2^nd International Conference on Respiratory and Pulmonary Medicine October 17-18, 2016 Chicago,Illinois, USA

Biography:

Dr. Philbin completed his PharmD from Nova Southeastern University and both MSc in Pharmacoeconomics and MBA at the University of Florida. He is a Senior Health Economics and Outcomes Research Liaison at Mallinckrodt Pharmaceuticals, where he specializes in the generation and dissemination of value evidence for innovative specialty pharmaceuticals to optimize population-health, payer and healthcare systems decision making.

Abstract:

The objective of this study was to provide a contemporary estimate of the healthcare resource use (HCRU) and costs borne by commercial payers for sarcoidosis patients in the US. Patients (aged 18-64 years) with a first diagnosis of sarcoidosis between 1/1/1998 and 3/31/2015 were selected from a large, de-identified, privately-insured administrative claims database (OptumHealth Reporting and Insights). Costs (inpatient, outpatient/physician office, emergency department/other, pharmacy) were assessed from the payer perspective over 12 months post-diagnosis. To assess incremental HCRU and costs, sarcoidosis patients were matched (1:1) to non-sarcoidosis controls based on Charlson Comorbidity Index and propensity-score calculated by logistic regression with covariates for demographic characteristics and baseline HCRU and costs. A total of 7,119 sarcoidosis patients who met the sample selection criteria were matched with a control. Overall, commercial payers incurred $19,714 in total annual healthcare costs per sarcoidosis patient. The principle drivers of costs were outpatient visits ($9,050, 46%) and inpatient admissions ($6,398, 32%). Relative to controls, sarcoidosis patients had, on average, $5,190 (36%) higher overall total healthcare costs ($19,714 vs. $14,524; p<0.001). Using US  population and prevalence statistics from published literature, these results suggest that sarcoidosis patients impose a total direct medical cost burden of approximately $1.3 to $8.7 billion (in 2015$) to commercial payers – comparable to estimates of other autoimmune diseases such as rheumatoid arthritis, psoriaisis, or ulcerative colitis. These estimates, moreover, likely understate the actual burden because they excluded out-of-pocket costs, supplemental insurer payments, costs associated with premature mortality, reduced quality of life, and/or informal caregiving.

Biography:

Flavio Fontes Pirozzi; endocrinologist of Brazilian Society of Endocrinology and Metabolism; master degree in Genetic by State of Sao Paulo University (UNESP/IBILCE - Sao Jose do Rio Preto/Brazil) and professor on Endocrinology Department of Unilago Medical School (Sao Jose do Rio Preto/Brazil). Speaker on World Congress of Diabetes 2015 (Kaohsiung/Taiwan).
 

Abstract:

Pulmonary Arterial Hypertension (PAH) is as unknown complication of metabolic syndrome (MS) and more than half of patients with idiophatic-PAH have criteria for MS. There are several mechanisms for the development of PAH in obeses and diabetic patients such as inflammation, angiogenesis, hypoxia, slepp apnea, insulin resistance, cardiac disorders,... . Theres is a important relationship between glycemic control and PAH; patients with HbA1c>5,7% presented a lower risk to survival and worst pulmonary capacity. When we serach about "weight loss and PAH" in PubMed we find few studies about this (only cases reports and after bariatric surgery). Bariatric surgery promotes weight loss but also increases GLP1 (glucagon like-peptide 1) levels and GLP1 has a unknown pleiotropic effect in the lung, it promotes pulmonary artery vasorelaxation. Our group showed that, using a DDP4 inhibitor (vildagliptin 50mg 2x/day - drug which increases native GLP1 without weight loss) in diabetic patients with obesity and  (idiophatic and symptomatic) PAHpromotes important improvement of PAH and dreacreses of systolic pressure of right ventricle in echocardiogram. Maybe increasing GLP1 is better than weight loss in patients with MS and PAH.

