NF-{\kappa}B$ and IRF3 activation by LPS, but it did not inhibit $NF-{\kappa}B$ or IRF3 activation by MyD88, inhibitor ${\kappa}B$ kinase $(IKK){\beta}$, TRIF, or TNF-receptor-associated factor family member-associated $NF-{\kappa}B$ activator (TANK)-binding kinase 1 (TBK1). Acrolein inhibited LPS-induced dimerization of TLR4, which resulted in the down-regulation of $NF-{\kappa}B$ and IRF3 activation. These results suggest that activation of TLRs and subsequent immune/inflammatory responses induced by endogenous molecules or chronic infection can be modulated by certain chemicals with a structural motif that enables Michael addition.
Acrolein, a known toxin in cigarette smoke, is the most abundant electrophilic $\alpha$, $\beta$-unsaturated aldehyde to which humans are exposed in a variety of environmental pollutants, and is also product of lipid peroxidation. Increased unsaturated aldehyde levels and reduced antioxidant status plays a major role in the pathogenesis of various diseases such as diabetes, Alzheimer's and atherosclerosis. The findings reported here show that low concentrations of acrolein induce heme oxygenase-1 (HO-1) expression in RAW 264.7 macrophages. HO-1 induction by acrolein and signal pathways was measured using reverse transcription-polymerase chain reaction, Western blot and immunofluorescence staining analyses. Inhibition of extracellular signal-regulated kinase activity significantly attenuated the induction of HO-1 protein by acrolein, while suppression of Jun N-terminal kinase and p38 activity did not affect induction of HO-1 expression. Moreover, rottlerin, an inhibitor of protein kinase $\delta$, suppressed the upregulation of HO-1 protein production, possibly involving the interaction of NF-E2-related factor 2 (Nrf2), which has a key role as a HO-1 transcription factor. Acrolein elevated the nuclear translocation of Nrf2 in nuclear extraction. The results suggest that RAW 264.7 may protect against acrolein-mediated cellular damage via the upregulation of HO-1, which is an adaptive response to oxidative stress.
Purpose : This study are the secondary data of Global Youth Tobacco Survey(GYTS) developed by the WHO and United State Center for Disease Control(CDC) and Prevention to trace tobacco use among youth in youth in countries across the world. This study was carried out to serve for a basis for antismoking campaigns and to prevent adolescents from smoking by analyzing the smoking by analyzing the smoking realities factors. Methods : This study is a cross-sectional school-based survey, which employed a two-stage cluster sample design to produce a nationally representative sample of middle school students aged 13 to 15 years olds. Seventy-five schools were selected. All schools containing grade 1, 2 and 3 that contained 40 or students were included in the sampling frame. Results : The results of this study were as follows ; 1. The proportion of smoking students in middle school was 6.4% and the rate of smoking in male students(7.4%) was higher than it of in female students(5.5%). 2. 26.5% of all respondent had a experience to try smoke and the results showed that the rate of trying smoking in male students was increased by grade more than female students. 3. According to test of significance in regression analysis, the independent variables such as sex, school grade, smoking parents, friends distinction, pocket money and others showed statistical significance. 4. There was a statistical significance between smokers and nonsmokers in proportion to the completing the preventive education for nonsmoking(p=0.0023) and the acquirement of knowledge on smoking(p<.0001). 5. Finally there was a statistical significance between the exposure to anti-smoking campaign(p=0.0053) and tobacco advertisement in the mass media and the smoking(p=0.0036). Conclusion : All things considered, the health education for tobacco control in school need to be developed from an elementary school. I suggest that prevent smoking program in school need to be revitalized and be made more accessible for everyone who wish to quit. And the government should develop the regulation on total banning promoting cigarette advertising and smoking scene in the movie for young people.
The effects of smoking and physical exercise on the plasma concentrations of lipid-soluble antioxidants were investigated in 62 healthy males, aged 34-65 years. Current smokers (n=21) and ex-smokers(n=16) had significantly lower plasma levels of carotenoids ($\alpha$-carotene, $\beta$-carotene, cryptoxanthin and lycopene), $\alpha$-tocopherol and ${\gamma}$-tocopherol than non-smokers (n=25). Plasma concentrations of retionl and ubiquinone (coenzyme Q10) were lower among ex-smokers and current smokers than among non-smokers, but the differences were not statistically significant. Regular physical exercise was associated with increased plasma levels of lipid-soluble antioxidants. Plasma concentrations of crytoxanthin, retinol and ubiquinone were significantly elevated in the group engaging in moderate amounts of exercise (more than 20 minutes per day) compared to the group engaging in small amounts of exercise (less than 10 minutes per day). Plasma $\alpha$-carotene, $\beta$-carotene, lycopene levels in the subjects were affected more by smoking than by exercise. However, plasma levels of cryptoxanthin, retinol and ubiquinone in the subjects were affected more by exercise than by smoking. These findings suggest than smoking may cause a decrease in plasma lipid-soluble antioxidants during neutralization of reactive oxygen species present in cigarette smoke and that poor exercise habits may accelerate this imbalance of oxidant/antioxidant homeostasis in middle-aged Korean men.
