Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 3rd Intrenational Conference on Chronic Obstructive Pulmonary Disease Brisbane, Australia.

Day 1 :

Keynote Forum

Joaquim Gea

Dean of the School of Medicine
Universitat Pompeu Fabra
Barcelona
Spain

Keynote: Low Physical Activity and COPD: Prognosis and handling of this clinical problem

Time : 09:55-10:35

OMICS International COPD 2016 International Conference Keynote Speaker Joaquim Gea photo
Biography:

Joaquim Gea obtained his MD (1979) and PhD (1989) degrees at the Universitat de Barcelona, being specialist in both Internal Medicine (1981) and Respiratory Medicine (1985). He is the Head of the Respiratory Department at Hospital del Mar, Full Professor and Dean in the School of Medicine at Universitat Pompeu Fabra and has been Visiting professor at McGill (94-95) and Johns Hopkins (2010-11) universities, and Deputy Director of the Spanish Network of Excellence for Research in Respiratory Diseases (CIBERES). He has been funded by 65 competitive grants, including 4 projects from the European Commission, and published more than 260 Original Articles and Reviews in peer reviewed journals as well as 50 book chapters.

Abstract:

Chronic obstructive pulmonary disease (COPD) is considered a multidimensional disorder since, in addition to the lung disease, it also has important systemic manifestations and is associated with significant comorbidities. Respiratory and anxious-depressive symptoms, together with the Western lifestyle, often lead to a progressive limitation in the level of physical activity. This leads to higher levels of depression as well as to cardiovascular and skeletal muscle deconditioning along with alterations in bone metabolism and quality. All these changes increase the negative impact on the level of physical activity, which continues its decline, generating a progressive vicious circle, with important consequences in different clinical outcomes: development of or increased severity in different comorbidities, more hospitalizations and increased mortality. Therefore, it is necessary to improve the clinical management of COPD patients by early detecting inappropriate low levels of activity and optimizing the treatment. The latter should necessarily include the treatment of both respiratory and psychological symptoms, while attempting to directly incentivate the increase in the level of activity. Thus, the strategy must include bronchodilators (long-acting beta-agonists and anticholinergic drugs), pulmonary rehabilitation (mainly general training) and behavioral changes. To determine and monitor the level of physical activity is also an important point of the management. For this purpose, different instruments have been developed and are now available, including actigraphs, pedometers and questionnaires. Conclusion: Physical activity is a key element in COPD prognosis, and therefore low levels of daily activity must be detected, monitored and properly treated.

OMICS International COPD 2016 International Conference Keynote Speaker Patrick Vanscheeuwijck photo
Biography:

Dr. Patrick Vanscheeuwijck is Director pre-clinical toxicology at Philip Morris International, Reduced Risk Products, and Switzerland, responsible for the in vitro and in vivo assessment of Reduced Risk Products (RRPs). The focus of his career at PMI has been on the development of approaches for the assessment of hazard associated with cigarette smoke and aerosols from RRPs, inhalation toxicology and animal models of disease; with more than 30 peer-reviewed publications. He has a Ph.D. in biochemical pharmacology (University of Gent, Belgium), performed postdocs at the University of Arizona, U.S. and the University of Leuven, Belgium in molecular pharmacology and molecular biology.rnrn

Abstract:

Chronic obstructive pulmonary disease (COPD) is a respiratory disease characterized by progressive airflow limitation, with globally increasing prevalence. Although efforts to simplify COPD diagnosis to a single repeatable test using spirometry has proved critical in the day-to-day diagnosis and management of the disease, it is clear that COPD is a complex disease whose phenotypes may not be adequately captured by spirometry alone. Moreover, suitable biomarkers for the diagnosis, treatment and prognosis are still lacking. Therefore, we conducted a case-control study designed to identify a biomarker (panel) for the differentiation of subjects with mild and moderate COPD, asymptomatic current, former and never-smokers and to compare physiological measurements and quality of life (QoL) across the study groups (NCT01780298). Our data shows that there are a number of subjects that would be diagnosed as healthy using spirometry alone. However, these data also suggest that complementary tests such as CT chest imaging or lung sound analysis may prove helpful in identifying asymptomatic smokers at risk or with subclinical disease. Potential biomarkers identified by ‘omics’ analyses may support this stratification further. For example, sputum analysis detected cigarette smoking-related alterations in the transcriptome and proteome, which were further augmented in COPD smokers. Strikingly, proteomics data could distinguish COPD from asymptomatic smokers with a similar accuracy as the combination of three commonly used physiological parameters, FEV1, TLCO % and total COPD score