Biography:

Toidi Adekambi has completed his PhD at the age of 32 years from Marseille University School of Medicine and postdoctoral studies from CDC and Emory University. He is research associate at Emory Vaccine Center. He discovered 6 new species of mycobacteria in different clinical context, including Mycobacterium bolletii and Mycobacterium massiliense that pose serious challenges for treatment because they are resistant to most anti-mycobacterial drugs. He has published more than 30 papers in reputed journals with 1500+ citations and is serving as an editorial board member of Dataset Papers in Science.

Abstract:

The identification and treatment of individuals with tuberculosis (TB) is a global public health priority. Accurate diagnosis of pulmonary active TB (ATB) disease remains challenging and relies on extensive medical evaluation and detection of Mycobacterium tuberculosis (Mtb) in the patient's sputum. Further, the response to treatment is monitored by sputum culture conversion, which takes several weeks for results. Here, we sought to identify blood-based host biomarkers associated with ATB and hypothesized that immune activation markers on Mtb-specific CD4+ T cells would be associated with Mtb load in vivo and could thus provide a gauge of Mtb infection.

Using polychromatic flow cytometry, we evaluated the expression of immune activation markers on Mtb-specific CD4+ T cells from individuals with asymptomatic latent Mtb infection (LTBI) and ATB as well as from ATB patients undergoing anti-TB treatment from US (test cohort) and South Africa (validation cohort).

Frequencies of Mtb-specific IFN-γ+CD4+ T cells that expressed immune activation markers CD38 and HLA-DR as well as intracellular proliferation marker Ki-67 were substantially higher in subjects with ATB compared with those with LTBI. These markers accurately classified ATB and LTBI status, with cutoff values of 18%, 60%, and 5% for CD38+IFN-γ+, HLA-DR+IFN-γ+, and Ki-67+IFN-γ+, respectively, with 100% specificity and greater than 96% sensitivity. These markers also distinguished individuals with untreated ATB from those who had successfully completed anti-TB treatment and correlated with decreasing mycobacterial loads during treatment.

We have identified host blood-based biomarkers on Mtb-specific CD4+ T cells that discriminate between ATB and LTBI and provide a set of tools for monitoring treatment response and cure.

Biography:

Samuel Dinkneh has completed his degree in Nursing from Gondar University. He is an Emergency Ward Head at St Peter TB Specialized Hospital, Ethiopia. He has conducted two researches and one is on the way for publication.

Abstract:

Tuberculosis (TB) is an infectious disease caused by the bacterium Mycobacterium tuberculosis. Tuberculosis generally affects the lung, but can also affect other parts of the body. The classic symptoms of active TB are chronic cough, sputum, fever, night sweat and weight loss. Tuberculosis spreads through the air from people who have active TB cough, when they spit, speak or sneeze. People with latent TB do not transmit the disease, active Tb occurs more often in people with HIV and those who smoke. Prevention of TB involves screening those at high risk, early detection and treatment of cases and vaccination with BCG. Those who are high risk include household, workplace and social contact of people with active TB. Treatment requires the use of multiple antibiotics over a long period of time. One third of world population thought to be infected with TB. New infection occurs in about 1% of the total population each year. In 2015 there were 9 million TB cases which resulted in 1.3 million deaths, more than 95% occurred in developing country. More than 80% of the cases TB affect the lung but some time it spread and affects other organs like the central nervous system, the lymphatic system, the genitourinary system, joints and bone, etc. Diagnosis of TB is culture, chest X-ray, sigh and symptom. The prevention is using BCG vaccine giving to infants. The most serious TB problem is drug resistance TB (MDR and XDR) occur due to inadequate treatment or not taking prescribed drug or drop out and need longer treatment and require more expensive drug.

Biography:

Toidi Adekambi has completed his PhD at the age of 32 years from Marseille University School of Medicine and postdoctoral studies from CDC and Emory University. He is research associate at Emory Vaccine Center. He discovered 6 new species of mycobacteria in different clinical context, including Mycobacterium bolletii and Mycobacterium massiliense that pose serious challenges for treatment because they are resistant to most anti-mycobacterial drugs. He has published more than 30 papers in reputed journals with 1500+ citations and is serving as an editorial board member of Dataset Papers in Science.

