14 results on '"Nathaniel, Marchetti"'
Search Results
2. Clinical Markers Associated With Risk of Suicide or Drug Overdose Among Individuals With Smoking Exposure
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Brigid A. Adviento, Elizabeth A. Regan, Barry J. Make, MeiLan K. Han, Marilyn G. Foreman, Anand S. Iyer, Surya P. Bhatt, Victor Kim, Jessica Bon, Xavier Soler, Gregory L. Kinney, Nicola A. Hanania, Katherine E. Lowe, Kristen E. Holm, Abebaw M. Yohannes, Gen Shinozaki, Karin F. Hoth, Jess G. Fiedorowicz, James D. Crapo, Edwin K. Silverman, Terri H. Beaty, Peter J. Castaldi, Michael H. Cho, Dawn L. DeMeo, Adel El Boueiz, Auyon Ghosh, Lystra P. Hayden, Craig P. Hersh, Jacqueline Hetmanski, Brian D. Hobbs, John E. Hokanson, Wonji Kim, Nan Laird, Christoph Lange, Sharon M. Lutz, Merry-Lynn McDonald, Dmitry Prokopenko, Matthew Moll, Jarrett Morrow, Dandi Qiao, Aabida Saferali, Phuwanat Sakornsakolpat, Emily S. Wan, Jeong Yun, Juan Pablo Centeno, Jean-Paul Charbonnier, Harvey O. Coxson, Craig J. Galban, Eric A. Hoffman, Stephen Humphries, Francine L. Jacobson, Philip F. Judy, Ella A. Kazerooni, Alex Kluiber, David A. Lynch, Pietro Nardelli, John D. Newell, Aleena Notary, Andrea Oh, James C. Ross, Raul San Jose Estepar, Joyce Schroeder, Jered Sieren, Berend C. Stoel, Juerg Tschirren, Edwin Van Beek, Bram van Ginneken, Eva van Rikxoort, Gonzalo Vegas Sanchez-Ferrero, Lucas Veitel, George R. Washko, Carla G. Wilson, Robert Jensen, Matthew Strand, Jim Crooks, Katherine Pratte, Aastha Khatiwada, Erin Austin, Gregory Kinney, Kendra A. Young, Alejandro A. Diaz, Barry Make, Susan Murray, Elizabeth Regan, Russell P. Bowler, Katerina Kechris, Farnoush Banaei-Kashani, Jeffrey L. Curtis, Perry G. Pernicano, Nicola Hanania, Mustafa Atik, Aladin Boriek, Kalpatha Guntupalli, Elizabeth Guy, Amit Parulekar, Craig Hersh, George Washko, R. Graham Barr, John Austin, Belinda D’Souza, Byron Thomashow, Neil MacIntyre, H. Page McAdams, Lacey Washington, Charlene McEvoy, Joseph Tashjian, Robert Wise, Robert Brown, Nadia N. Hansel, Karen Horton, Allison Lambert, Nirupama Putcha, Richard Casaburi, Alessandra Adami, Matthew Budoff, Hans Fischer, Janos Porszasz, Harry Rossiter, William Stringer, Amir Sharafkhaneh, Charlie Lan, Christine Wendt, Brian Bell, Ken M. Kunisaki, Eric L. Flenaugh, Hirut Gebrekristos, Mario Ponce, Silanath Terpenning, Gloria Westney, Russell Bowler, Richard Rosiello, David Pace, Gerard Criner, David Ciccolella, Francis Cordova, Chandra Dass, Gilbert D’Alonzo, Parag Desai, Michael Jacobs, Steven Kelsen, A. James Mamary, Nathaniel Marchetti, Aditi Satti, Kartik Shenoy, Robert M. Steiner, Alex Swift, Irene Swift, Maria Elena Vega-Sanchez, Mark Dransfield, William Bailey, Anand Iyer, Hrudaya Nath, J. Michael Wells, Douglas Conrad, Andrew Yen, Alejandro P. Comellas, John Newell, Brad Thompson, Ella Kazerooni, Wassim Labaki, Craig Galban, Dharshan Vummidi, Joanne Billings, Abbie Begnaud, Tadashi Allen, Frank Sciurba, Divay Chandra, Joel Weissfeld, Antonio Anzueto, Sandra Adams, Diego Maselli-Caceres, Mario E. Ruiz, and Harjinder Singh
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Pulmonary and Respiratory Medicine ,Cardiology and Cardiovascular Medicine ,Critical Care and Intensive Care Medicine - Published
- 2023
3. The Association Between Lung Hyperinflation and Coronary Artery Disease in Smokers
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Divay Chandra, Aman Gupta, Gregory L. Kinney, Carl R. Fuhrman, Joseph K. Leader, Alejandro A. Diaz, Jessica Bon, R. Graham Barr, George Washko, Matthew Budoff, John Hokanson, Frank C. Sciurba, James D. Crapo, Edwin K. Silverman, Barry J. Make, Elizabeth A. Regan, Terri Beaty, Ferdouse Begum, Adel R. Boueiz, Peter J. Castaldi, Michael Cho, Dawn L. DeMeo, Marilyn G. Foreman, Eitan Halper-Stromberg, Lystra P. Hayden, Craig P. Hersh, Jacqueline Hetmanski, Brian D. Hobbs, John E. Hokanson, Nan Laird, Christoph Lange, Sharon M. Lutz, Merry-Lynn