  • Track-3: Pathophysiology of COPD
    Track-5: COPD and its Co-Morbidities
Speaker

Chair

Ping Yang

Mayo Clinic College of Medicine, USA

Speaker

Co-Chair

Tsuyoshi Shuto

Kumamoto University

Session Introduction

Esther Barreiro

Professor
Research Institute of Hospital del Mar
Barcelona
Spain

Title: Biological Mechanisms of Muscle Mass Loss and Cachexia in Patients with COPD

Time : 11:35 - 12:00

Speaker
Biography:

Dr. Esther Barreiro (MD, PhD) coordinates a research group at Hospital del Mar-IMIM and Pompeu Fabra University (Barcelona). She has obtained more than 40 grants to conduct medical research in COPD, and has published more than 140 articles in peer-reviewed international journals and several book chapters. She is Editor-in-Chief of Archivos de Bronconeumología (July 2012), Associate Editor of Journal of Applied Physiology (July 2011), and a member of the Editorial Board of American Journal of Respiratory and Critical Care Medicine (January 2012). She is also a member of the American Thoracic, American Physiological, European Respiratory and Spanish Respiratory Societies

Abstract:

Muscle dysfunction is a major systemic manifestation in patients with lung diseases, especially in those with chronic obstructive pulmonary disease (COPD). The difference between respiratory and limb muscle dysfunction needs to be made as the diaphragm must contract at a specific resting length, which is not the case in the limb muscles. A reduction in lower limb muscle strength (namely quadriceps weakness) and atrophy (smaller size of the muscle fibers) have important clinical implications as they are predictors of disease prognosis and mortality in COPD patients. In the last two decades, many different factors and biological mechanisms have been shown to participate in the multifactorial etiology of skeletal muscle dysfunction in COPD. Our group has extensively contributed to the understanding of part of those mechanisms such as muscle oxidative stress and inflammation, oxidation of specific key muscle proteins, systemic inflammation, proteolysis mediated by the ubiquitin-proteasome system, structural muscle alterations (myofibers and sarcomere disruptions), deficiency in key muscle proteins, nutritional abnormalities, signaling pathways of muscle atrophy, apoptosis, autophagy, epigenetics, unfolding of muscle proteins, and modifications of these molecular and cellular events in response to several therapeutic strategies such as exercise and/or muscle training and rehabilitation. The conclusions are that until effective and safer pharmacological therapies emerge, exercise and muscle training modalities, alone or in combination with nutritional support, are undoubtedly the best treatment options to improve muscle mass and function, and quality of life in COPD patients. In my talk, the most recent results shown to be involved in the pathophysiology of skeletal muscle dysfunction in patients with COPD will be shown and discussed.

Phil Hansbro

Professor
University of Newcastle and Hunter Medical Research Institute
New South Wales
Australia

Title: The Role of the Microbiome in COPD

Time : 12:00-12:25

Speaker
Biography:

Professor Hansbro holds a tenured chair of immunology & microbiology at the University of Newcastle and a National Health and Medical Research Council (NHMRC) of Australia Principal Research Fellowship. He has established and leads a team that investigates the pathogenesis of infectious and respiratory diseases, including asthma, COPD and recently lung cancer. He has extensive expertise in the development and utilization of mouse models that recapitulate the hallmark features of human disease and complimentary human studies using state of the art facilities. He has developed unique short-term mouse models of severe, steroid-resistant asthma, COPD and lung cancer. These models enable novel studies that identify new therapeutic targets and to test emerging therapies for respiratory diseases. He has established expertise and techniques in assessing inflammation and pathophysiology in experimental infections, asthma, COPD and lung cancer. His group routinely performs analysis of inflammatory cell influx and cytokine/chemokine levels, assess remodeling in terms of mucus secreting cell hyperplasia, collagen levels/deposition/fibrosis and epithelial thickening, and emphysema. This occurs using cytospins, microscopy with moving stages, real time qPCR, ELISA, western blot and multiplex protein assays, flow cytometry and FACS sorting, perfusion, histology and staining and morphometric analysis. They have particular expertise in the measurement of lung function using invasive plethysmography and routinely perform forced manoeuvre and oscillation techniques. His group has expertise in assessing inflammatory processes including inflammasomes, microRNAs, microbiomes, epigenetic, oxidative stress, etc, in these systems.

Abstract:

Recent technical advances have enabled the assessment of entire microbiomes in tissues. This had led to the elucidation of their roles in health and disease. Until recently the lower respiratory tract was thought to be sterile but microbiome studies have shown this not to be the case and that there is a core lung microbiome. Alterations in the microbiome indicate and may be causal in disease. In dysbiosis commensals are displaced by pathgens that drive inflammation and inflammatory diseases including the in the respiratory tract. It is now established thatthere is infectious and inflammatory cross talk between the lung and gut and so changes in gut microbiomes may also be involved in respiratory disease potentially through the induction of systemic inflammation. The current state of the field in COPD will be assessed and new data from our lab on the role of changes in the gut microbiome in this disease will be presented.

Md. Rashidul Hassan

Director
National Institute of Diseases of the Chest & Hospital
Bangladesh

Title: SEF Classification for COPD Management

Time : 12:25 - 12:50

Speaker
Biography:

Prof. Md. Rashidul Hassan Director cum Professor, National Institute of Diseases of the Chest & Hospital, Dhaka 1212 is a Bangladeshi, completed his MD Respiratory Medicine from Dhaka University in the Year 1995. He is now Professor, Department of Respiratory Medicine, National Institute of Diseases of the Chest and Hospital [NIDCH], Dhaka 1212, Bangladesh. He is now Founding President of Bangladesh Lung Foundation and Founding Vice President of Evidence Based Clinical Practice Society of Bangladesh. He has published 63 papers in reputed Journals and has been serving as editorial board member of Journal of Asia Pacific Society of Respirology (APSR)

Abstract:

Chronic Obstructive Pulmonary Disease (COPD) is one of the most common respiratory ailments encountered by the physicians. This disease is a burden for both developed and developing countries. In 2007, a study on COPD known as BOLD-BD (Burden of Obstructed Lung Disease in Bangladesh) revealed the prevalence of COPD in general population to be 4.32% Chronic Obstructive Lung Diseases (COPD) may cause significant inflammation and narrowing of small airways which is not reflected very well by FEV1. Moreover, FEV1 correlated well with exertional dyspnea, not with chronic productive cough even with wheeze. Patients with chronic productive cough are more prone to exacerbations than emphysema patient, so management of Chronic Obstructive Lung Diseases (COPD) depends on both symptoms and exacerbations besides FEV1. GOLD classification ABCD sub-classification is not friendly for GPs . Considering limitations of FEV1, presence of complications (respiratory failure, other comorbidities), frequency of exacerbations and impact of disease on patients’ life a new management plan for Chronic Obstructive Lung Diseases (COPD) patients is formulated which is more effective than Gold management plan. So, a modified staging and management of Chronic Obstructive Lung Diseases (COPD) is formulated which is based on symptoms (S) frequency of exacerbations (E) and Function (Lung Function= FEV1) and depending on these three parameters, SEF(symptom, exacerbation and Function) classification has been made. According to SEF classification, COPD patients are dividing into four stages on the basis of FEV1 and each stage is again sub-classified on the basis of symptoms (a) and exacerbation (b)

Tsukasa Kadota

Research Associate
The Jikei University School of Medicine
Japan

Title: The biological role of extracellular vesicles in COPD

Time : 13:35 - 14:20

Speaker
Biography:

Tsukasa Kadota graduated from Jikei University School of Medicine where he also completed his residency in pulmonary medicine. He is a research associate at The Jikei University School of Medicine and a visiting scientist at National Cancer Center Research Institute.