Abstract:

The identification and treatment of individuals with tuberculosis (TB) is a global public health priority. Accurate diagnosis of pulmonary active TB (ATB) disease remains challenging and relies on extensive medical evaluation and detection of Mycobacterium tuberculosis (Mtb) in the patient's sputum. Further, the response to treatment is monitored by sputum culture conversion, which takes several weeks for results. Here, we sought to identify blood-based host biomarkers associated with ATB and hypothesized that immune activation markers on Mtb-specific CD4+ T cells would be associated with Mtb load in vivo and could thus provide a gauge of Mtb infection.

Using polychromatic flow cytometry, we evaluated the expression of immune activation markers on Mtb-specific CD4+ T cells from individuals with asymptomatic latent Mtb infection (LTBI) and ATB as well as from ATB patients undergoing anti-TB treatment from US (test cohort) and South Africa (validation cohort).

Frequencies of Mtb-specific IFN-γ+CD4+ T cells that expressed immune activation markers CD38 and HLA-DR as well as intracellular proliferation marker Ki-67 were substantially higher in subjects with ATB compared with those with LTBI. These markers accurately classified ATB and LTBI status, with cutoff values of 18%, 60%, and 5% for CD38+IFN-γ+, HLA-DR+IFN-γ+, and Ki-67+IFN-γ+, respectively, with 100% specificity and greater than 96% sensitivity. These markers also distinguished individuals with untreated ATB from those who had successfully completed anti-TB treatment and correlated with decreasing mycobacterial loads during treatment.

We have identified host blood-based biomarkers on Mtb-specific CD4+ T cells that discriminate between ATB and LTBI and provide a set of tools for monitoring treatment response and cure.

Biography:

Samuel Dinkneh has completed his Degree in Nursing at age of 22 years from Gondar University. He is an Emergency Ward Head at St Peter TB Specialized Hospital. He conducted two researches and one is on the way for publication.

Abstract:

Tuberculosis (TB) is an infectious disease caused by the bacterium mycobacterium tuberculosis. Tuberculosis generally affects the lung, but can also affects other parts of the body. The classic symptoms of active TB are chronic cough, sputum, fever, night sweat, weight loss. Tuberculosis spread through the air when people who have active TB cough, spit, speak or sneeze. People with latent TB do not5 transmit the disease, active Tb occurs more often in people with HIV and those who smokes. Prevention of TB involves screening those at high risk, early detection and treatment of cases and vaccination with BCG. Those who are high risk include household, workplace, and social contact of people with active TB. Treatment requires the use of multiple antibiotics over a long period of time. One third of world population thought to be infected with TB. New infection occur in about 1% of the total population each year. In 2015 there were 9million TB cases which resulted in 1.3million deaths, more than 95% occurred in developing country. More than 80% of the cases TB affects the lung but some time it spread and affect other organs like the central nervous system, the lymphatic system, the genitourinary system, joints and bone, etc… Diagnosis of TB are culture, chest X-ray, sigh and symptom. The prevention is using BCG vaccine giving to infants. The most serious TB problem is drug resistance TB (MDR and XDR) occur due to inadequate treatment or not taking prescribed drug or drop out and need longer treatment and require more expensive drug.

Biography:

Collins kirui has completed master of science in public health. He is currently working in Kapkatet county referral hospital

Abstract:

Prospectivestudy was conducted in Tengecha boy’s high school for active case finding by the hospital team. This was triggered by smear positive students screened and treated for TB in the hospital. The study was conducted in the school from July, 2014 to November 2014.Screening was conducted to all student and teachers, those found with signs and symptoms; sputum smears was done. Those found to be smear positive were initiated on anti-TB drugs and were followed up in the hospital. Health education was conducted weekly by the hospital staff in the school during the study period.

Biography:

Weizhong Jin has completed MD Nanjing Medical University.He is currently working in the Department of Pulmonary Disease, Hangzhou First People’s Hospital, Zhejiang Province, China

Abstract:

Endobronchial ultrasound (EBUS) can be of value in prompt diagnosis of the disorder.