McDonald, Margaret M. Parker, Dmitry Prokopenko, Dandi Qiao, Phuwanat Sakornsakolpat, Emily S. Wan, Sungho Won, Mustafa Al Qaisi, Harvey O. Coxson, Teresa Gray, MeiLan K. Han, Eric A. Hoffman, Stephen Humphries, Francine L. Jacobson, Philip F. Judy, Ella A. Kazerooni, Alex Kluiber, David A. Lynch, John D. Newell, James C. Ross, Raul San Jose Estepar, Joyce Schroeder, Jered Sieren, Douglas Stinson, Berend C. Stoel, Juerg Tschirren, Edwin Van Beek, Bram van Ginneken, Eva van Rikxoort, Carla G. Wilson, Robert Jensen, Jim Crooks, Douglas Everett, Camille Moore, null Strand, John Hughes, Gregory Kinney, Katherine Pratte, Kendra A. Young, Surya Bhatt, Carlos Martinez, Susan Murray, Xavier Soler, Farnoush Banaei-Kashani, Russell P. Bowler, Katerina Kechris, Jeffrey L. Curtis, Perry G. Pernicano, Nicola Hanania, Mustafa Atik, Aladin Boriek, Kalpatha Guntupalli, Elizabeth Guy, Amit Parulekar, Craig Hersh, John Austin, Belinda D’Souza, Byron Thomashow, Neil MacIntyre, H. Page McAdams, Lacey Washington, Charlene McEvoy, Joseph Tashjian, Robert Wise, Robert Brown, Nadia N. Hansel, Karen Horton, Allison Lambert, Nirupama Putcha, Richard Casaburi, Alessandra Adami, Hans Fischer, Janos Porszasz, Harry Rossiter, William Stringer, Michael E. DeBakey, Amir Sharafkhaneh, Charlie Lan, Christine Wendt, Brian Bell, Ken M. Kunisaki, Eugene Berkowitz, Gloria Westney, Russell Bowler, Richard Rosiello, David Pace, Gerard Criner, David Ciccolella, Francis Cordova, Chandra Dass, Gilbert D’Alonzo, Parag Desai, Michael Jacobs, Steven Kelsen, Victor Kim, A. James Mamary, Nathaniel Marchetti, Aditi Satti, Kartik Shenoy, Robert M. Steiner, Alex Swift, Irene Swift, Maria Elena Vega-Sanchez, Mark Dransfield, William Bailey, Surya P. Bhatt, Anand Iyer, Hrudaya Nath, J. Michael Wells, Joe Ramsdell, Paul Friedman, Andrew Yen, Alejandro P. Comellas, Karin F. Hoth, John Newell, Brad Thompson, Ella Kazerooni, Carlos H. Martinez, Joanne Billings, Abbie Begnaud, Tadashi Allen, Frank Sciurba, Carl Fuhrman, Joel Weissfeld, Antonio Anzueto, Sandra Adams, Diego Maselli-Caceres, and Mario E. Ruiz
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Male ,Pulmonary and Respiratory Medicine ,medicine.medical_specialty ,Coronary Artery Disease ,Critical Care and Intensive Care Medicine ,COPD: Original Research ,Coronary artery disease ,03 medical and health sciences ,FEV1/FVC ratio ,0302 clinical medicine ,Functional residual capacity ,Risk Factors ,Internal medicine ,medicine ,Humans ,Lung volumes ,030212 general & internal medicine ,Myocardial infarction ,Lung ,Subclinical infection ,COPD ,business.industry ,Smoking ,Organ Size ,Middle Aged ,respiratory system ,medicine.disease ,Coronary Vessels ,United States ,Respiratory Function Tests ,respiratory tract diseases ,Airway Obstruction ,Plethysmography ,Biological Variation, Population ,Pulmonary Emphysema ,030228 respiratory system ,Asymptomatic Diseases ,Cohort ,Cardiology ,Airway Remodeling ,Female ,Tomography, X-Ray Computed ,Cardiology and Cardiovascular Medicine ,business - Abstract
BACKGROUND: Smokers manifest varied phenotypes of pulmonary impairment. RESEARCH QUESTION: Which pulmonary phenotypes are associated with coronary artery disease (CAD) in smokers? STUDY DESIGN AND METHODS: We analyzed data from the University of Pittsburgh COPD Specialized Center for Clinically Oriented Research (SCCOR) cohort (n = 481) and the Genetic Epidemiology of COPD (COPDGene) cohort (n = 2,580). Participants were current and former smokers with > 10 pack-years of tobacco exposure. Data from the two cohorts were analyzed separately because of methodologic differences. Lung hyperinflation was assessed by plethysmography in the SCCOR cohort and by inspiratory and expiratory CT scan lung volumes in the COPDGene cohort. Subclinical CAD was assessed as the coronary artery calcium score, whereas clinical CAD was defined as a self-reported history of CAD or myocardial infarction (MI). Analyses were performed in