There are 3 clinical trials

Clinical Trials

1 Smokers' Response to Nicotine Dependence Genotyping

Innovative strategies to reduce adult smoking prevalence include using genetic information to motivate cessation and, ultimately, to tailor cessation pharmacotherapy. Success of these interventions depends, in part, on smokers' interest and participation in genetic testing related to cessation and their understanding and use of the results (i.e., their genetic literacy). The recent availability of genetic risk testing for a nicotinic acetylcholine receptor gene (CHRNA3) variant (rs105173) associated with nicotine dependence makes it highly feasible to investigate smokers' interest in and use of genetic information about nicotine dependence. Therefore, the primary purpose of this study is to determine the impact of an intervention that provides smokers with an educational session about genetic contributions to smoking and nicotine dependence plus their genotype results for rs1051730 on smoking cessation outcomes compared to those who receive only the educational session. Secondary purposes are to determine: (a) the impact of genetic education and knowing personal genotype results on genetic literacy outcomes and (b) the feasibility of recruitment and retention methods in a study addressing genotyping for nicotine dependence. Primary outcomes are cessation-related behaviors and cognitions indicating abstinence. Secondary outcomes are cognitions and emotions indicating genetic literacy. Knowledge gained from this study has the potential for clinical translation so that as genotyping becomes part of smoking cessation, health-care providers can understand and address factors influencing smokers' adaptation to genetically-informed cessation treatment. The study will use a longitudinal, repeated measures design (experimental, control; N=90; 45/group). All participants will receive a 90-minute educational session about genetic contributions for smoking and nicotine dependence and will donate a buccal swab sample for genotyping. The investigators will then randomize participants to two groups: those who receive genotyping results in a genetic counseling session (experimental) and those who do not (control). Follow-up data will be collected from both groups at baseline and weeks 2, 6, 10 after the experimental group receives genotyping results, with a brief follow-up and study termination occurring at week 12. Control group participants will be offered their genotyping results at the end of the study.

NCT01780038 Cigarette Smoking Nicotine Dependence Behavioral: Receipt of Genetic Results Behavioral: No results given

MeSH:Tobacco Use Disorder

Therefore, the primary purpose of this study is to determine the impact of an intervention that provides smokers with an educational session about genetic contributions to smoking and nicotine dependence plus their genotype results for rs1051730 on smoking cessation outcomes compared to those who receive only the educational session.

2 Molecular, Cytological Features and Genetic Susceptibility of Occupational Chronic Obstructive Pulmonary Disease Attributable to Different Environmental Exposures

The objective of this study is to investigate molecular, cytological and genetic features of occupational chronic obstructive pulmonary disease (COPD) in conditions of different occupational exposures. In order to achieve this goal serum pro-inflammatory cytokines and standard inflammation markers level, hemostasis, cytological analysis of bronchoalveolar lavage and associations of single nucleotide polymorphisms (SNPs) rs1800470 transforming growing factor β1 (TGF β1) gene, rs1828591 hedgehog interacting protein (HHIP) gene, rs4129267 interleukin 6 receptor (IL-6R) gene, rs1051730 nicotinic acetylcholine receptor 3 (CHRNA3) gene with COPD in subjects exposed to silica dust and in those exposed to polycyclic aromatic hydrocarbons exhaust will be investigated. The relationship between genotype and phenotype characteristics, such as an inflammation activity, assessed by C-reactive protein (hsCRP) and tumor necrosis factor-α (TNF α) serum concentration, in different occupational COPD groups will be studied. The hypothesis is that the mechanisms underlying disease development and progression are different due to environmental risk factor that reflex in differs in disease attributes - molecular biomarkers, cytology results and genetic susceptibility between COPD due to dust, COPD due to chemicals and COPD in smokers therefore COPD can be subdivided into ecological phenotypes according to environmental risk factor.