Essential oil in tobacco leaves influences the taste and aroma of cigarette smoke and is important to tobacco quality. This study was conducted to investigate the change in the level of essential oil components during flue-curing process of two flue-cured tobaccos, NC82 and KEl14. Flue-curing process was divided by six steps; harvest stage, the end of yellowing stage, the middle of color fixing stage, the end of color fixing stage, the middle of midrib drying stage, full-cured stage. NC82 in each stage contained 0.28%, 0.30%, 0.35%, 0.36%, 0.40% and 0.42% essential oil, respectively, and KF114 were 0.29%, 0.31%, 0.34%, 0.36%, 0.39% and 0.41%, respectively. Almost all hydrocarbons on the basis of relative peak area were gradually increased in two varieties with curing, neophytadiene content in them was highest at the full-cured stage. Most of alcohols and esters with curing showed a declining trend, but benzyl alcohol was increased in two tobaccos. Ketones were largely increased at the midrib drying stage during the curing process, especially, the most largely increasing constituent was $\beta$-damascenone among them. The content of 2-butylterahydrofuran, heterocyclic compounds, was largely increased at tile color fixing stage. There was no considerable difference between NC82 and KFl14 at the GC profile of essential oil and the pattern of each components during flue-curing process.
Cigarette smoking has long been recognized as a major risk factor in the development of coronary heart disease. Several investigators have reported the strong association between smoking and high serum cholesterol, triglyceride concentration, SFA and low HDL cholesterol, PUFA and $\omega$6 concentrations. Therefore, this study was done to investigate the effect of smoking on the serum lipid profile and fatty acid composition of college women. Sixty-one non-smokers and twenty-seven smokers were selected from college women students in the Seoul area. Their lipid intake, serum lipid concentration and fatty acid composition were examined. There were no differences in the general characteristics and anthropometric indices between the smokers and non-smokers. However, alcohol consumption was significantly higher in smokers than non-smokers (p<0.001). The daily caloric intake of smokers and non-smokers were 1875.84 kcal and 1915.53 kacl, respectively. On the other hand, the mean daily intake of lipids and cholesterol were significantly lower in smokers (p<0.05). In smokers, the mean concentrations of serum total cholesterol, LDL-cholesterol and the LDL-C/HDL-C ratio were higher, and the compositions of EPA and DHA were lowe than in non-smokers. There was a negative correlation between the serum triglyceride and PUFA levels in the two groups. Also, serum HDL-C correlated negatively with MUFA in smokers and non-smokers (p<0.01). These results suggest that smoking cause inadequate changes in serum lipid profile and serum fatty acid composition, thereby increasing the tendency for coronary heart disease.
Objective This study aimed to evaluate the effects of Sagan-tang (SGT) on COPD mouse model. Methods The study was carried out by two ways (in vitro, in vivo). In vitro RAW264.7 cells (mouse macrophage) were used and analysed by flow cytometry, ELISA, Western blot. In vivo LPS and CSS challenged mice were used and its BALF had been analysed by cytospin image, FACS, ELISA, lung tissue by real-time PCR. Results In vitro, SGT maintained 80-100% rate of viablilty on 10 ~ 500 ㎍/㎖ concentration. In ELISA analysis with RAW264.7 cells, SGT significantly decreased NO over 30 ㎍/㎖. In flow cytometry, SGT 100 ㎍/㎖ dosage group displayed a tendency for decrease ROS. In Western blot analysis, SGT 100 ㎍/㎖ dosage group decreased NF-κB. In ELISA analysis, SGT significantly decreased TNF-α, IL-6 over 200 ㎍/㎖. In vivo SGT 200 ㎎/㎏ dosage group, application of SGT significantly decreased increase of neutrophils, TNF-α, IL-6 in BALF, muc5AC, TGF-β, TNF-α, expression of mRNA in lung tissue and histological lung injury. Conclusion This Study suggests usability of SGT for COPD patients by controlling lung tissue injury.
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