all smokers and then repeated in those with airflow obstruction (FEV(1) to FVC ratio, < 0.70). RESULTS: Pulmonary phenotypes, including airflow limitation, emphysema, lung hyperinflation, diffusion capacity, and radiographic measures of airway remodeling, showed weak to moderate correlations (r < 0.7) with each other. In multivariate models adjusted for pulmonary phenotypes and CAD risk factors, lung hyperinflation was the only phenotype associated with calcium score, history of clinical CAD, or history of MI (per 0.2 higher expiratory and inspiratory CT scan lung volume; coronary calcium: OR, 1.2; 95% CI, 1.1-1.5; P = .02; clinical CAD: OR, 1.6; 95% CI, 1.1-2.3; P = .01; and MI in COPDGene: OR, 1.7; 95% CI, 1.0-2.8; P = .05). FEV(1) and emphysema were associated with increased risk of CAD (P < .05) in models adjusted for CAD risk factors; however, these associations were attenuated on adjusting for lung hyperinflation. Results were the same in those with airflow obstruction and were present in both cohorts. INTERPRETATION: Lung hyperinflation is associated strongly with clinical and subclinical CAD in smokers, including those with airflow obstruction. After lung hyperinflation was accounted for, FEV(1) and emphysema no longer were associated with CAD. Subsequent studies should consider measuring lung hyperinflation and examining its mechanistic role in CAD in current and former smokers.
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- 2021
4. Design and rationale of the CHILL phase II trial of hypothermia and neuromuscular blockade for acute respiratory distress syndrome
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Carl B. Shanholtz, Michael L. Terrin, Thelma Harrington, Caleb Chan, Whittney Warren, Robert Walter, Faith Armstrong, Jeffrey Marshall, Rachel Scheraga, Abjihit Duggal, Perry Formanek, Michael Baram, Majid Afshar, Nathaniel Marchetti, Sunit Singla, John Reilly, Dan Knox, Nitin Puri, Kevin Chung, Clayton H. Brown, and Jeffrey D. Hasday
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Pharmacology ,General Medicine - Published
- 2023
5. Prevalence of abnormal spirometry in individuals with a smoking history and no known obstructive lung disease
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Thuonghien V. Tran, Gregory L. Kinney, Alejandro Comellas, Karin F. Hoth, Arianne K. Baldomero, A. James Mamary, Jeffrey L. Curtis, Nicola Hanania, Richard Casaburi, Kendra A. Young, Victor Kim, Barry Make, Emily S. Wan, Alejandro A. Diaz, John Hokanson, James D. Crapo, Edwin K. Silverman, Surya P. Bhatt, Elizabeth Regan, Spyridon Fortis, Barry J. Make, Elizabeth A. Regan, Terri H. Beaty, Peter J. Castaldi, Michael H. Cho, Dawn L. DeMeo, Adel El Boueiz, Marilyn G. Foreman, Auyon Ghosh, Lystra P. Hayden, Craig P. Hersh, Jacqueline Hetmanski, Brian D. Hobbs, John E. Hokanson, Wonji Kim, Nan Laird, Christoph Lange, Sharon M. Lutz, Merry-Lynn McDonald, Dmitry Prokopenko, Matthew Moll, Jarrett Morrow, Dandi Qiao, Aabida Saferali, Phuwanat Sakornsakolpat, Jeong Yun, Juan Pablo Centeno, Jean-Paul Charbonnier, Harvey O. Coxson, Craig J. Galban, MeiLan K. Han, Eric A. Hoffman, Stephen Humphries, Francine L. Jacobson, Philip F. Judy, Ella A. Kazerooni, Alex Kluiber, David A. Lynch, Pietro Nardelli, John D. Newell, Aleena Notary, Andrea Oh, James C. Ross, Raul San Jose Estepar, Joyce Schroeder, Jered Sieren, Berend C. Stoel, Juerg Tschirren, Edwin Van Beek, Bram van Ginneken, Eva van Rikxoort, Gonzalo Vegas Sanchez Ferrero, Lucas Veitel, George R. Washko, Carla G. Wilson, Robert Jensen, Douglas Everett, Jim Crooks, Katherine Pratte, Matt Strand, Erin Austin, Gregory Kinney, Jessica Bon, Susan Murray, Xavier Soler, Russell P. Bowler, Katerina Kechris, Farnoush BanaeiKashani, Perry G. Pernicano, Mustafa Atik, Aladin Boriek, Kalpatha Guntupalli, Elizabeth Guy, Amit Parulekar, Craig Hersh, George Washko, R. Graham Barr, John Austin, Belinda D'Souza, Byron Thomashow, Neil MacIntyre, H. Page