Methods and results

Based on the EBUS, we currently have made diagnosis of Dieulafoy’s disease of bronchi in three patients with unexplained hemoptysis. Of which these patients, one was a 44-year-old male suffered from recurrent hemoptysis. Computed tomography of bronchial artery showed an absence of left upper pulmonary artery and patchy shadows in the left lower basal segmental lobe on CT scan. Flexible bronchoscopy revealed an elevated lesion in the left lower bronchus. The radial probe endobronchial ultrasound showed a circular anechoic area within the submucosa, circumscribed with a hyperechoic margin highly suggestive of vascular structures (figure 1). Of note, the anechoic area beat rhythmically in keeping with the pulse. The DSA revealed a left tortuous bronchial artery. The diagnosis was established. After transcatheter

embolization of the hypertrophic bronchial artery, DSA revealed complete disappearance of the

abnormal bronchial artery.

Conclusions

EBUS is competent to the diagnosis of Dieulafoy's disease of bronchi.

Biography:

Abstract:

The aim of this study was to determine the role of protein deacetylase SIRT1, one of the nicotinamide adenine dinucleotide(NAD+)-dependent intracellular silent information regulators, in lipopolysaccharide (LPS)-induced lung endothelial barrier dysfunction and lung injury in vivo.

Methods

The cultured human pulmonary endothelial cells (HPECs) were exposed to LPS and C57BL/6 mice administered intratracheally, and were treated with SIRT1 activator SRT1720 or inhibitor EX527 after LPS exposure, respectively. The endothelial permeability was measured in transwell by use of FITC-dextra. Lung injury was studied by measuring vascular permeability, histopathological examination, nature of infiltrating cells, inflammatory cytokine induction in the broncho-alveolar fluid.

Results

In cultured HPECs, LPS increased endothelial permeability in parallel with a decrease in SIRT1 expression. Consistent with this observation, SIRT1 activation with the potent sirt1 activator SRT1720 attenuated LPS-induced endothelial hyper-permeability in vitro, but increased by the SIRT1 inhibitor EX527. Intra-tracheal administration of LPS (5 mg/kg) in mice reduced sirts expression in lung tissue extracts, increased protein content and cell count in bronchial alveolar lavage fluid, and increased Evans Blue dye infiltration into the lung. Pretreatment with SRT1720 reduced the lung injury in LPS-treated WT mice, and EX527 accentuated the lung injury.

Conclusions

We concluded that SIRT1 play a role in LPS-induced endothelial barrier dysfunction and that its activation attenuated the endothelial barrier dysfunction and lung injury.

Biography:

Flavio Fontes Pirozzi; endocrinologist of Brazilian Society of Endocrinology and Metabolism; master degree in Genetic by State of Sao Paulo University (UNESP/IBILCE - Sao Jose do Rio Preto/Brazil) and professor on Endocrinology Department of Unilago Medical School (Sao Jose do Rio Preto/Brazil). Speaker on World Congress of Diabetes 2015 (Kaohsiung/Taiwan).
 

Abstract:

Pulmonary Arterial Hypertension (PAH) is as unknown complication of metabolic syndrome (MS) and more than half of patients with idiophatic-PAH have criteria for MS. There are several mechanisms for the development of PAH in obeses and diabetic patients such as inflammation, angiogenesis, hypoxia, slepp apnea, insulin resistance, cardiac disorders,... . Theres is a important relationship between glycemic control and PAH; patients with HbA1c>5,7% presented a lower risk to survival and worst pulmonary capacity. When we serach about "weight loss and PAH" in PubMed we find few studies about this (only cases reports and after bariatric surgery). Bariatric surgery promotes weight loss but also increases GLP1 (glucagon like-peptide 1) levels and GLP1 has a unknown pleiotropic effect in the lung, it promotes pulmonary artery vasorelaxation. Our group showed that, using a DDP4 inhibitor (vildagliptin 50mg 2x/day - drug which increases native GLP1 without weight loss) in diabetic patients with obesity and  (idiophatic and symptomatic) PAHpromotes important improvement of PAH and dreacreses of systolic pressure of right ventricle in echocardiogram. Maybe increasing GLP1 is better than weight loss in patients with MS and PAH.