Abstract:

Extracellular vesicles (EVs), such as exosomes and microvesicles, are released by many cell type into their environment. EVs contain a subset of proteins and nucleic acids such as messenger RNA and microRNA. EVs are thought to serve as a means of cell-to-cell communication and contribute to a number of disease states as they transfer their contents. COPD is a chronic inflammatory lung disease that causes obstructed airflow from the lungs. The main pathological changes of COPD are emphysema and small airway remodeling. Cigarette smoking have been widely recognized as the main causes of COPD. The noxious effects of smoking induce airway epithelial injury. Injured lung epithelial cells act as a source of various autocrine and paracrine factors. These suggest that the reciprocal interactions between the epithelium and mesenchyme are part of the important mechanism in COPD pathogenesis. Therefore the major aim of our study is to reveal the cell-to-cell interaction via EVs in COPD pathogenesis. Within research of our group, we investigated an EV-mediated intercellular communication mechanism between primary human bronchial epithelial cells (HBECs) and lung fibroblasts (LFs) and discovered that cigarette smoke extract (CSE)-induced HBEC-derived EVs promote myofibroblast differentiation in LFs. Remarkably, we elucidated that the novel mechanism of myofibroblast differentiation in LFs is attributed to the CSE-induced HBEC-derived EV miR-210 regulating autophagy machinery. Defining these mechanisms has potential as a new therapeutic target for COPD. The results will be presented and discussed.

Speaker
Biography:

Dr. Patrick Vanscheeuwijck is Director pre-clinical toxicology at Philip Morris International, Reduced Risk Products, and Switzerland, responsible for the in vitro and in vivo assessment of Reduced Risk Products (RRPs). The focus of his career at PMI has been on the development of approaches for the assessment of hazard associated with cigarette smoke and aerosols from RRPs, inhalation toxicology and animal models of disease; with more than 30 peer-reviewed publications. He has a Ph.D. in biochemical pharmacology (University of Gent, Belgium), performed postdocs at the University of Arizona, U.S. and the University of Leuven, Belgium in molecular pharmacology and molecular biology

Abstract:

Smoking cigarettes is a major risk factor in the development and progression of chronic obstructive pulmonary disease (COPD). Potential Reduced Risk Products (RRPs*), are being developed to reduce smoking-related health risks compared to smoking cigarettes. Here we report on mouse studies that have been conducted comparing different aspects of COPD after exposure of different strains to mainstream smoke (MS) from the reference cigarette 3R4F and aerosols from RRPs. Exposures were carried out for up to 8 months for several hours per day and at concentrations up to 30 µg nicotine/l test atmosphere. MS from 3R4F caused significant lung inflammation as evidenced by recruitment of inflammatory cells and pro-inflammatory cytokines in broncho-alveolar lavage fluid, changed pulmonary function parameters (e.g. resistance, PV-loops) indicative for emphysema and quantifiable emphysematous changes in the lung parenchyma. Exposure to high concentrations of aerosols from RRPs resulted in changes of a much lower magnitude and in a number of cases changes were not different from Sham (air)-exposed animals. Switching mice from exposure to MS for 2 months to aerosol from RRPs, resulted in the reversal of the emphysematous changes similar to those noticed when animals are switched from exposure of MS to fresh air. In summary, we have demonstrated in different mouse models that the RRPs, in contrast to 3R4F, cause a low level of lung inflammation and minimal pulmonary emphysema.
*RRPs is the term the company uses to refer to products with the potential to reduce individual risk and population harm in comparison to smoking cigarettes.