McAdams, Lacey Washington, Charlene McEvoy, Joseph Tashjian, Robert Wise, Robert Brown, Nadia N. Hansel, Karen Horton, Allison Lambert, Nirupama Putcha, Alessandra Adami, Matthew Budoff, Hans Fischer, Janos Porszasz, Harry Rossiter, William Stringer, Amir Sharafkhaneh, Charlie Lan, Christine Wendt, Brian Bell, Ken M. Kunisaki, Eric L. Flenaugh, Hirut Gebrekristos, Mario Ponce, Silanath Terpenning, Gloria Westney, Russell Bowler, Richard Rosiello, David Pace, Gerard Criner, David Ciccolella, Francis Cordova, Chandra Dass, Gilbert D'Alonzo, Parag Desai, Michael Jacobs, Steven Kelsen, Nathaniel Marchetti, Aditi Satti, Kartik Shenoy, Robert M. Steiner, Alex Swift, Irene Swift, Maria Elena Vega-Sanchez, Mark Dransfield, William Bailey, Anand Iyer, Hrudaya Nath, J. Michael Wells, Douglas Conrad, Andrew Yen, Alejandro P. Comellas, John Newell, Brad Thompson, Ella Kazerooni, Wassim Labaki, Craig Galban, Dharshan Vummidi, Joanne Billings, Abbie Begnaud, Tadashi Allen, Frank Sciurba, Divay Chandra, Joel Weissfeld, Antonio Anzueto, Sandra Adams, Diego Maselli-Caceres, Mario E. Ruiz, and Harjinder Singh
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Pulmonary and Respiratory Medicine - Published
- 2023
6. Mitochondrial dysfunction in human primary alveolar type II cells in emphysema
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Sudhir Bolla, Dhanendra Tomar, Karim Bahmed, Loukmane Karim, Beata Kosmider, Muniswamy Madesh, Liudmila Vlasenko, Gerard J. Criner, Chih-Ru Lin, and Nathaniel Marchetti
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0301 basic medicine ,FIS1 ,Mitochondrial DNA ,Pathology ,medicine.medical_specialty ,Research paper ,DNA damage ,Mitochondrion ,DNA, Mitochondrial ,General Biochemistry, Genetics and Molecular Biology ,03 medical and health sciences ,Adenosine Triphosphate ,0302 clinical medicine ,Superoxides ,Smoke ,Humans ,COPD ,Medicine ,MFN1 ,Lung ,Emphysema ,Phosphoric Diester Hydrolases ,business.industry ,General Medicine ,respiratory system ,medicine.disease ,Mitochondria ,Alveolar type II cells ,respiratory tract diseases ,3. Good health ,Oxidative Stress ,Protein Transport ,030104 developmental biology ,medicine.anatomical_structure ,Pulmonary Emphysema ,Alveolar Epithelial Cells ,030220 oncology & carcinogenesis ,Disease Progression ,Energy Metabolism ,Reactive Oxygen Species ,business ,TDP1 - Abstract
Background Cigarette smoke is the main risk factor of pulmonary emphysema development, which is characterized by alveolar wall destruction. Mitochondria are important for alveolar type II (ATII) cell metabolism due to ATP generation. Methods We isolated ATII cells from control non-smoker and smoker organ donors, and after lung transplant of patients with emphysema to determine mitochondrial function, dynamics and mitochondrial (mt) DNA damage. Findings We found high mitochondrial superoxide generation and mtDNA damage in ATII cells in emphysema. This correlated with decreased mtDNA amount. We also detected high TOP1-cc and low TDP1 levels in mitochondria in ATII cells in emphysema. This contributed to the decreased resolution of TOP1-cc leading to accumulation of mtDNA damage and mitochondrial dysfunction. Moreover, we used lung tissue obtained from areas with mild and severe emphysema from the same patients. We found a correlation between the impaired fusion and fission as indicated by low MFN1, OPA1, FIS1, and p-DRP1 levels and this disease severity. We detected lower TDP1 expression in severe compared to mild emphysema. Interpretation We found high DNA damage and impairment of DNA damage repair in mitochondria in ATII cells isolated from emphysema patients, which contribute to abnormal mitochondrial dynamics. Our findings provide molecular mechanisms of mitochondrial dysfunction in this disease. Fund This work was supported by National Institutes of Health (NIH) grant R01 HL118171 (B.K.) and the Catalyst Award from the American Lung Association (K.B.).