Biography:

Dr. Weizhong Jin got his degree from FudanUniversity in 2012 and has been working as a internal resident in Hangzhou First People's Hospital, China since graduation.

Abstract:

Objectives: We conducted a meta-analysis to assess the association of pre-hospital APT in adults with ARDS.

Data Sources: We searched the PubMed, Web of Science, EMBASE, Cochrane Central Register of Controlled Trials, and Cochrane Database of Systematic Reviews.

Study Eligibility Criteria, Participants & Interventions: All human studies published in full text, abstract, or poster form, were eligible for inclusion. We included cohort, case control trials or RCT. We included trials comparing the incidence of ARDS in patients with pre-hospital anti-platelet agents or without. The date of the most recent search was on October 2015.

Study Appraisal and Synthesis Methods: Two authors independently assessed study risk of bias and extracted data. The primary outcome was ARDS morbidity, while secondary outcome was ICU or hospital mortality. We identified 7 studies meeting the eligibility criteria.

Results: Meta-analysis of 7 studies of 30291 patients showed that pre-hospital APT was associated with a decrease in the odds of ARDS compared with those without APT (OR 0.68, 95% CI 0.56 - 0.83 and p=0.0001), but not the hospital mortality and ICU mortality.

Conclusion: The findings suggested that pre-hospital APT is associated with the lower rate of ARDS, but not mortality in patients at risk.

Biography:

Dr. Magitta received medical training from the University of Dar es Salaam in Tanzania in 2001. He obtained a PhD in Medicine from the University of Bergen in Norway in 2010, where he studied the genetics of Autoimmune Polyendocrine Syndrome Type 1. He is currently a Senior Research Scientist at Ifakara Health Institute (IHI) and a Lecturer of Biochemistry at the School of Health Sciences, University of Dar es Salaam in Tanzania. His research interest is on chronic non-communicable diseases of public health importance in Africa.

Abstract:

Chronic Obstructive Pulmonary Disease (COPD) is an important contributor to mortality and morbidity in developed countries but there is limited data from Africa. Apart from tobacco smoking, household air pollution is a potential risk factor for COPD, but its contribution has not been adequately studied in Africa. We aimed to provide prevalence estimates of COPD in Tanzania and further identify factors associated with risk and disease exacerbations.  In this cross-sectional, descriptive survey in the rural setting of Maswa district in Tanzania, adults aged ≥ 35 years were randomly selected from 150 households across 6 villages from 2 wards. We collected data on respiratory symptoms, occupation and exposure to biomass using the BOLD questionnaire. Spirometry was performed using a 3L-syringe daily-calibrated NDD EasyOne^TM spirometer with COPD defined based on post-bronchodilator FEV₁/FVC<70%. Indoor carbon monoxide pollution levels were measured using the Langan T15x samplers. The pre-determined risk factors were tested for associations. A total of 869 participants (49.1% women) with a mean age of 51.8± 10.58 years completed the questionnaires. Of these 57% completed post-bronchodilator spirometry, with over 98% good quality spirometry and 25% were smokers. The prevalence of COPD was estimated at 17.5% ⦋21.7% in men, 12.9% in women⦌. COPD was associated with level of education (p<0.0001) and cigarette smoking (p<0.002). The severity of COPD was significantly associated with history of cough, phlegm production and wheezing (p<0.02, p<0.03 and p<0.002). Half of COPD patients presented with cough and 85% had mild-to-moderate airway limitation. Furthermore, over 35% of women had dyspnoea and increased exacerbations while men had poor FEV₁ and FVC. Pulmonary tuberculosis was reported in about 10% of COPD patients. Intermittent aminophylline was the most commonly prescribed drug for COPD.

Biography:

Dr. Weizhong Jin got his degree from FudanUniversity in 2012 and has been working as a internal resident in Hangzhou First People's Hospital, China since graduation.

Abstract:

Introduction: It is not completely clear about the mechanism of the endothelial hyper-permeability in acute lung injury.

