3rd Intrenational Conference on Chronic Obstructive Pulmonary Disease July 11-12, 2016 Brisbane, Australia

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.

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.

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)

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.

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.

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.

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.

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.

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.

Biography:

T.M.Sooronbaev is the National Coordinator of FRESH AIR study in Kyrgyzstan, and Scientific Coordinator of Kyrgyz-Japanese Research Centre of NCCIM, He is also a Head of Respiratory, Critical Care and Sleep Medicine Department of National Center of Cardiology and Internal Medicine and Chief Pulmonologist of MoH Kyrgyz Republic, Chief Pulmonologist of MoH Kyrgyz Republic and also President of Kyrgyz Thoracic Society. He was joined in many collobrations with National GARD (WHO) Coordinator MoH Kyrgyz Republic and Chief Scientific Coordinator of Euro-Asian Respiratory Society. He is also an Co-chair of Central Asian PVRI Task Force and Head of PVRI excellence PH Centre in Kyrgyzstan

Abstract:

COPD is very important problems, especially for highlanders. Particularly bad situation for COPD mortality among residents of high mountains, the mortality rate among the highlanders are 2-3 times higher than that among lowlanders, also a high prevalence of COPD among the highlanders than lowlanders. The distribution of patients by age showed an increase in the prevalence of COPD in patients older than 40 years to 25.4%. It is 4 times higher than the official statistics. Smoking is a major risk factor of COPD among highlanders, we found 60% male smokers. Indoor pollution is a very important reason for the development and progression of COPD among highlanders, especially for women and children. Each highlander’s family has large reserves of biomass (dung), which are the main fuel for heating and cooking. Noteworthy is the negative impact of smoke, when many highlanders use open fire for cooking. Also an important risk factor could be the smoke from cooking. We got interesting results, the frequency of respiratory symptoms in 2 times higher in families where they use of biomass than in families where they use of other fuels. What we can say about the clinical features of COPD in the inhabitants of the mountains. We observed a significant dyspnoea in highlanders with COPD, also in GOLD stages I and II. The quality of life of the mountain people with COPD was also worse than lowlanders. We also found a significant reduction in physical activity in highlanders with COPD. For 6 minutes, they could go much smaller distance than lowlanders. Thus, COPD is one of highly prevalent diseases of highlanders which causes high mortality. COPD in highlanders is severe and progressive. We have new approaches for the treatment of COPD in the highlands with oxygen therapy and other methods.

Biography:

Udantha Abeyratne earned a PhD in Biomedical Engineering from Drexel University, Philadelphia and a Postgraduate Certificate in Pediatric Sleep Science from the Faculty of Medicine, U of Western Australia. Dr. Abeyratne is an Associate Professor and the director of the Master of Engineering Science program at The University of Queensland, Australia

Abstract:

Introduction: spirometry is an essential tool to diagnose COPD. The reliability of spirometry depends on the expertise of the technologist who administers the test and the patient’s efforts. Laboratory spirometry is not suitable for patient-centred COPD management plans in home settings. Automated technologies independent of patient efforts to monitor COPD are urgently needed for laboratory as well as home use. Cough is a cardinal symptom of COPD but it is not sufficiently used in diagnosing COPD beyond noting it as a symptom. Adventitious sounds such as crackles and wheezing generated in a diseased lung as well as information on airflow limitations due to obstructive illnesses should be available via a cough. Our target is to develop mathematical techniques for cough analysis for the diagnosis of COPD and associated illnesses such as asthma and emphysema. We also implement this technology on a smartphone, together with automated cough detection and counting software. No network connection or extra attachements are required. Method: cough sounds were recorded at the Princess Alexandra Hospital (PAH), Brisbane from adults referred for routine spirometry. We recorded voluntary cough events using an iPhone (in air, outside the mouth) and analyzed them following a technique similar to our pediatric pneumonia technology (Ann Biomed Eng, 41(11):2448-62)). We explored the performance of the method using a leave-one-out validation technology, against the clinical diagnosis supported by spirometry and other tests deemed clinically necessary. At the time of writing, our database at PAH consists of 66 subjects (COPD (n=15), no respiratory disease (n=42) and obesity hypoventilation (n=6)). Results: the cough sound based algorithm achieved a classification sensitivity and specificity of 80% and 88% respectively in separating COPD patients from the rest. The technology can be implemented on a smart phone such as an iPhone. Conclusion: our preliminary results were obtained on a small dataset, but they suggest cough sounds carry vital information on COPD. Results we have obtained – accuracies in the order of 90% – from pediatric subjects on illnesses such as pneumonia, bronchiolitis and asthma/viral-wheeze further encourage us to apply our methods on adult populations. Our database of adult patients is growing and we expect to present further improvements to the technology at the conference.

Biography:

Director and Coordinator of the "Chronic Cough” Guideliness of the Spanish Society of Respiratory, 2014. Proposed by the European Respiratory Society for the formation in Spain of a research group (Ramon y Cajal Hospital) for multicenter project in 5 European countries, entitled "Mechanisms of Neuropathic symdrome cough hypersensitivity (CHS) Member: biomarkers and treatment targets for new Approaches (NEuroCough), in September 2014 within the European research program Horizon 2020

Abstract:

The relationship between COPD, asthma and gastroesophageal reflux has been the subject of many publications for decades because many epidemiological studies they approve. But still remain obscure mechanisms that explain it chiefly for two reasons, one, the lack of exploration with sufficient statistical power, especially those concerning the physiology of extraesophageal reflux and gastro-esophageal junction and two, the need to understand that by means of mechanism bidirectionality sharp, several vicious circles between the two entities are established. Comorbidities in COPD-asthma, obesity and obstructive sleep apnea probably also involved in the control of asthma having the reflux material as the link. The end result is that COPD-asthma and gastroesophageal reflux are multifactorial entities with many points of connection between them still scarcely analyzed as a whole, which favors that must involve at least three specialties, Pneumology, ENT and Gastroenterology to explore carefully reflux in each COPD or asthmatic patient in order to optimize therapy. In this paper, an update on this relationship be made and future directions of research will target