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- 2019
7. Ventilatory Mechanics in Early vs Late Intubation in a Cohort of Coronavirus Disease 2019 Patients With ARDS
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Aloknath Pandya, Navjot Ariyana Kaur, Daniel Sacher, Oisin O’Corragain, Daniel Salerno, Parag Desai, Sameep Sehgal, Matthew Gordon, Rohit Gupta, Nathaniel Marchetti, Huaqing Zhao, Nicole Patlakh, Gerard J. Criner, and Temple University
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Pulmonary and Respiratory Medicine ,ARDS ,medicine.medical_specialty ,2019-20 coronavirus outbreak ,Coronavirus disease 2019 (COVID-19) ,business.industry ,medicine.medical_treatment ,Ventilatory mechanics ,Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ,medicine.disease ,Single Center ,Critical Care and Intensive Care Medicine ,Emergency medicine ,Cohort ,medicine ,Intubation ,business ,Cardiology and Cardiovascular Medicine - Published
- 2021
- Full Text
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8. Lobar Emphysema Distribution Is Associated With 5-Year Radiological Disease Progression
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Adel Boueiz, Yale Chang, Michael H. Cho, George R. Washko, Raul San José Estépar, Russell P. Bowler, James D. Crapo, Dawn L. DeMeo, Jennifer G. Dy, Edwin K. Silverman, Peter J. Castaldi, James Crapo, Edwin Silverman, Barry Make, Elizabeth Regan, Terri Beaty, Nan Laird, Christoph Lange, Stephanie Santorico, John Hokanson, Dawn DeMeo, Nadia Hansel, Craig Hersh, Peter Castaldi, Merry-Lynn McDonald, Emily Wan, Megan Hardin, Jacqueline Hetmanski, Margaret Parker, Marilyn Foreman, Brian Hobbs, Robert Busch, Dandi Qiao, Eitan Halper-Stromberg, Ferdouse Begum, Sungho Won, Sharon Lutz, David A. Lynch, Harvey O. Coxson, MeiLan K. Han, Eric A. Hoffman, Stephen Humphries, Francine L. Jacobson, Philip F. Judy, Ella A. Kazerooni, John D. Newell, James C. Ross, Raul José Estépar, Berend C. Stoel, Juerg Tschirren, Eva van Rikxoort, Bram van Ginneken, Carla G. Wilson, Mustafa Al Qaisi, Teresa Gray, Alex Kluiber, Tanya Mann, Jered Sieren, Douglas Stinson, Joyce Schroeder, Edwin Van Beek, Robert Jensen, Douglas Everett, Anna Faino, Matt Strand, Carla Wilson, John E. Hokanson, Gregory Kinney, Kendra Young, Katherine Pratte, Lindsey Duca, Jeffrey L. Curtis, Carlos H. Martinez, Perry G. Pernicano, Nicola Hanania, Philip Alapat, Venkata Bandi, Mustafa Atik, Aladin Boriek, Kalpatha Guntupalli, Elizabeth Guy, Amit Parulekar, Arun Nachiappan, Francine Jacobson, R. Graham Barr, Byron Thomashow, John Austin, Belinda D’Souza, Gregory D.N. Pearson, Anna Rozenshtein, Neil MacIntyre, Lacey Washington, H. Page McAdams, Charlene McEvoy, Joseph Tashjian, Robert Wise, Robert Brown, Karen Horton, Nirupama Putcha, Richard Casaburi, Alessandra Adami, Janos Porszasz, Hans Fischer, Matthew Budoff, Harry Rossiter, Amir Sharafkhaneh, Charlie Lan, Christine Wendt, Brian Bell, Gloria Westney, Eugene Berkowitz, Russell Bowler, David Lynch, Richard Rosiello, David Pace, Gerard Criner, David Ciccolella, Francis Cordova, Chandra Dass, Gilbert D’Alonzo, Parag Desai, Michael Jacobs, Steven Kelsen, Victor Kim, A. James Mamary, Nathaniel Marchetti, Aditi Satti, Kartik Shenoy, Robert M. Steiner, Alex Swift, Irene Swift, Maria Elena Vega-Sanchez, Mark Dransfield, William Bailey, J. Michael Wells, Surya Bhatt, Hrudaya Nath, Joe Ramsdell, Paul Friedman, Xavier Soler, Andrew Yen, Alejandro Cornellas, John Newell, Brad Thompson, MeiLan Han, Ella Kazerooni, Carlos Martinez, Joanne Billings, Tadashi Allen, Frank Sciurba, Divay Chandra, Joel Weissfeld, Carl Fuhrman, Jessica Bon, Antonio Anzueto, Sandra Adams, Diego Maselli-Caceres, and Mario E. Ruiz
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Male ,Pulmonary and Respiratory Medicine ,medicine.medical_specialty ,Pathology ,Genome-wide association study ,Comorbidity ,Critical Care and Intensive Care Medicine ,Severity of Illness Index ,Gastroenterology ,03 medical and health sciences ,FEV1/FVC ratio ,0302 clinical medicine ,Forced Expiratory Volume ,Internal medicine ,medicine ,Humans ,COPD ,Distribution (pharmacology) ,030212 general & internal medicine ,Aged ,business.industry ,Middle Aged ,respiratory system ,medicine.disease ,respiratory tract diseases ,Pulmonary Emphysema ,030228 respiratory system ,Genetic epidemiology ,Radiological weapon ,Cohort ,Disease Progression ,Inflammatory diseases Radboud Institute for Health Sciences [Radboudumc 5] ,Female ,Metabolic syndrome ,Tomography, X-Ray Computed ,Cardiology and Cardiovascular Medicine ,business ,Rare cancers Radboud Institute for Health Sciences [Radboudumc 9] - Abstract