Roger Mark Engel

Senior Lecturer
Department of Chiropractic
Macquarie University
Sydney
Australia

Title: The effect of including manual therapy in the management of mild chronic obstructive pulmonary disease – a randomized controlled trial

Time : 14:45 - 15:10

Speaker
Biography:

Dr Roger Engel is a Senior Lecturer and Co-ordinator of Research in the Department of Chiropractic at Macquarie University. He is an osteopath and chiropractor with over 30 years clinical experience in hospitals in Australia and South-East Asia. In 2012, Roger was awarded a PhD from Macquarie University for his work in the field of chronic respiratory disease, in particular his work on the use of manual therapy in the management of chronic obstructive pulmonary disease. He has presented the results from his research at national and international conferences in Australia, Canada, China, Indonesia, Japan, the UK and the US.

Abstract:

Chronic obstructive pulmonary disease (COPD) is a major cause of disability, hospital admission and premature death in Australia. Estimates put the number of people affected at just over half a million. While exercise capacity is a prognostic indicator in COPD, the primary source of exercise limitation is dyspnoea with an increase in chest tightness identified as one of the causes. Manual therapy (MT) increases mobility of musculoskeletal structures and has the potential to alter chest tightness. Two pilot trials that used MT in conjunction with exercise reported greater improvements in exercise capacity in the group that received MT and exercise compared to exercise alone. This presentation will report on the design and progress of a fully-powered randomised controlled trial designed to investigate the effect of MT and exercise on patients with mild COPD. METHODS: 202 participants with stable mild COPD, between the ages of 50 and 65 years were randomly allocated to one of two groups: standardised exercise (Ex) or MT plus Ex (MT+Ex). Outcome measures including lung function, exercise capacity, dyspnoea levels and systemic inflammatory biomarkers were recorded at baseline, 4, 8, 16, 32 and 48 weeks. RESULTS: Preliminary analysis of results from the first group of participants show a trend towards greater increases in exercise capacity and lung function in the MT plus Ex group compared to Ex alone. DISCUSSION: Combining MT with exercise enhances exercise performance in people with mild COPD. If the increase in exercise capacity is sustained it appears to have a beneficial effect on lung function.

Speaker
Biography:

Al-Said A. Haffor is the Professor of Physiology, College of Medicine, Dar Aluloom University, Riyadh, Saudi Arabia. He completed his Ph.D., Applied Physiology, The Ohio State University, Columbus, Ohio, USA, 1985. He has served as the Professor of Physiology, College Science, and College of Applied Medical Science, King Saud University in the year 2013. He worked as a Principal Investigator and main research area is focused on Differentiation of Different Stages of Bronchial Responsiveness in Asthma Patients using X-Ray in Relation to Blood Cells Changes, and also – Effects of Selenium on the Activities of Glutathione Peroxidase and Lactate Dehydrogenase and their Relations to Free Radical Production in the Lungs.

Abstract:

Emphysema is characterized by destruction of lungs units and increased load on the diaphragm. The purpose of the present study was to examine the effects of O2 breathing (OB) on ultrastructural pathological alterations in the diaphragm and the lungs in relation to free radicals (FR) accumulation. Twenty adult male rats were randomly assigned to two groups; control (C); and OB. Animals of the OB were breathing 100%O2 for 72 hr continuously. Serum, lungs and diaphragm tissue supernatant analysis showed significantly higher (p<0.05) FR in HP group, as compared with control group. Ultrastructure examinations showed that OB resulted in variety of pathological alterations in the mitochondria and endoplasmic reticulum that were associated with disarrangement of myofibrils, loss of I-banding for myosin, focal myolysis of the myofilaments, complete fragmentation of myosin, tearing of myofilaments from Z plates and tearing of the endothelial cell of the interstitial blood capillaries. Ultrastructure examination of lungs showed that OB breathing resulted in desquamated pneumocyte Type II with degenerated surfactant materials, thickened alveolar wall and thickening of alveolar septum due to proliferation of endothelial cells lining the pulmonary capillaries as a result of an active transmigration. Based on the results of the present study, it can be concluded that OB inducted acceleration ROS formation, damaged the lungs' parenchyma and damaged the contractile apparatuses of the diaphragm and related endomembrane proteins that could involve intracellular calcium channels proteins.