Biography:

Researcher and Master course student, Department of Molecular Medicine, Graduate School of Pharmaceutical Sciences, Kumamoto University 2016-present, Doctor course student, Department of Molecular Medicine, Graduate School of Pharmaceutical Sciences, Kumamoto University

Abstract:

Chronic obstructive pulmonary disease (COPD) is mainly characterized by airway mucus obstruction, chronic inflammation and emphysema. Identification of novel factors that control the COPD pulmonary phenotypes is an important issue for better treatment of COPD patients. Glucagon-like peptide-1 (GLP-1) is a gastrointestinal hormone, and because of its pancreatic supporting function, GLP-1 receptor agonist is clinically used as a drug for the treatment of type 2 diabetes. Interestingly, GLP-1 receptor is highly expressed in lung tissue compared with other tissues. But little is known about the physiological and pathophysiological roles of GLP-1 in lung. Here, we showed that intratracheal treatment of airway specific βENaC (epithelial Na+ channel β subunit)-transgenic mice, a murine model of COPD that basically exhibits airway mucus obstruction, with GLP-1 receptor agonist Exendin-4 (10 pmol/day, 2 weeks) significantly up-regulates mucin gene expression in lung tissue. Moreover, Exendin-4 significantly increased the alveolar mean linear intercept (MLI), a measure of emphysema, in βENaC-Tg mice. Notably, GLP-1 receptor agonist (Exendin-4 and Liraglutide) treatment (0.1 nM, 6-12 hrs) also enhanced mucin expression in β/γENaC-overexpressing 16HBE14o-cells, and the effect was possibly induced by p38 MAP kinase pathway. Despite observations of Exendin-4-dependent mucin up-regulation in WT mice and parental 16HBE14o- cells, exacerbation of pulmonary phenotypes were not observed in these conditions. Together, our studies demonstrate that pulmonary GLP-1 signal exacerbates the phenotypes of βENaC-Tg mice at least partly via p38 MAPK-dependent mucin induction, and our data may caution against the clinical use of inhaled GLP-1 receptor agonist in COPD patients with type 2 diabetes.

Biography:

Reseracher and present, Master course student, Dpartment of Molecular Medicine, Graduate School of Pharmaceutical Sciences, Kumamoto University, Japan

Abstract:

One of the major pathophysiological hallmarks of COPD is oxidative stress. Our microarray analysis using the lung tissue of COPD-like murine models (ENaC-transgenic mice) suggested an imbalance between oxidants and antioxidants. Uric acid (UA), a product of purine metabolism, is one of the strongest endogenous anti-oxidants in the body. Interestingly, recent cohort studies showed that low levels of serum UA are associated with higher rates of COPD (Horsfall LJ, et al., Thorax 2014; Nicks ME, et al., COPD, 2011). However, the experimental evidence remains inconclusive. To clarify how serum UA levels affect pulmonary phenotypes of COPD, we treated βENaC-Tg mice with oxonate, a pharmacological inhibitor of uricase, which is an enzyme that oxidizes UA to allantoin, to increase blood concentration of UA in the mice. Notably, oxonate treatment (500 mg/kg/day, p.o., 4-5 weeks) in βENaC-Tg mice revealed that typical phenotypes of COPD, such as emphysema demonstrated by an alteration of the mean linear intercept (MLI), and pulmonary function (FEV0.1%) determined by the ventilator-based flexiVent system, tended to be improved in oxonate-treated βENaC-Tg female but not male mice. Moreover, a cross-sectional study and a retrospective longitudinal study with Japanese participants in a health screening program also demonstrated the association between plasma UA level and pulmonary function in a female-specific manner. Thus, ours studies demonstrate plasma UA as a protective factor of respiratory dysfunction and emphysema in female mice and human with obstructive pulmonary diseases.

Biography:

Dr. Olfert completed his PhD in Physiology from Loma Linda University (Loma Linda, CA) and postdoctoral studies in pulmonary physiology in School of Medicine at University of California San Diego (La Jolla, CA). He is currently an Associate Professor (with Tenure) at West Virginia University School of Medicine, and Member in the Center for Cardiovascular and Respiratory Sciences, the Mary Babb Randolph Cancer Center, and the West Virginia Clinical and Translational Science Institute. He has published more than 45 papers in ruptable peer reviewed journals and is currently serving as an editorial board member on 3 respected journals. He is a standing member on 2 national grant reveiw panels within the USA, as well as ad hoc reveiwer for several international grant agencies.

Abstract:

Exercise limitation is a hallmark of chronic lung diseases, such as COPD. There is evidence of systemic contributions that contribute to exercise limitation above and beyond central pulmonary dysfunction, but the cellular mechanisms remain poorly understood. This talk will review currentl and new data obtain from muscle biopsys in patients with COPD in the regards to exercise function and expression of angiogenic regulators and inflammatory molecules in skeletla muscle. Importantly, this discussion will highlight evidence obtained in a diversity of COPD patients, which include cigarette smoked induced COPD, as well as the genetic variant of COPD resulting from alpha-1-antitrypsin deficient (AATD) individuals. Further insight will be glean from data obtain in AATD individuals that have developed COPD and AATD who have not develop COPD. The focus of the presentation will address whether abnormalities in the muscle angiogenic response to exercise are a consequence of systemic inflammation stemming from lung damage, or if these are based on O2 transport limitation, and what effect exercise training and/or physical fitness exhibits in this context. The central premise of the talk is based on observation that deregulation of several key angiogenic regulators is responsible for many of the structural and functional alterations found in skeletal muscle of patients with COPD, especially those with a cachectic phenotype, and that these abnormalities produce a phenotype that is unable to protect skeletal muscle from chronic inflammation. Exercise training can help to restore and/or minimize the abnormal angio-metabo signal axis in muscle, thereby increasing muscle capillarity and improving muscle function.