Objectives: The aim of this study was to determine the role of protein deacetylase SIRT1, one of the nicotinamide adenine dinucleotide (NAD+)-dependent intracellular silent information regulators, in lipopolysaccharide (LPS) induced lung endothelial barrier dysfunction and lung injury in vivo.

Methods: The cultured human pulmonary endothelial cells (HPECs) were exposed to LPS and C57BL/6 mice administered intratracheally, and were treated with SIRT1 activator SRT1720 or inhibitor EX527 after LPS exposure, respectively. The endothelial permeability was measured in transwell with the use of FITC-dextran. Lung injury was studied by measuring vascular permeability, histopathological examination, nature of infiltrating cells and inflammatory cytokine induction in the bronchoalveolar fluid.

Results: In cultured HPECs, LPS increased endothelial permeability in parallel with a decrease in SIRT1 expression. Consistent with this observation, SIRT1 activation with the potent sirt1 activator SRT1720 attenuated LPS-induced endothelial hyper-permeability in vitro, but increased by the SIRT1 inhibitor EX527. Intra-tracheal administration of LPS (5 mg/kg) in mice reduced SIRTs expression in lung tissue extracts, increased protein content and cell count in bronchial alveolar lavage fluid, and increased Evans blue dye infiltration into the lung. Pretreatment with SRT1720 reduced the lung injury in LPS-treated WT mice, and EX527 accentuated the lung injury.

Conclusions: We concluded that, SIRT1 plays a role in LPS-induced endothelial barrier dysfunction and that its activation attenuated the endothelial barrier dysfunction and lung injury.

Biography:

Dr. Weizhong Jin got his degree from FudanUniversity in 2012 and has been working as a internal resident in Hangzhou First People's Hospital, China since graduation.

Abstract:

Based on the EBUS, we currently have made diagnosis of Dieulafoy’s disease of bronchi in three patients with unexplained hemoptysis. Of which, in these patients, one was a 44-year-old male suffered from recurrent hemoptysis. Computed tomography of bronchial artery showed an absence of left upper pulmonary artery and patchy shadows in the left lower basal segmental lobe on CT scan. Flexible bronchoscopy revealed an elevated lesion in the left lower bronchus. The radial probe endobronchial ultrasound showed a circular anechoic area within the sub-mucosa, circumscribed with a hyperechoic margin highly suggestive of vascular structures. Of note, the anechoic area beat rhythmically in keeping with the pulse. The DSA revealed a left tortuous bronchial artery. The diagnosis was established. After transcatheter embolization of the hypertrophic bronchial artery, DSA revealed complete disappearance of the abnormal bronchial artery.

Biography:

Dr. Sonia Shahid is a final year M.B.B.S student of Karachi Medical and Dental College, Karachi Pakistan. She has been a part of several national and international researches and many are on-going. She has attended several national and international seminars and conferences. She has good knowledge of clinical practices and protocols in variety of settings. Sonia is an inquisitive student with a passion for education as a power for change and improvement in the healthcare field of her country and is very ambitious in pursuing her career.

Abstract:

OBJECTIVE: Objective of this study was to analyse the coexistence of cystic fibrosis, with

positive sweat chloride test in children, with celiac disease.

INTRODUCTION: Cystic fibrosis is an inherited disorder that causes severe damage to the lungs and digestive system. Cystic fibrosis affects the cells that produce mucus, sweat and

digestive juices. These secreted fluids are normally thin and slippery. But in people with cystic fibrosis, a defective gene causes the secretions to become thick and sticky. Instead of acting as a lubricant, the secretions plug up tubes, ducts and passageways, especially in the lungs and pancreas. Cystic fibrosis signs and symptoms vary, depending on the severity of the disease.

INCLUSION CRITERIA: Paediatric patients of age ≤ 7 years regardless of gender presenting to paediatric department of tertiary care hospitals of Karachi with principal complain of chronic productive cough, recurrent wheezing and dyspnoea on exertion were included.

METHODOLOGY: This cross‐sectional study was conducted from July 2014 ‐ July 2016.