Speaker
Biography:

Tsuyoshi Shuto has received his PhD degree from Kumamoto University, Kumamoto, Japan, in 2006. He has joined Kumamoto University in 2001 as a Research Associate and in 2006 as a Lecturer/Assistant Professor in the Department of Molecular Medicine, Graduate School of Pharmaceutical Sciences of Kumamoto University, where he is currently an Associate Professor since 2013. During 1999 to 2001 he was at House Ear Institute, USA as a Research Associate. From 2004 to 2005, he was engaged as a Visiting Researcher at California Pacific Medical Center Research Institute, USA. He has published more than 75 papers in reputed journals.

Abstract:

Protease-antiprotease imbalance and oxidative stress are considered to be major pathophysiological hallmarks of severe lung diseases including chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF), but their role in the regulation of mucus obstructive phenotypes including pulmonary emphysema and dysfunction of βENaC-transgenic (Tg) mice, a murine model of COPD/CF, is unknown. Here, DNA microarray analysis revealed that protease- and oxidative stress-dependent pathways are activated in the lung tissue of βENaC-Tg mice. Treatments of βENaC-Tg mice with a serine protease inhibitor ONO3403 and an antioxidant N-acetylcystein significantly improved pulmonary emphysema and dysfunction. Moreover, depletion of a murine endogenous antioxidant Vitamin C (VC), by genetic disruption of VC-synthesizing enzyme senescence marker protein-30 (SMP30) in βENaC-Tg mice, increased inflammatory status in lung tissue and exaggerated pulmonary emphysema with a significant decrease in pulmonary function, possibly due to an increased oxidative stress. Thus, our results define protease and oxidative stress as factors that exacerbate mucus obstructive phenotypes of a mouse model of COPD/CF.

Shoude Jin

Professor
The Fourth Hospital of Harbin Medical University
china

Title: Mechanisms of Chronic obstructive pulmonary disease and airway smooth muscle remodeling: the potential roles of Abhd2

Time : 16:40 - 17:05

Speaker
Biography:

Shoude Jin has completed her PhD in the year of 2009 from Chinese Medicine University. She is the director of the department of Respiratory Medicine, academic leader, professor and a tutor of graduate student. Her research direction: chronic obstructive pulmonary disease pathogenesis, diagnosis and treatment of Respiratory Critical Care. She has published more than 20 papers as the first or corresponding author in reputed journals,including 8 papers of SCI, the cumulative impact factor of 25 points.

Abstract:

Chronic obstructive pulmonary disease(COPD)is a complex multifactorial illness involving both genetic and environmental factors and is one of the leading causes of death worldwide. Although considerable improvements have been made on the control of environmental factors, the morbidity and mortality of COPD are still continually increasing. Over the past years, we have concentrated on the genetic factors contributing to COPD, starting with ABHD2 mutations. We found that Abhd2 gene trap mice spontaneously developed into emphysema. These findings strongly suggest the roles of ABHD2 mutations in the development of COPD, but the exact mechanisms and whether ABHD2 mutations can be used as warning markers of COPD remain largely unknown. Based on the findings that Abhd2 is expressed in airway smooth muscle cell, in the next research project, we propose to test our hypothesis that ABHD2 regulates alveolar epithelial type Ⅱcells apoptosis in cell and animal levels and elucidate the effects of specific ABHD2 mutations on COPD, and use ovalbumin to stimulate Abhd2 deficient mice with COPD genetic background and trigger asthma attacks. The aim is to clarify the function and structure of airway smooth muscle cell changes to promote inflammation and remodeling, facilitating COPD to develop into ACOS in Abhd2 deficient mice. Eventually we hope to provide a theoretical basis and the potential key drug targets for early screening and early intervention for people with high COPD risk and identify the potential key drug targets and provide novel strategies for clinical precise treatment.