Biography:

Monika Szturmowicz is a Professor of Medicine afficiated at I Department of Lung Diseases, National Tuberculosis and Lung Diseases Research Institute, Warsaw Poland. In 2010—2014 she was the Editor-in-Chief of Polish Pneumonology and Allergology, the peer-reviewed official Journal of the Polish Respiratory Society. Dr. Szturmowicz is an active member of ACCP (FCCP since 2003), ERS and IASLC, directly involved in the clinical research concerning pulmonary hypertension in lung diseases. She is the author of 99 papers published in peer-reviewed international journals, Hirsh Index -13.

Abstract:

Pulmonary hypertension (PH) defined as mean resting pulmonary artery pressure (mPAP) equal or higher than 25 mmHg ( measured directly), is found in 50% of the patients with end-stage COPD. In most cases mild PH is observed. Nevertheless in 2-7% of patients, severe PH (defined as mPAP>35 mmHg or CI<2.5 l/min) develops. What’s most interesting, severe PH in COPD is not always combined with end-stage disease. The differential diagnosis on such occassion should exclude the influence of other comorbidities on PH ( left heart disease, venous thromboembolism and sleep disordered breathing). Latest publications indicate that clinical phenotype of severe PH in COPD is characterised by: profound hypoxemia, hypocapnia and very low diffusion capacity of the lung for carbon dioxide (DLCO), despite mild or moderate aiway obstruction. It is still not known, if such phenotype is combined with certain genetic rearangements. According to latest PH guidelines, optimal COPD treatment combined with long therm oxygen therapy in the patients with PaO2 below 60 mmHg, is indicated in PH-COPD. Nevertheless in the patients with servere PH, the referral to an expert center is advised. Latest results of clinical trials with PH-specific drugs are disappointing. Despite the improvement in pulmonary haemodynamics, no significant changes in exercise capacity or quality of life of the patients are reported. Future research should be directed towards the identification of those PH-COPD patients, in whom maximal exercise capacity is limited by low cardiac output, and not by the exhaused ventilatory reserve.

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 of the School of Medicine at Universitat Pompeu Fabra and Deputy Director at the Spanish Network of Excellence for Research in Respiratory Diseases (CIBERES). He has been funded by 65 competitive grants, including 4 projects funded by the European Commission, and published more than 260 Original Articles and Reviews in peer reviewed journals as well as 50 book chapters.

Abstract:

Nutritional abnormalities are often associated with Chronic Obstructive Pulmonary Disease (COPD). Their early detection is important, since they determine the patient's prognosis independently of the degree of lung function impairment. In addition, nutritional abnormalities are involved in muscle dysfunction, which in turn leads to exercise limitation, loss of quality of life and increased mortality. However, the presence/absence of malnutrition is a factor that has not been included in the majority of clinical guidelines. The diagnostic techniques include both anthropometry and measurement of body composition (mainly through bioelectrical impedance). The most commonly used anthropometric variables are body mass index (BMI) and the percentage of ideal body weight, while fat-free mass index (FFMI) is the most commonly used impedance variable. The causes of malnutrition associated with COPD include smoking, systemic inflammation, imbalance between nutrient intakes and energy consumption, impairment in respiratory gas exchange and the effects of anabolic hormones, effects of some drugs, decreased physical activity and comorbidities. All these causes lead mainly to an imbalance between protein synthesis and destruction and a predominance of bone resorption, with loss of muscle, fat and bone mass. The treatment includes an improvement in lifestyle (avoid tobacco smoking, better quality in nutrient intake, increase in physical activity, exercise training) and, if necessary, the use of nutritional support (enteral or even parenteral) and anabolic agents (eg, selective androgen receptor modulators [SARM] or secretagogues of the growth hormone). These drugs seem to be more effective when associated with training.

Biography:

Prof. Ping Yang has completed her MD from Beijing Medical College in China and PhD at Johns Hopkins University in USA. She has been leading a comprehesive lung cancer research program at Mayo Clinic since 1997, emphasizing patient-centered outcome research with COPD as one of the key interaested areas. She has published more than 200 peer-reviewed papers and has been serving as an editorial board member of Jounal of Clinical Oncology and Associate Editir of Journal of Thoracic Oncology.

Abstract:

COPD is present in 40-60% of LC patients; some existed long before LC diagnosis and others were identified at the time of LC diagnosis. Our clinical research team has been evaluating the impact of different diagnostic time (prior vs. concurrent), severity of COPD, and a subgroup of CT-defined emphysema on long-term survival of patients with early stage non-small cell lung cancer (NSCLC). Two patient cohorts include ~1400 NSCLC with known COPD status and ~1100 with known emphysema status. COPD was defined according to pulmonary function tests (post-bronchodilator FEV1/FVC<0.70) or recorded medical diagnosis; severity was grouped by GOLD criteria (Global Initiative for Chronic Obstructive Lung Disease). Emphysema was based on standard-dose CT scan; percentage quantification was determined through direct inspection and categorized into <5%, 6-24% and 25-60%. Five key findings are summarized as follows: (1) Patients with a prior COPD had a significantly higher proportion of former smokers and moderate airflow obstruction than those with concurrent COPD. (2) Worse survival was significantly associated with prior COPD and moderate to severe airflow obstruction regardless of COPD diagnosis time. (3) In surgically-treated patients, the overall postoperative complications were higher in patients with a greater emphysema score. (4) Increasing emphysema score was significantly associated with worse survival. (5) More specific to resected LC in the predominant emphysematous region, patients with >6% emphysema experienced a mild decrease in FEV1 and an increase in FEV1/FVC. We conclude that COPD in general and emphysema in particular should be taken into careful consideration in LC treatment

Biography:

Geertjan Wesseling has studied Biology and Medicine at the Free University of Amsterdam, Netherland. He has completed his Training in Respiratory Medicine in 1991 and obtained his PhD in 1993. He is a Professor of Respiratory Medicine in Maastricht and coordinates the International Master in Medicine of Maastricht University. He is a former President of the Dutch Pulmonology Society

Abstract:

Comorbidities are very common in COPD. Of patients referred for pulmonary rehabilitation more than 50% report at least one chronic comorbid disorder that is of importance for the rehabilitation and its outcomes. Also, comorbidities have a huge impact on the disease burden, on the risk of hospitalization and on mortality. Recently it was reported that comorbidities come in clusters of which cardiovascular and psychological comorbidities are the most frequently seen. It appears that these comorbidities are in part related to systemic inflammation. Other mechanisms may be relevant as well. Several studies have demonstrated effects of comorbidities on outcomes of pulmonary rehabilitation. These may implicate differentiation of rehabilitation programs according to clusters of comorbidities.