Contains fulltext : 194255.pdf (Publisher’s version ) (Open Access) BACKGROUND: Emphysema has considerable variability in its regional distribution. Craniocaudal emphysema distribution is an important predictor of the response to lung volume reduction. However, there is little consensus regarding how to define upper lobe-predominant and lower lobe-predominant emphysema subtypes. Consequently, the clinical and genetic associations with these subtypes are poorly characterized. METHODS: We sought to identify subgroups characterized by upper-lobe or lower-lobe emphysema predominance and comparable amounts of total emphysema by analyzing data from 9,210 smokers without alpha-1-antitrypsin deficiency in the Genetic Epidemiology of COPD (COPDGene) cohort. CT densitometric emphysema was measured in each lung lobe. Random forest clustering was applied to lobar emphysema variables after regressing out the effects of total emphysema. Clusters were tested for association with clinical and imaging outcomes at baseline and at 5-year follow-up. Their associations with genetic variants were also compared. RESULTS: Three clusters were identified: minimal emphysema (n = 1,312), upper lobe-predominant emphysema (n = 905), and lower lobe-predominant emphysema (n = 796). Despite a similar amount of total emphysema, the lower-lobe group had more severe airflow obstruction at baseline and higher rates of metabolic syndrome compared with subjects with upper-lobe predominance. The group with upper-lobe predominance had greater 5-year progression of emphysema, gas trapping, and dyspnea. Differential associations with known COPD genetic risk variants were noted. CONCLUSIONS: Subgroups of smokers defined by upper-lobe or lower-lobe emphysema predominance exhibit different functional and radiological disease progression rates, and the upper-lobe predominant subtype shows evidence of association with known COPD genetic risk variants. These subgroups may be useful in the development of personalized treatments for COPD.
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- 2018
9. VIEWS OF US PULMONOLOGISTS ON THE PREVALENCE OF UNCONTROLLED ASTHMA, TREATMENT DECISIONS, AND THE ROLE OF TREATABLE TRAITS: RESULTS FROM THE CHEST PULSE SURVEYS
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Diego Maselli Caceres, Robson Lima, Xavier Soler, Navitha Ramesh, Matthew J. Hegewald, Nathaniel Marchetti, Christopher J. Lettieri, Sarah Chang, and Erika Gonzalez
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Pulmonary and Respiratory Medicine ,medicine.medical_specialty ,Pulse (signal processing) ,business.industry ,medicine ,Treatment decision making ,Cardiology and Cardiovascular Medicine ,Critical Care and Intensive Care Medicine ,Intensive care medicine ,business ,Pulmonologists ,Uncontrolled asthma - Published
- 2020
10. Executive Summary
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Michael K. Stickland, Paul Hernandez, Donna Goodridge, Pat G. Camp, Jeremy Road, Mohit Bhutani, Meyer Balter, Marilyn G. Foreman, Nathaniel Marchetti, Stanley B. Fiel, Gerard J. Criner, Darcy D. Marciniuk, Daniel R. Ouellette, Joseph Ornelas, Gail Dechman, Nicola A. Hanania, Mark T. Dransfield, Belinda K. Ireland, Rebecca L. Diekemper, Kristen Curren, Bartolome R. Celli, Richard A. Mularski, and Jean Bourbeau
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Pulmonary and Respiratory Medicine ,medicine.medical_specialty ,COPD ,Exacerbation ,business.industry ,Evidence-based medicine ,Guideline ,Disease ,Critical Care and Intensive Care Medicine ,medicine.disease ,respiratory tract diseases ,Pulmonary function testing ,Clinical trial ,medicine ,Cardiology and Cardiovascular Medicine ,Intensive care medicine ,business ,Cause of death - Abstract
COPD is a common disease with substantial associated morbidity and mortality. Patients with COPD usually have a progression of airflow obstruction that is not fully reversible and can lead to a history of progressively worsening breathlessness, affecting daily activities and health-related quality of life.1-3 COPD is the fourth leading cause of death in Canada4 and the third leading cause of death in the United States where it claimed 133,965 lives in 2009.5 In 2011, 12.7 million US adults were estimated to have COPD.6 However, approximately 24 million US adults have evidence of impaired lung function, indicating an underdiagnosis of COPD.7 Although 4% of Canadians aged 35 to 79 years self-reported having been given a diagnosis of COPD, direct measurements of lung function from the Canadian Health Measures Survey indicate that 13% of Canadians have a lung function score indicative of COPD.4 COPD is also costly. In 2009, COPD caused 8 million office visits, 1.5 million ED visits, 715,000 hospitalizations, and 133,965 deaths in the United States.8 In 