Wn because of our small sample size. Additional, there is certainly also a opportunity that these associations could possibly be impacted by the SNPs of nearby genes with which the IREB2 SNPs are in LD. Our study has few limitations. Firstly, only male subjects had been incorporated in the study. This was as a consequence of lack of affected female subjects readily available under smoking category. Exposure to biomass fuel smoke could be the predominant threat issue for COPD in females in India. Consequently only smokers have been chosen together with the assumption that the mechanism by which tobacco smoke, which is a carrier of a number of Group I and Group II carcinogens, initiates COPD might be distinct from that of biomass fuel smoke. Second limitation of our study could be the sample size. One factor that significantly contributed to this was the strict adherence to bidi smokers. Cigarette is pricey than bidi. As many of the interviewed subjects have been every day wage labors, the option of smoking medium depended hugely on the person’s day to day variable monetary status. There had been subjects who smoked both bidi and cigarette. Such subjects were excluded to prevent misinterpretation of pack years. Lastly, our patient population will not be uniformly distributed across distinctive GOLD stages of COPD. COPD was unknown to all our subjects until diagnosis or our take a look at. Sufferers consulted physician only when they had extreme respiratory challenges due to illness progression. Hence, in the time of initial diagnosis, the majority of the sufferers had been either in GOLD stage III or GOLD stage IV. Conclusion Our study managed to reinforce the theories of oxidantantioxidant imbalance, protease-antiprotease imbalance and inflammation upon which the etiology of COPD has been built. While many of the associations discovered in this study have already been reported elsewhere, the associations found with IREB2 have to be investigated with larger sample sizes. Supporting Information Author Contributions Conceived and made the experiments: KRK PR CSA KMS. Performed the experiments: CA RRR. Analyzed the information: CA RRR VNP. Wrote the paper: AC RRR KRK. References 1. Jain NK, 14636-12-5 Thakkar MS, Jain N, Rohan KA, Sharma M Chronic obstructive pulmonary disease: Does gender actually matter Lung India 28: 258 262. two. Jindal SK, Aggarwal AN, Gupta D A evaluation of population Hexaconazole biological activity research from India to estimate national burden of chronic obstructive pulmonary disease and its association with smoking. Indian J.Chest Dis. Allied Sci 43: 13947. three. Lopez AD, Shibuya K, Rao C, Mathers CD, Hansell AL, et al. Chronic obstructive pulmonary disease: current burden and future projections. Eur Respir J 27: 397412. 4. Mahadeva R, Lomas D Alpha1-antitrypsin deficiency, cirrhosis and emphysema. Thorax 53: 501505. five. Wood AM, Stockley RA The genetics of chronic obstructive pulmonary illness. Respir Res 7: 130. 6. Hersh CP, DeMeo DL, Silverman EK National Emphysema Treatment Trial State on the Art. Genetics of Emphysema. Proc Am Thorac Soc 5: 486 493. 7. International Initiative for Chronic Obstructive Lung Illness. International approach for the diagnosis, management, and prevention of COPD. Executive summary. National Institutes of Health. 2006. Available: http://www.who.int/ respiratory/copd/GOLD_WR_06.pdf. Accessed: 2012 Nov. 22. eight. Purcell S, Neale B, Todd-Brown K, Thomas L, Ferreira MAR PLINK: A Tool Set for Whole-Genome Association and Population-Based Linkage Analyses. Am J Hum Genet. 81: 559575. 9. Purcell S, Daly MJ, Sham Computer WHAP: haplotype-based association evaluation. Bioinformatics. 23: 2556. 10. Shili Lin, Hongyu Z.Wn because of our little sample size. Additional, there is also a chance that these associations could be impacted by the SNPs of nearby genes with which the IREB2 SNPs are in LD. Our study has couple of limitations. Firstly, only male subjects were included within the study. This was as a result of lack of impacted female subjects obtainable beneath smoking category. Exposure to biomass fuel smoke is definitely the predominant threat factor for COPD in females in India. Therefore only smokers had been selected together with the assumption that the mechanism by which tobacco smoke, which is a carrier of a number of Group I and Group II carcinogens, initiates COPD could be unique from that of biomass fuel smoke. Second limitation of our study is the sample size. 1 element that greatly contributed to this was the strict adherence to bidi smokers. Cigarette is expensive than bidi. As many of the interviewed subjects had been everyday wage labors, the selection of smoking medium depended very around the person’s day to day variable monetary status. There were subjects who smoked both bidi and cigarette. Such subjects have been excluded to avoid misinterpretation of pack years. Lastly, our patient population is not uniformly distributed across diverse GOLD stages of COPD. COPD was unknown to all our subjects till diagnosis or our check out. Individuals consulted doctor only when they had severe respiratory challenges as a result of disease progression. Hence, at the time of initial diagnosis, a lot of the sufferers have been either in GOLD stage III or GOLD stage IV. Conclusion Our study managed to reinforce the theories of oxidantantioxidant imbalance, protease-antiprotease imbalance and inflammation upon which the etiology of COPD has been built. Even though the majority of the associations found within this study have been reported elsewhere, the associations found with IREB2 have to be investigated with larger sample sizes. Supporting Data Author Contributions Conceived and developed the experiments: KRK PR CSA KMS. Performed the experiments: CA RRR. Analyzed the data: CA RRR VNP. Wrote the paper: AC RRR KRK. References 1. Jain NK, Thakkar MS, Jain N, Rohan KA, Sharma M Chronic obstructive pulmonary illness: Does gender actually matter Lung India 28: 258 262. two. Jindal SK, Aggarwal AN, Gupta D A assessment of population research from India to estimate national burden of chronic obstructive pulmonary illness and its association with smoking. Indian J.Chest Dis. Allied Sci 43: 13947. 3. Lopez AD, Shibuya K, Rao C, Mathers CD, Hansell AL, et al. Chronic obstructive pulmonary illness: current burden and future projections. Eur Respir J 27: 397412. four. Mahadeva R, Lomas D Alpha1-antitrypsin deficiency, cirrhosis and emphysema. Thorax 53: 501505. five. Wood AM, Stockley RA The genetics of chronic obstructive pulmonary disease. Respir Res 7: 130. 6. Hersh CP, DeMeo DL, Silverman EK National Emphysema Remedy Trial State of the Art. Genetics of Emphysema. Proc Am Thorac Soc five: 486 493. 7. Global Initiative for Chronic Obstructive Lung Illness. International strategy for the diagnosis, management, and prevention of COPD. Executive summary. National Institutes of Health. 2006. Readily available: http://www.who.int/ respiratory/copd/GOLD_WR_06.pdf. Accessed: 2012 Nov. 22. 8. Purcell S, Neale B, Todd-Brown K, Thomas L, Ferreira MAR PLINK: A Tool Set for Whole-Genome Association and Population-Based Linkage Analyses. Am J Hum Genet. 81: 559575. 9. Purcell S, Daly MJ, Sham Pc WHAP: haplotype-based association analysis. Bioinformatics. 23: 2556. 10. Shili Lin, Hongyu Z.