Biography:

Md Rashidul Hassan is the Director cum Professor at National Institute of Diseases of the Chest & Hospital, Dhaka. He has completed his MD Respiratory Medicine from Dhaka University in the year 1995. He is currently a Professor at the Department of Respiratory Medicine, National Institute of Diseases of the Chest and Hospital [NIDCH], Dhaka, Bangladesh. He is also a 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:

Background: Understanding of basic concept of COPD is an important issue for the practicing physicians. Seamless management of COPD needs to understand basic concept of asthma. Use of simile is the best way to understand any basic concepts. A positive role of physicians after proper understanding of basic concept is essential for successful management of COPD. To achieve this goal in Bangladesh, we developed a module COPD presentations and carried out several seminars entitled “COPD: BASIC CONCEPT AND MANANAGEMENT” in different regions of the country. The outcome is encouraging and we assume the module can be used for general physicians as an effective instrument in switching to standard treatment of COPD from conventional treatment. Objectives: Similarity between water movement air movement and pathophysiology of COPD helps in understanding the basic mechanism of COPD and thereby physicians can be easily motivated to switch over to standard treatment of COPD. Methods: An audio-visual module comprising of an interactive lecture were prepared and presented in front of the primary care physicians and respiratory specialists. For this a nation-wide campaign will be out entitled “COPD: BASIC CONCEPT AND MANANAGEMENT” in different regions of Bangladesh including all medical colleges. Atleast two pulmonologists of Bangladesh presented the papers and answered the different questions of the audiences. Discussion: Water movement, like conduction, convection and Diffusion can be easily described and resulting in difficulty in breathing. After water movement simile it is described clearly irritation of smoke and recurrent infection is the main cause of sputum production and exacerbations. After an episode of COPD exacerbation small airway and alveolar destruction leads to different types of emphysema formations and mismatch of Ventilation Perfusion ratio and right to left shunt. This V/Q mismatch and shunted blood leads to progressive exertional dyspnea, Hypoxemia, Hypoventilation, Polycythemia or anemia and ultimately leads to Respiratory Failure. Conclusions: What we don’t see through our necked eyes (pathophysiology of COPD) may be understandable by drawing simile with an event, which we can see with our eyes. The lesson can be remembered like stories by anybody even a layman. This may help to facilitate patient education programs. Recommendations: We may carry this mode pf presentation to popularize COPD management and Update knowledge of physicians. 1.Attract physicians “towards Basic Cocept of COPD” by using such simple simile like water movement 2.Integrate physicians with appropriate knowledge of COPD Management 3.Deal with physicians to take care patients’ value regarding COPD management.

Biography:

Hiroaki Kume obtained his MD from Toyama Medical and Pharmaceutical University in 1982. He has completed his PhD in Department of Medicine (II), Nagoya University School of Medicine in 1990, and postdoctoral studies from School of Veterinary Medicine, University of Pennsylvania (Dr. Michael I. Kotlikoff’s Lab). Currently, he works at Department of Respiratory Medicine and Allergology, Kindai University Faculty of Medicine and Department of Respiratory Medicine, Rinku General Medical Center, Izumisano City, Osaka 598-8577, Japan, and focuses on investigating the characteristics of COPD with the goal of rational therapy for COPD

Abstract:

Rationale: Eosinophil inflammation in the airways is observed in some patients with chronic obstructive pulmonary disease (COPD) independent of asthma. However, little is known about not only mechanisms but also therapy in this clinical phenotype of COPD. This clinical study was designed to determine whether inhaled glucocorticosteroids (ICS) are useful for airway eosinophilia in COPD. Methods: Once-daily inhalation of indacaterol (LABA) was firstly administrated to the patient with COPD. After symptoms were stable, sputum examination was done. When a percentage of eosinophil in the induction sputum is >3%, once-daily inhalation of ciclesonide (ICS) was administered. Results: 20 patients with COPD (GOLD 2-3) with airway eosinophilia were enrolled. After administration of indacaterol, COPD Assessment Test (CAT) score was decreased from 15.1 to 7.9 (P<0.05), and frequency of SABA on demand for symptom relief was also decreased from 1.6 to 0.8 puffs/week (P<0.05). In lung function test, forced expiratory volume in 1 sec (FEV1) and inspiratory capacity (IC) were increased by 210.0 (P<0.05) and 311.5 mL (P<0.01), respectively. After addition to ciclesonide, values of CAT score and frequency of SABA were markedly decreased to 4.9 points and 0.3 puffs/week, respectively (each P<0.05 vs LABA). Moreover, FEV1 and IC were further increased by 147.0 and 227.6 mL, respectively (each P<0.05 vs LABA). Conclusions: Not only LABA but also ICS is needed to improve lung function and to achieve better maintenance in COPD with airway eosinophilia. Ciclesonide is effective for these cases. Eosinophil infiltration to airways may be indication of ICS therapy for COPD.