Pediatric patients under 7 years of age were recruited in this study. A history and examination

form designed from an application “Forms”,particularly for the study. Children were tested for tissue transglutaminase (tTG) to confirm the disease and also for sweat chloride to access the relation between two diseases. For data analysis SPSS 16.0 software was used.

RESULTS: During 2 years time, total 103 patients were inspected out of which 42.28% were

male and 57.72% were females. The mean age was 2.7(+) 2.38 months. The incidence of cysticfibrosis were significantly more frequent with celiac disease than in the general population.Positive IgA tTG was documented in 64 (62.14 %) of CF patients.

CONCLUSION: Frequency of cystic fibrosis is higher among celiac disease patients. It suggests the need for targeted screening for cystic fibrosis in children with celiac disease. Many patients with celiac disease has a positive sweat chloride test. However, our results suggests that cystic fibrosis coexists with celiac disease in children.

Biography:

Feng has completed her PhD from Purdue University. Currently, she is a tenure-track Assistant Professor at the Department of Kinesiology at California State University-Chico. She has published 10 papers in reputed journals and has been serving in review board member of reputed journal, Frontiers in Physiology.            
 

Abstract:

Chronic obstructive pulmonary disease (COPD) is one of the leading causes of death in the United States. Although the exact pathophysiological mechanism of COPD is not clear, the increased reactive oxygen species (ROS) play important role in the pathogenesis of COPD. Numerous studies have shown that cigarette smoking is the most significant risk factor to induce COPD. However, early smoking cessation does not effectively alleviate the symptoms of COPD. Impaired immune function activated via long-term exposure to cigarette smoke elicits detrimental effect on the lungs. An extensive literature research demonstrated the strong relationship among chronic tobacco exposure, oxidative stress, and immune response in COPD. We aim to develop potential therapeutic approaches targeting restoring immune homeostasis and host defenses via regulating the disrupted balance of oxidant production and antioxidant defense. The combination of pharmacological therapy and non-pharmacological approaches are more effective in halting COPD exacerbation. In particular, development of new drugs with high selectivity and bioavailability targeting epigenetic regulation of redox status and inflammatory response at the different stages of COPD will be the future challenge. Moreover, moderate intensity structured exercise not only reduces the risk of the development of COPD but also improves respiratory muscle function in COPD patients.

Biography:

Li Zuo obtained his PhD at Ohio State University (OSU). Currently, he is an Assistant Professor and  Director of the Molecular Physiology and Rehabilitation Research Lab at OSU Medical center. He authored and editted over 140 original papers, abstracts, book chapters, review articles and edited publications. He is serving as associate editor for Frontiers in Physiology (the 2016 #1 most cited open-access journal in Physiology with an impact factor of 4.031). He also earned recognition as a fellow by American College of Sports Medicine (ACSM) in 2015 and won S&R Foundation Ryuji Ueno Award, the largest American Physiological Society (APS) award in 2016.

Abstract:

Hypoxia is a major factor contributed to respiratory muscle dysfunction in chronic obstructive pulmonary diseases (COPD). Recently, hypoxic preconditioning (HPC, muscle treatment with alternative low and high oxygen) was proposed as a novel strategy that can protect diaphragm against hypoxia-induced muscle injuries; yet its underlying mechanism remains elusive in COPD. In this study, we tested the hypothesis that reactive oxygen species (ROS) play a signaling role in HPC protective effects on COPD diaphragm. C57BL6 mice were smoked for three consecutive months to develop COPD symptoms. When smoking was ceased, mice diaphragms were isolated and mounted in a contractile chamber. Diaphragm muscle strips were either treated (n = 6) or non-treated (n = 10) with HPC or exposed to an antioxidant combination of Tiron and N-acetyl cysteine (NAC, 1mM each, n = 7) prior to HPC, followed by 30-min hypoxia. Muscles were electrically stimulated for 5 min during hypoxia. Contraction force at the end of 5-min contraction was normalized by baseline force as an indicator of muscle function. Data were analyzed using multi-way ANOVA, expressed as means ± SE. The results demonstrate that HPC significantly enhanced diaphragm function during hypoxia (29±2.8% for HPC vs. 6±1.3 for control, p < 0.05); while elimination of muscular ROS abolished such protective effects (29±2.8% for HPC vs. 8±3.1% for Tiron+NAC+HPC, p < 0.05). These data collectively suggest that HPC may protect diaphragm against hypoxia-induced muscle dysfunction in COPD via ROS-involved pathways.  