2010, US costs for COPD were projected to be approximately $49.9 billion, including $29.5 billion in direct health-care expenditures, $8.0 billion in indirect morbidity costs, and $12.4 billion in indirect mortality costs.9 Exacerbations account for most of the morbidity, mortality, and costs associated with COPD. The economic burden associated with moderate and severe exacerbations in Canada has been estimated to be in the range of $646 million to $736 million per annum.10 This value may be an underestimate given that the prevalence of moderate exacerbations is not well documented, COPD is underdiagnosed, and the rate of hospitalization due to COPD is increasing.11 Exacerbations are to COPD what myocardial infarctions are to coronary artery disease: They are acute, trajectory-changing, and often deadly manifestations of a chronic disease. Exacerbations cause frequent hospital admissions, relapses, and readmissions12; contribute to death during hospitalization or shortly thereafter12; reduce quality of life dramatically12,13; consume financial resources12,14; and hasten a progressive decline in pulmonary function, a cardinal feature of COPD. Hospitalization due to exacerbations accounts for > 50% of the cost of managing COPD in North America and Europe.15,16 COPD exacerbation has been defined as an event in the natural course of the disease characterized by a baseline change in the patient’s dyspnea, cough, and/or sputum that is beyond the normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD.17,18 Exacerbation in clinical trials has been defined for operational reasons on the basis of whether an increase in treatment beyond regular or urgent care is required in an ED or a hospital. Exacerbation treatment in clinical trials usually is defined by the use of antibiotics, systemic corticosteroids, or both.19 The severity of the exacerbation is then ranked or stratified according to the outcome: mild, when the clinical symptoms are present but no change in treatment or outcome is recorded; moderate, when the event results in a change in medication, such as the use of antibiotics and systemic corticosteroids; or severe, when the event leads to a hospitalization.1 Two-thirds of exacerbations are associated with respiratory tract infections or air pollution, but one-third present without an identifiable cause.17 Exacerbations remain poorly understood in terms of not only cause but also treatment and prevention. Although the management of an acute exacerbation has been the primary focus of clinical trials, the prevention of acute exacerbations has not been a major focus until recently. Most current COPD guidelines focus on the general diagnosis and evaluation of the patient with COPD, the management of stable disease, and the diagnosis and management of acute exacerbations.1,20 Although current COPD guidelines state that prevention of exacerbations is possible, little guidance is provided to the clinician regarding current available therapies for the prevention of COPD exacerbations.1,20 Moreover, new therapies have promise in preventing acute exacerbations of COPD (AECOPD) and would benefit from critical review of their efficacy in the exacerbation prevention management.21-23 The American College of Chest Physicians (CHEST) and Canadian Thoracic Society (CTS) jointly commissioned this evidence-based guideline on the prevention of COPD exacerbations to fill this important void in COPD management. The overall objective of this CHEST and CTS joint evidence-based guideline (AECOPD Guideline) was to create a practical, clinically useful document describing the current state of knowledge regarding the prevention of AECOPD according to major categories of prevention therapies. We accomplished this by using recognized document evaluation tools to assess and choose the most appropriate studies and evidence to extract meaningful data and to grade the level of evidence supporting the recommendations in a balanced and unbiased fashion. The AECOPD Guideline is unique not only for its topic but also for the first-in-kind partnership between two of the largest thoracic societies in North America. The CHEST Guidelines Oversight Committee in partnership with the CTS COPD Clinical Assembly launched this project with the objective that a systematic review and critical evaluation of the published literature by clinical experts and researchers in the field of COPD would lead to a series of recommendations to assist clinicians in their management of the patient with COPD. This guideline is unique because a group of interdisciplinary clinicians who have special expertise in COPD clinical research and care led the development of the guideline process with the assistance of methodologists.