Biography:

Gunilla Lindqvist is a Registered Nurse (RN), Master´s degree in Public Health, Senior Lecturer, Doctor of Philosophy (PhD) and Post doctor within the subject of Health and Caring Science. Gunilla is working as a Senior Lecturer at School of Health and Caring Sciences, Linnaeus University Campus Kalmar and Växjö and has now a postdoctoral position at Linnaeus University. Gunilla Lindquist’s research focuses on Chronic Obstructive Pulmonary Disease, the sufferer themselves and their spouses. Gunilla works in a research project focusing on innovative solutions to meet future healthcare needs and preferences of older people and their carers.

Abstract:

Chronic obstructive pulmonary disease (COPD) is an increasing health problem that affects about 600 million people globally, and it is expected to be the third most common cause of death worldwide by 2020. COPD is a chronic long-term condition that is irrevocable. Cigarette smoking is the most commonly encountered risk factor for COPD, and it has also been shown that passive smoking impairs lung function. When the disease progresses, not only is the lung fiction impaired, but there are also other consequences as physical, psychological and social. Aim The aim of the study was to generate a theory, grounded in empirical data, to reveal the main concerns of people who suffer from COPD and how they handle everyday life. Method The constant comparative method of grounded theory, developed by Glaser and Strauss (1967), was used. Data was collected by interviewing 23 people with COPD all having different grades of the disease, from mild to severe. Findings A substantive theory was generated showing that the main concern for people suffering from COPD was feelings of guilt due to self-inflicted disease associated with smoking habits. This includes feelings of living in the shadow of death. This core category was linked to five categories termed making sense of existence, adjusting to bodily restrictions, surrendering to faith, making excuses for the smoking related cause, and creating compliance with daily medication. These categories form a pattern of behavior that explains how feelings of guilt were handled by people living with COPD.

Biography:

Dr. Qian Zeng made Self-research on anti-inflammatory therapy for chronic inflammatory diseases from 2001 to 2011, and Working as a general practitioner at Medi7 Clinic Bentleigh, Melbourne and continuing research on anti- inflammatory therapy from 2012 until now. His main Interest is to combine Modern Western Medicine with Traditional Chinese Medicine to develop a new anti-inflammatory therapy for treating chronic inflammatory diseases.

Abstract:

COPD is a chronic progressive inflammatory lung disease. It is caused by various stimuli, like smoking, air pollution, exposing to noxious chemicals and recurrent infections. All these stimuli can cause small airway and lung tissue injury, which induces an inflammatory reaction. Prolonged inflammation further damages small airway and lung tissue, subsequently the inflammation becomes self-perpetuating, i.e. the inflammation will last for ever even when the initial stimuli are eliminated. The activated neutrophil and alveolar macrophage produce neutrophil elastase and macrophage elastase, these two proteolytic enzymes cause disruption of the wall of alveoli and fusion of alveoli, resulting in decreased gas-exchanging surface. Activated inflammatory cells also produce various inflammatory factors, which stimulate secretion of mucus and cause fibrosis and thickening of the wall of small airway, all these increase the obstruction of small airway, reduce the air flow. The ongoing inflammation in small airway and lung tissue will continue to cause tissue damage, as a result, the lung function in COPD patients will progressively deteriorate. The key in treating COPD is to treat the inflammation. Current treatment of COPD are LAMA, LABA and ICS. LAMA and LABA only treat the symptoms of COPD by dilating the small airway, they do not target the underlying mechanism of COPD (the inflammation). ICS can only temporarily supress the inflammation in COPD, cannot really terminate the inflammatory reaction and therefore it cannot stop the progression of COPD, though it is the mainstay of treatment of COPD. The inflammation in COPD is partially resistant to steroid. The underlying mechanism sustaining the chronic inflammation in COPD is due to a bidirectional intercellular reactions between T cell and alveolar macrophage and/or neutrophil. The activated T cell produces cytokines, which activate alveolar macrophage and/or neutrophil, in turn, activated alveolar macrophage and neutrophil produce interleukins XII and other cytokines to activate T cell. Once this vicious intercellular reaction established, it cannot be disrupted and will last for ever. This is the common mechanism of all self-perpetuating chronic inflammation, no matter what the initial stimuli are or in what tissue or organ the inflammatory reaction occurs. Steroid resistant is a big issue in treating COPD and other chronic inflammatory lung diseases, like asthma, pulmonary fibrosis. In order to effectively treat COPD, we must find new anti-inflammatory therapies or developing new anti-inflammatory drugs.

Biography:

Geertjan Wesseling (1956) studied biology and medicine at the Free University of Amsterdam. He completed his training in Respiratory Medicine in 1991 and obtained his PhD in 1993. He is a professor of Respiratory Medicine in Maastricht and coordinates the international master in medicine of Maastricht University. He is a former president of the Dutch Pulmonology Society

Abstract:

Chronic Obstructive Pulmonary Disease causes significant morbidity and mortality worldwide. Most patients can be treated in primary care. However, even in patients with relatively mild airflow obstruction referral to a specialist may lead to important findings, both related to the COPD and to comorbidities. Several classifications and gradings have been proposed throughout the years that help in categorizing patients, yet not all have direct consequences for the management, that typically includes lifestyle changes, of which smoking cessation and increased physical activity or even rehabilitation are paramount, and pharmacotherapy. Inhaled medication is aimed at improving expiratory flow, reducing hyperinflation and inflammation, to slow-down disease progression and improve quality of life and prognosis. Longacting bronchodilators have clinically significant effects and are widely used, also in mild-to-moderate disease. In recent years the Astma COPD Overlap Syndrome has been proposed, which is a misnomer and often an excuse to skip an adequate diagnostic process and prescribe triple-therapy in patients who would do well with only one or two different drugs. Unfortunately, the majority of COPD patients are on inhaled steroids, but effects are small, often not clinically relevant and side-effects such as an increased risk of pneumonia should warrant clinicians to be more prudent in prescribing those. Selfmanagement is considered an important component of management strategies, even if effects on various outcomes are limited. Repeated lung function measurements are often performed both in primary care and in the hospital.with limited if any effects on management. Taken together, appropriate COPD management is not only about what we should do but certainly also about what we shouldn’t.

