The meeting proved of great interest to those developing an animal model of chronic obstructive pulmonary disease (COPD). COPD is caused by cigarette smoking, evidenced by deterioration in lung function. Lung function is only rarely assessed in animal models. A cigarette smoke driven pathology should provide the best in vivo model for COPD. However, as lesions produced this way take 8–12 months to develop other strategies have to be employed. Emphysematous lesions were also achieved by treatment with elastase, lipopolysaccharide, ozone and other inducers. Several studies described treatments that have shown activity in these models. Transgenic models were discussed, as was the importance of species and strain selection.

Evidence for a role of diet in asthma and chronic obstructive pulmonary disease (COPD) has been accumulating rapidly over the past decade. Associations have been reported between the intake of fruit, fish, antioxidant vitamins, fatty acids, sodium or magnesium, and indicators of asthma and COPD. Several issues need to be addressed before causality of these associations can be established. The role of diet in the development of disease and the induction time and reversibility of the effect needs further investigation. The role of smoking habits in the relation of diet and respiratory disease also needs to be elucidated. Nevertheless, based on the available evidence, dietary guidelines could be proposed for the primary and secondary prevention of asthma and COPD that are in line with existing dietary guidelines for the prevention of coronary heart disease and cancer.

Asthma and associated phenotypes are complex traits most probably caused by an interaction of multiple disease susceptibility genes and environmental factors. Major achievements have occurred in identifying chromosomal regions and polymorphisms in candidate genes linked to or associated with asthma, atopic dermatitis, IgE levels and response to asthma therapy. The aims of this review are to explain the methodology of genetic studies of multifactorial diseases, to summarize chromosomal regions and polymorphisms in candidate genes linked to or associated with asthma and associated traits, to list genetic alterations that may alter response to asthma therapy, and to outline genetic factors that may render individuals more susceptible to asthma and atopy due to environmental changes.

[개요] -COPD 는 만성 폐쇄성 폐질환을 말하며, 해당 데이터는 이러한 질환을 앓고 있는 환자를 대상으로 수집된 데이터 - 시험군 , 대조군을 두어 임상시험이 실시되며 시험군 대조군의 선정 방식은 무작위 배정 방식을 사용 - 시험군에겐 혈압계, 혈당계, 활동량계, 스마트줄자, 폐기능검사기, 체성분계, 체온계, 실내측정기가 제공되며, 대조군에겐 혈압계, 혈당계, 활동량계, 체성분계,실내측정기가 제공됨 - 임상시험은 총 5회 방문으로 이뤄지며, 처음 방문시 IoT의료기기, IoT 웰니스기기사용, 폐활량 측정 등 임상시험에 대한 설명 및 혈액검사 시행 - 첫 방문 이후 2차 방문 전까지 IoT 기기를 사용하여 정해진 횟수와 시간에 따라 자가 측정 및 연동 앱을 통하여 대상자의 분석을 통해 메시지를 통한 중재 받음(시험군의 경우만 중재를 받음, 대조군의 경우엔 우을 증상을 방지하고자 최소한의IoT기기 제공 및 제한된 분석 추이 제공) - 모든 대상자는 5차 방문 시(12개월간의 임상시험 참여 후) 이상반응 유무 확인 - 폐활량 측정 및 만족도 설문지 조사, IoT의료기기 및 IoT웰니스기기 반납 후 임상시험을 종료 위와 같은 과정을 통하여 만성폐쇄성폐질환 환자의 데이터가 수집 [제공항목] - COPD 대상자의 폐기능검사 내용을 제공

Exposure of the airways to cigarette smoke (CS) is the primary risk factor for developing several lung diseases such as Chronic Obstructive Pulmonary Disease (COPD). CS consists of a complex mixture of over 6000 chemicals including the highly reactive α,β-unsaturated aldehyde acrolein. Acrolein is thought to be responsible for a large proportion of the non-cancer disease risk associated with smoking. Emerging evidence suggest a key role for CS-induced abnormalities in mitochondrial morphology and function in airway epithelial cells in COPD pathogenesis. Although in vitro studies suggest acrolein-induced mitochondrial dysfunction in airway epithelial cells, it is unknown if in vivo inhalation of acrolein affects mitochondrial content or the pathways controlling this. In this study, rats were acutely exposed to acrolein by inhalation (nose-only; 0-4 ppm), 4 hours/day for 1 or 2 consecutive days (n=6/group). Subsequently, the activity and abundance of key constituents of mitochondrial metabolic pathways as well as expression of critical proteins and genes controlling mitochondrial biogenesis and mitophagy were investigated in lung homogenates. A transient decreasing response in protein and transcript abundance of subunits of the electron transport chain complexes was observed following acrolein inhalation. Moreover, acrolein inhalation caused a decreased abundance of key regulators associated with mitochondrial biogenesis, respectively a differential response on day 1 versus day 2. Abundance of components of the mitophagy machinery was in general unaltered in response to acrolein exposure in rat lung. Collectively, this study demonstrates that acrolein inhalation acutely and dose-dependently disrupts the molecular regulation of mitochondrial metabolism in rat lung. Hence, understanding the effect of acrolein on mitochondrial function will provide a scientifically supported reasoning to shortlist aldehydes regulation in tobacco smoke. This dataset is not publicly accessible because: EPA does not own the data and therefore EPA does not have right to publish the data. It can be accessed through the following means: Data can be obtained from corresponding author of the paper. Format: The data in this paper are collected from lung tissue that were isolated from air or acrolein-exposed Wistar Kyoto rats. All data are derived from lung tissue assessment of many biological markers associated with mitochondrial homeostasis. For these data n=8 animals were used for each group of samples. This dataset is associated with the following publication: Tulen, C., S. Snow , P. Leermakers, U. Kodavanti, F. van Schooten, A. Opperhuizen, and A. Remels. Acrolein inhalation acutely affects the regulation of mitochondrial metabolism in rat lung. TOXICOLOGY. Elsevier Science Ltd, New York, NY, USA, 469(153129): 1, (2022).

[개요] -COPD 는 만성 폐쇄성 폐질환을 말하며, 해당 데이터는 이러한 질환을 앓고 있는 환자를 대상으로 수집된 데이터 - 시험군 , 대조군을 두어 임상시험이 실시되며 시험군 대조군의 선정 방식은 무작위 배정 방식을 사용 - 시험군에겐 혈압계, 혈당계, 활동량계, 스마트줄자, 폐기능검사기, 체성분계, 체온계, 실내측정기가 제공되며, 대조군에겐 혈압계, 혈당계, 활동량계, 체성분계,실내측정기가 제공됨 - 임상시험은 총 5회 방문으로 이뤄지며, 처음 방문시 IoT의료기기, IoT 웰니스기기사용, 폐활량 측정 등 임상시험에 대한 설명 및 혈액검사 시행 - 첫 방문 이후 2차 방문 전까지 IoT 기기를 사용하여 정해진 횟수와 시간에 따라 자가 측정 및 연동 앱을 통하여 대상자의 분석을 통해 메시지를 통한 중재 받음(시험군의 경우만 중재를 받음, 대조군의 경우엔 우을 증상을 방지하고자 최소한의IoT기기 제공 및 제한된 분석 추이 제공) - 모든 대상자는 5차 방문 시(12개월간의 임상시험 참여 후) 이상반응 유무 확인 - 폐활량 측정 및 만족도 설문지 조사, IoT의료기기 및 IoT웰니스기기 반납 후 임상시험을 종료 위와 같은 과정을 통하여 만성폐쇄성폐질환 환자의 데이터가 수집 [제공항목] - COPD 대상자의 혈액검사 내용을 제공