Biography:

Zewen Liu is currently a Postdoctoral Reseacher at The Ohio State University Medical Center and an Associate Chief Physician, Associate Director of Medical Affiars from Ezhou Central Hospital of Wuhan University. He has published more than 15 papers in reputed journals and has been serving as an review board member of repute.    

Abstract:

Asthma, characterized by reversible airflow obstruction and airway hyper-reactivity associated with chronic inflammation, are often observed in younger populations. Although current research primarily focuses on childhood asthma, studies have shown that the mortality rate of asthma is higher in the elderly compared to younger populations due to age-related immunosenescence, underdiagnosis, and inadequate treatment. Asthma that is developed later in life, termed non-atopic asthma, is related to elevated levels of neutrophils in serum and sputum and Th1-type inflammatory responses. However, the pathophysiological and redox mechanisms relating to asthma have not been fully elucidated in the seniors. In addition, few studies have been focused on the aging effect on the progression of asthma. Reactive oxygen species (ROS) have been shown to be involved in inflammatory reactions and the immune response  likely due to the immunosenescence in the elderly. The major challenge is to develop an effective therapeutic strategy against asthma in the older populations, as misdiagnoses of such disease to COPD or congestive heart failure can lead to the more serious consequence. Other reactive species such as nitric oxide (·NO) has also been shown to be associated with asthma via nitrosative stress exerted on the airway. Considering the critical roles of ROS in asthma progression, in clinical settings, interplay effects between inflammatory factors, ROS and ·NO should be intensively explored. Particularly, it is imperative to establish a consistent guideline to address the  increasing asthma incidences in elderly population.   

Biography:

Lung cancer is the leading cause of cancer death and radiation is the standard therapy for patients with unresectable disease. Intensity-modulated proton therapy (IMPT), the next evolutionary step in radiotherapy, has the extraordinary capability to precisely deposit maximum cell killing energy in tumors and minimum exposure to surrounding normal tissues; therefore, IMPT will improve the therapeutic ratio, resulting in fewer adverse effects. However, use of IMPT for lung cancer is hindered by a serious limitation: it is highly sensitive to uncertainties caused by patient setup and range uncertainties, respiratory motion, anatomic changes due to tumor shrinkage and patient weight change. These uncertainties can cause under-treatment of tumors or over-exposure of surrounding normal tissue, resulting in unfavorable clinical consequences. Therefore, it is essential to implement robustness quantification (quantifying the sensitivity of IMPT plans to uncertainties) and robust optimization (delivering precise and predictable IMPT plans to ensure the highest clinical benefit). The root mean square dose volume histograms (RVH) can be used to measure the sensitivity of the dose to uncertainties and the areas under the RVH curve (AUCs) can be used to evaluate plan robustness. Robustly optimized plans have better target coverage, improved dose homogeneity, and lower or equivalent dose to organs at risk (OARs). Additionally, robust optimization provides significantly more robust dose distributions to targets and organs than conventional optimization. Planning directly based on CTV provides better or equivalent OAR sparing. Also 4D robust optimization mitigates the influence of interplay effect than 3D robust optimization in lung cancer.

Abstract:

Wei Liu obtained his PhD at Princeton University. Currently, he is an Associate Professor of Department of Radiation Oncology of Mayo Clinic College of Medicine. He authored 43 (23 are fist-authored) peer-reviewed journal publications, 4 US pending patients, and 1 book chapter. He has served as an Editor/reviewer for many top-ranked international journals. He was a recipient of National Institute of Health (NIH)/National Cancer Institute (NCI) Career Developmental Award (K25) and serve as a NIH/NCI Early Career Reviewer (ECR).