Biography:

Abstract:

Chronic obstructive pulmonary disease (COPD) is a complex multi-component condition whose clinical presentation is often complicated by co-morbidities and extrapulmonary clinical features. This presentation will highlight three of them. Affecting between 17% and 78% of people is gastro-oesophageal reflux disease (GORD). Due to the possibility of pulmonary microaspiration GORD may influence lung disease severity and is a predictor of acute exacerbations. Pain is common in people with COPD, affecting 66% of individuals with moderate to very severe disease. Higher pain intensity is associated with increased dyspnea, fatigue, poorer quality of life, lower levels of physical activity and a greater number of comorbidities. Pain imposes limitations on exercise behaviour and participation in pulmonary rehabilitation. The common locations of pain are the upper and lower back and lower limbs. In COPD, postural alterations may be influenced by musculoskeletal comorbidities including osteoarthritis and osteoporosis. Common postural abnormalities include alterations in the degree of cervical lordosis and thoracic kyphosis, and altered scapula position. Postural alterations are associated with reduced pulmonary function and may contribute to exercise limitations and increased functional impairment.

Biography:

Sulaiman Obtained his MBBS degree from Mumbai University in 1996 and Post graduation in Respiratory medicine and Tuberculosis in 2002 from B Y L Nair Hospital Mumbai. he has more than 13 years experience in private practice and research . Areas of expertise include Asthma,COPD, Interstial lung disease,Sleep apnea syndrome and Tuberculosis esp multi drug resistant and XDR tuberculosis Awarded Mahatma Gandhi gold medal in 2014 for outstanding contribution in field of Respiratory medicine, community health and research. Have many publications in Internarional journals and participated in many international conferences . Am Principal Investigator in many research projects at present and part of Advisory committee of ICMR and CCDC Delhi for Non communicable diseases Have been Director with Aga Khan Health Service India for 7 years and at present am a Governing board of Prince Aly khan. Hospital since 2012. Am also the Chairman of Hospital based Authorisation commitee and Brainstem Death committee at Prince Aly Khan hospital

Abstract:

A global healthcare survey of WHO highlighted some health concerns for India viz. vulnerability of young children, poor sanitation and limited insurance with only 3%-5% of Indians covered under health insurance. There is a high percentage of ageing population as well. Chronic diseases like COPD add to this pre-existing burden on healthcare systems. The current COPD burden is limited but is expected to increase as the population ages.There is a lot of variation in COPD prevalence in India in rural and urban population.In India, cigarette smoking is just one of the major risk factors for COPD. Exposure to tobacco smoke from hookahs, chillums and bidis, burning of biomass fuel like animal dung and wood, burning of mosquito coils, also poses a great risk. This is coupled with under-diagnosis of COPD withSpirometry still being underutilized. Comorbid conditions like ischemic heart disease, hypertension, skeletal muscle dysfunction, osteoporosis, depression, diabetes and renal conditions add to the morbidity. The Indian guidelines for COPD classify severity simply as mild, moderate and severe whereas GOLD guidelines have a combined assessment of COPD in the form of a grid which is classified as mild, moderate, severe and very severe. Management options include SABAs/SAMAs, LAMAs and LABAs, inhaled corticosteroids, antibiotics and the preferred device being MDI with spacer or nebulization. Due to diversity of COPD stages at which patients present themselves along with urban and rural prevalence, it will be interesting to ponder over different treatment algorithms based on some case studies.

Biography:

Dr. Olfert completed his PhD in Physiology from Loma Linda University (Loma Linda, CA) and postdoctoral studies in pulmonary physiology in School of Medicine at University of California San Diego (La Jolla, CA). He is currently an Associate Professor (with Tenure) at West Virginia University School of Medicine, and Member in the Center for Cardiovascular and Respiratory Sciences, the Mary Babb Randolph Cancer Center, and the West Virginia Clinical and Translational Science Institute. He has published more than 45 papers in ruptable peer reviewed journals and is currently serving as an editorial board member on 3 respected journals. He is a standing member on 2 national grant reveiw panels within the USA, as well as ad hoc reveiwer for several international grant agencies.

Abstract:

Exercise limitation is a hallmark of chronic lung diseases, such as COPD. There is evidence of systemic contributions that contribute to exercise limitation above and beyond central pulmonary dysfunction, but the cellular mechanisms remain poorly understood. This talk will review currentl and new data obtain from muscle biopsys in patients with COPD in the regards to exercise function and expression of angiogenic regulators and inflammatory molecules in skeletla muscle. Importantly, this discussion will highlight evidence obtained in a diversity of COPD patients, which include cigarette smoked induced COPD, as well as the genetic variant of COPD resulting from alpha-1-antitrypsin deficient (AATD) individuals. Further insight will be glean from data obtain in AATD individuals that have developed COPD and AATD who have not develop COPD. The focus of the presentation will address whether abnormalities in the muscle angiogenic response to exercise are a consequence of systemic inflammation stemming from lung damage, or if these are based on O2 transport limitation, and what effect exercise training and/or physical fitness exhibits in this context. The central premise of the talk is based on observation that deregulation of several key angiogenic regulators is responsible for many of the structural and functional alterations found in skeletal muscle of patients with COPD, especially those with a cachectic phenotype, and that these abnormalities produce a phenotype that is unable to protect skeletal muscle from chronic inflammation. Exercise training can help to restore and/or minimize the abnormal angio-metabo signal axis in muscle, thereby increasing muscle capillarity and improving muscle function.

Biography:

Dr. D. Behera is the Senior Professor & Head,Dept. of Pulmonary Medicine,(WHO Collaborating Centre for Research & Capacity Building in Chronic Respiratory Diseases)Postgraduate Institute of Medical Education & Research, Chandigarh - 160012 (INDIA). He has the experience as a teacher, researcher and clinician over 35 years. He has 425 scientific publications and is the author of two text books on Pulmonary Medicine and Respiratory Diseases. Has also has authored books on bronchial asthma and lung cancer, and tuberculosis. He has many National and International Scientific awards to his credit. He has been A Fellow and Member of many International and National scientific bodies. He has been the President and office bearer of a couple of scientific bodies and is associated with a number of scientific journals.