NCT02220387 Chronic Obstructive Pulmonary Disease Other: exposure to respirable silica dust Other: exposure to polycyclic aromatic hydrocarbons exhaust

MeSH:Lung Diseases Lung Diseases, Obstructive Pulmonary Disease, Chronic Obstructive Genetic Predisposition to Disease

HPO:Abnormal lung morphology Chronic pulmonary obstruction Pulmonary obstruction

In order to achieve this goal serum pro-inflammatory cytokines and standard inflammation markers level, hemostasis, cytological analysis of bronchoalveolar lavage and associations of single nucleotide polymorphisms (SNPs) rs1800470 transforming growing factor β1 (TGF β1) gene, rs1828591 hedgehog interacting protein (HHIP) gene, rs4129267 interleukin 6 receptor (IL-6R) gene, rs1051730 nicotinic acetylcholine receptor 3 (CHRNA3) gene with COPD in subjects exposed to silica dust and in those exposed to polycyclic aromatic hydrocarbons exhaust will be investigated.

Association of SNPs rs1800470 TGF β1 gene, rs1828591 HHIP gene, rs4129267 IL-6R gene, rs1051730 CHRNA3 gene with COPD in subjects exposed to dust and in those exposed to chemicals.. Odds ratio and 95% confidence interval will be calculated for each occupational group.

3 Molecular, Cytological Features and Genetic Susceptibility of Occupational Chronic Obstructive Pulmonary Disease Attributable to Different Environmental Exposures 2.

The objective of this study is to investigate molecular, cytological and genetic features of occupational chronic obstructive pulmonary disease (COPD) in conditions of different occupational exposures. In order to achieve this goal serum pro-inflammatory cytokines and standard inflammation markers level, hemostasis, cytological analysis of bronchoalveolar lavage fluid and association of single nucleotide polymorphisms (SNPs) rs1800470 transforming growing factor β1 (TGF β1) gene, rs1828591 hedgehog interacting protein (HHIP) gene, rs4129267 interleukin 6 receptor (IL-6R) gene, rs1051730 nicotinic acetylcholine receptor 3 (CHRNA3) gene with COPD in subjects exposed to silica dust and in those exposed to polycyclic aromatic hydrocarbons exhaust will be investigated. The relationship between genotype and phenotype characteristics, such as an inflammation activity, assessed by C-reactive protein (hsCRP) and tumor necrosis factor alpha (TNF α) serum concentration, in different occupational COPD groups will be studied. The hypothesis is that the mechanisms underlying disease development and progression are different due to environmental risk factor that reflex in differs in disease attributes - molecular biomarkers, cytology results and genetic susceptibility between COPD due to dust, COPD due to chemicals and COPD in smokers therefore COPD can be subdivided into ecological phenotypes according to environmental risk factor.

NCT02284295 Chronic Obstructive Pulmonary Disease Other: exposure to respirable silica dust Other: exposure to aromatic hydrocarbons

MeSH:Lung Diseases Lung Diseases, Obstructive Pulmonary Disease, Chronic Obstructive Genetic Predisposition to Disease

HPO:Abnormal lung morphology Chronic pulmonary obstruction Pulmonary obstruction

In order to achieve this goal serum pro-inflammatory cytokines and standard inflammation markers level, hemostasis, cytological analysis of bronchoalveolar lavage fluid and association of single nucleotide polymorphisms (SNPs) rs1800470 transforming growing factor β1 (TGF β1) gene, rs1828591 hedgehog interacting protein (HHIP) gene, rs4129267 interleukin 6 receptor (IL-6R) gene, rs1051730 nicotinic acetylcholine receptor 3 (CHRNA3) gene with COPD in subjects exposed to silica dust and in those exposed to polycyclic aromatic hydrocarbons exhaust will be investigated.

Association of SNPs rs1800470 TGF β1 gene, rs1828591 HHIP gene, rs4129267 IL-6R gene, rs1051730 CHRNA3 gene with COPD in subjects exposed to dust and in those exposed to chemicals.

HPO Nodes