Abstract:

More than 400 million people worldwide suffer from COPD. The estimated burden in India is about 15 million cases (~9 million males and ~6 million females)[INSEARCH study IJTLD 2012]. Besides smoking air pollution, particularly indoor air pollution is one important risk factor for COPD in iNdia and other developing countries. Women who cook with solid fuels have increased respiratory symptoms including chronic cough and phlegm. Decrease in lung function and COPD is present in 7 % of biomass using women who never smoked in their life. In contrast, only 1.8% of never-smoking LPG users had COPD. A number of studies have showed that in India, the incidence of chronic cor pulmonale is similar in men and women despite the fact that 75% of the men and only 10% women are smokers. In women, chronic cor pulmonale was found to be more common in younger age. This has been attributed to domestic air pollution as a result of the burning of solid biomass fuels leading to chronic bronchitis and emphysema which result in chronic cor pulmonale. A number of studies by us (Behera et al) have shown that exposure to biomass fuel produces various respiratory symptoms including COPD, impaired lung functions (Lung function, particularly FVC, is affected by indoor air pollution due to domestic cooking more so with biomass fuel), high levels of blood carboxyhemoglobin levels, and respiratory symptoms in children (Mixed fuel and kerosene fuel had worst effects on respiratory system in children whose households used these fuels).

Biography:

MH Boskabady Finished MD in Mashhad University of Medical in 1981 and PhD in London University, Charring Cross and Westminister Medical School in 1991. He Published more than 170 papers in English language and more than 10 in Farsi and Presented more than 240 abstract in National and International Congresses He Received several national research awards His main intersts are; Asthma, COPD, Airway Pharmacology, Chemical warfare and Respiratory Diseases, Inhaled toxicology, Smoking

Abstract:

Increased airway responsiveness to different stimuli is the main characteristic feature of asthma. However, airway hyper responsiveness is reported in COPD patients and smokers. In a series of studies airway responsiveness to various pharmacological agonists and antagonists were examined. In animal studies, increased tracheal responsiveness to histamine as histamine concentration caused 50% of maximum response (EC50) and hisataminie (H1) receptor blockade by chlorpheniramine as shift in concentration response to histamine (CR-1) in guinea pig model of COPD by their exposing to cigarette smoke as well as in sensitized animals were shown. Tracheal responsiveness to both isoprenaline and beta-adrenoreceptor blockade by propranolol in cigarette smoke exposed and sensitized guinea pigs and a close correlation in responsiveness to isoprenaline and propranolol between COPD and asthmatic animals were demonstrated. Increased tracheal responsiveness to methacoline and muscarinic receptor blockade by atropine in an animal model of COPD was also reported. Tracheal hyper responsiveness to methacholine in sulfur mustard exposed guinea pigs was also shown. In human studies, increased airway responsiveness to methacholine and salbutamol and the relationship between the two was demonstrated in smokers. Airway hyper responsiveness to salbutamol in COPD patients was also shown. Airway hyper responsiveness to methacholine as well as to salbutamol in chemical war victims were also shown in two studies. Increased airway responsiveness to different pharmacological agonists and antagonists in exposed animal to cigarette smoke and sulfur mustard, smokers, COPD patients and chemical war victims were documented.

Biography:

Monika Szturmowicz is a Professor of Medicine afficiated at I Department of Lung Diseases, National Tuberculosis and Lung Diseases Research Institute, Warsaw Poland. In 2010—2014 she was the Editor-in-Chief of Polish Pneumonology and Allergology, the peer-reviewed official Journal of the Polish Respiratory Society. Dr. Szturmowicz is an active member of ACCP (FCCP since 2003), ERS and IASLC, directly involved in the clinical research concerning pulmonary hypertension in lung diseases. She is the author of 99 papers published in peer-reviewed international journals, Hirsh Index -13.

Abstract:

Pulmonary hypertension (PH) defined as mean resting pulmonary artery pressure (mPAP) equal or higher than 25 mmHg ( measured directly), is found in 50% of the patients with end-stage COPD. In most cases mild PH is observed. Nevertheless in 2-7% of patients, severe PH (defined as mPAP>35 mmHg or CI<2.5 l/min) develops. What’s most interesting, severe PH in COPD is not always combined with end-stage disease. The differential diagnosis on such occassion should exclude the influence of other comorbidities on PH ( left heart disease, venous thromboembolism and sleep disordered breathing). Latest publications indicate that clinical phenotype of severe PH in COPD is characterised by: profound hypoxemia, hypocapnia and very low diffusion capacity of the lung for carbon dioxide (DLCO), despite mild or moderate aiway obstruction. It is still not known, if such phenotype is combined with certain genetic rearangements. According to latest PH guidelines, optimal COPD treatment combined with long therm oxygen therapy in the patients with PaO2 below 60 mmHg, is indicated in PH-COPD. Nevertheless in the patients with servere PH, the referral to an expert center is advised. Latest results of clinical trials with PH-specific drugs are disappointing. Despite the improvement in pulmonary haemodynamics, no significant changes in exercise capacity or quality of life of the patients are reported. Future research should be directed towards the identification of those PH-COPD patients, in whom maximal exercise capacity is limited by low cardiac output, and not by the exhaused ventilatory reserve.

Biography:

Department of Respiratory Medicine, King George’s Medical University, Lucknow-226003, Uttar Pradesh, India

Abstract:

Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease (COPD). Oxidative stress has been known for having a key role in pathogenesis of many diseases. The aim of this study was to investigate the serum cytokines levels in [Interleukin-1β (IL-1β), Interleukin-6 (IL-6), Tumor necrosis factor-α (TNF-α)] and their correlation with smoking categories, oxidative stress and also the relationship between antioxidant system statuses and lung function in patients with COPD and smokers and non-smokers subjects. Diagnosis was made by spirometry. METHODS: Total 100 newly diagnosed patients from 30-80 years were included in the study. Participants diagnosed as COPD were selected for the systemic serum cytokines levels. 5 ml of venous blood were collected from each patient in a plain vial and centrifuged for 10 minutes at 2655 g at 40 C, serum collected; it was stored at -80° C for further analysis. For oxidative stress 30 subjects with COPD, 30 smokers, and 30 healthy non-smokers participated in this study. The investigation included determination of the lung function and the measurements of total antioxidant capacity, and also erythrocyte glutathione peroxidase, glutathione reductase, superoxide dismutase, and catalase. RESULTS: The results shows that among the smoking categories there was significant difference in the level of TNF-α (p=0.03), IL-6 (p=0.01) and IL-1β (p=0.02) among the different categories of smoking habit. The pos-hoc analysis revealed TNF- α (pg/ml) was significantly (p<0.05) higher among ex-smoker than non-smokers. Erythrocyte glutathione peroxidase and glutathione reductase were not significantly different between the studied groups. Subjects with COPD and smokers had lower catalase and superoxide dismutase activity (P < .001) than the non-smoker group. Levels of antioxidant capacity were significantly lower in subjects with COPD and smokers than in the non-smoker group (P < .001). Regression analysis revealed no correlations between antioxidant status and spirometric data. CONCLUSION: Decreased total antioxidant capacity in plasma of subjects with COPD and smokers suggests an increased oxidative stress in this group. However, no relationship was found between lung function and antioxidant systems status in COPD subjects. Smoking may influence TNF-α mediated systemic inflammation, which, in turn, may account for some of the benefits observed in patients with COPD who stop smoking.

Biography:

MH Boskabady Finished MD in Mashhad University of Medical in 1981 and PhD in London University, Charring Cross and Westminister Medical School in 1991. He Published more than 170 papers in English language and more than 10 in Farsi and Presented more than 240 abstract in National and International Congresses He Received several national research awards His main intersts are; Asthma, COPD, Airway Pharmacology, Chemical warfare and Respiratory Diseases, Inhaled toxicology, Smoking

Abstract:

In a series of studies various possible therapeutic potential of natural product and stem cell for treatment of COPD were examined. The effect of adipose derived stromal cells (ASCs) on tracheal responsiveness, interleukin-8 (IL-8), total and differential white blood cells (WBC) counts in animal model of COPD was shown. The effect of ASCs on lung histopathologic changes and serum level of malondialdehyde (MDA) in COPD animals was also demonstrated in another study. The effect of Zataria multiflora and its constituent, carvacrol on systemic inflammation including serum levels of IL-8 and MDA as well as total and differential white blood cell (WBC) in the blood of guinea pig COPD model was documented in two studies. The preventive effect of Zataria multiflora and carvacrol on thiol groups, IL-8, total and differential WBC broncho-alveolar lavage fluid (BALF), lung pathology and tracheal responsiveness, were also demonstrated. Tracheal responsiveness to both methacholine and ovalbumin reduced in COPD animal model due to Nigella sativa extract and vitamin C treatment. The preventive effect of vitamine E, dexamethazone and the extract of Nigella sativa on tracheal responsiveness and lung inflammation of sulfur mustard exposed animals was studied. Significant improvement in pulmonary function tests and respiratory symptoms in chemical war victims treated with the extract of Nigella sativa for two month was also observed. The results of these studies indicated a promising therapeutic potential for stem cell and natural product in the treatment of COPD which should be clinically evaluated in further

Biography:

Dr. Reddy, currently faculty member in the Division of Human Genetics, Department of Anthropology. His expertise is clinical nutrition, clinical trials and genetic epidemiology. He has published 67 research papers in various journals of repute and completed three ad-hoc projects funded by Government of India and one clinical trial is under progress.

Abstract:

The development of chronic obstructive pulmonary disease, upon exposure to tobacco smoke, is the cumulative effect of defects in several genes. With the aim of understanding the genetic structure that is characteristic of our patient population, we selected forty two single nucleotide polymorphisms of twenty genes based on previous studies and genotyped a total of 382 samples, which included 236 patients and 146 controls using Sequenom Mass ARRAY system. Allele frequencies of rs2276109 (MMP12) and rs1800925 (IL13) differed significantly between patients and controls (p = 0.013 and 0.044 respectively). Genotype analysis showed association of rs2276109 (MMP12) under additive and dominant models (p = 0.017, p = 0.012 respectively), rs1800925 (IL13) under additive model (p = 0.047) and under recessive model, rs1695 (GSTP1; p = 0.034), rs729631, rs975278, rs7583463 (SERPINE2; p = 0.024, 0.024 and 0.012 respectively), rs2568494, rs10851906 (IREB2; p = 0.026 and 0.041 respectively) and rs7671167 (FAM13A; p = 0.029). The minor alleles of rs1695 (G), rs7671167 (T), rs729631 (G), rs975278 (A) and rs7583463 (A) showed significant negative association whereas those of rs2276109 (G), rs2568494 (A), rs10851906 (G) and rs1800469 (T; TGF-b) showed significant positive association with lung function under different genetic models. Haplotypes carrying A allele of rs2276109, G allele of rs1695 showed negative correlation with lung function. Haplotypes carrying major alleles of rs7671167 (C) of FAM13A and rs729631 (C), rs975278 (G), rs7583463 (C) of SERPINE2 had protective effect on lung function. Haplotypes of IREB2 carrying major alleles of rs2568494 (G), rs2656069 (A), rs10851906 (A), rs965604 (C) and minor alleles of rs1964678 (T), rs12593229 (T) showed negative correlation with lung function. In conclusion, our study replicated the results of most of the previous studies. However, the positive correlation between the minor alleles of rs2568494 (A) and rs10851906 (G) of IREB2 and lung function needs further investigation.