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- 2015
11. Prevention of Acute Exacerbations of COPD
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Pat G. Camp, Donna Goodridge, Nathaniel Marchetti, Joseph Ornelas, Jean Bourbeau, Richard A. Mularski, Stanley B. Fiel, Bartolome R. Celli, Kristen Curren, Paul Hernandez, Mark T. Dransfield, Belinda K. Ireland, Mohit Bhutani, Rebecca L. Diekemper, Gerard J. Criner, Meyer Balter, Darcy D Marciniuk, Marilyn G. Foreman, Jeremy Road, Daniel R. Ouellette, Michael K. Stickland, Nicola A. Hanania, and Gail Dechman
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Pulmonary and Respiratory Medicine ,COPD ,medicine.medical_specialty ,education.field_of_study ,Exacerbation ,business.industry ,Population ,Evidence-based medicine ,Guideline ,Critical Care and Intensive Care Medicine ,medicine.disease ,respiratory tract diseases ,law.invention ,Quality of life (healthcare) ,Randomized controlled trial ,law ,medicine ,Disease management (health) ,Cardiology and Cardiovascular Medicine ,Intensive care medicine ,education ,business - Abstract
BACKGROUND:COPD is a major cause of morbidity and mortality in the United States as well as throughout the rest of the world. An exacerbation of COPD (periodic escalations of symptoms of cough, dyspnea, and sputum production) is a major contributor to worsening lung function, impairment in quality of life, need for urgent care or hospitalization, and cost of care in COPD. Research conducted over the past decade has contributed much to our current understanding of the pathogenesis and treatment of COPD. Additionally, an evolving literature has accumulated about the prevention of acute exacerbations. METHODS:In recognition of the importance of preventing exacerbations in patients with COPD, the American College of Chest Physicians (CHEST) and Canadian Thoracic Society (CTS) joint evidence-based guideline (AECOPD Guideline) was developed to provide a practical, clinically useful document to describe the current state of knowledge regarding the prevention of acute exacerbations according to major categories of prevention therapies. Three key clinical questions developed using the PICO (population, intervention, comparator, and outcome) format addressed the prevention of acute exacerbations of COPD: nonpharmacologic therapies, inhaled therapies, and oral therapies. We used recognized document evaluation tools to assess and choose the most appropriate studies and to extract meaningful data and grade the level of evidence to support the recommendations in each PICO question in a balanced and unbiased fashion. RESULTS:The AECOPD Guideline is unique not only for its topic, the prevention of acute exacerbations of COPD, but also for the first-in-kind partnership between two of the largest thoracic societies in North America. The CHEST Guidelines Oversight Committee in partnership with the CTS COPD Clinical Assembly launched this project with the objective that a systematic review and critical evaluation of the published literature by clinical experts and researchers in the field of COPD would lead to a series of recommendations to assist clinicians in their management of the patient with COPD. CONCLUSIONS:This guideline is unique because it provides an up-to-date, rigorous, evidence-based analysis of current randomized controlled trial data regarding the prevention of COPD exacerbations.
- Published
- 2015
12. Cigarette Smoke Silences Innate Lymphoid Cell Function and Facilitates an Exacerbated Type I Interleukin-33-Dependent Response to Infection
- Author
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Gerard J. Criner, Tomas Mustelin, Caroline Sanden, Nathaniel Marchetti, Zheng Liu, Tuyet-Hang Pham, Alison A. Humbles, Christine K. Ward, Jonas S. Erjefält, Jennifer Kearley, Aaron A Berlin, Roland Kolbeck, Jonathan S. Silver, Natalie White, and Michiko Mori
- Subjects
Immunology ,Interleukin-1 Receptor-Like 1 Protein ,Mice, Transgenic ,Inflammation ,Respiratory Mucosa ,Biology ,Proinflammatory cytokine ,Pulmonary Disease, Chronic Obstructive ,Orthomyxoviridae Infections ,Immunity ,Smoke ,Tobacco ,Weight Loss ,medicine ,Animals ,Humans ,Immunology and Allergy ,Lymphocytes ,Lung ,COPD ,Interleukins ,Macrophages ,Innate lymphoid cell ,Receptors, Interleukin ,Interleukin-33 ,medicine.disease ,Immunity, Innate ,Killer Cells, Natural ,Interleukin 33 ,Infectious Diseases ,Gene Expression Regulation ,Influenza A virus ,Female ,medicine.symptom ,Signal transduction ,Signal Transduction - Abstract
SummaryCigarette smoking is a major risk factor for chronic obstructive pulmonary disease and is presumed to be central to the altered responsiveness to recurrent infection in these patients. We examined the effects of smoke priming underlying the exacerbated response to viral infection in mice. Lack of interleukin-33 (IL-33) signaling conferred complete protection during exacerbation and prevented enhanced inflammation and exaggerated weight loss. Mechanistically, smoke was required to upregulate epithelial-derived IL-33 and simultaneously alter the distribution of the IL-33 receptor ST2. Specifically, smoke decreased ST2 expression on group 2 innate lymphoid cells (ILC2s) while elevating ST2 expression on macrophages and natural killer (NK) cells, thus altering IL-33 responsiveness within the lung. Consequently, upon infection and release, increased local IL-33 significantly amplified type I proinflammatory responses via synergistic modulation of macrophage and NK cell function. Therefore, in COPD, smoke alters the lung microenvironment to facilitate an alternative IL-33-dependent exaggerated proinflammatory response to infection, exacerbating disease.
- Published
- 2015
13. Prediction of Acute Respiratory Disease in Current and Former Smokers With and Without COPD
- Author
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Lacey Washington, Kalpalatha K. Guntupalli, John Newell, Adam L. Friedlander, Joyce D. Schroeder, Rebecca Leek, Robert H. Brown, Tadashi Allen, Edwin K. Silverman, Barry J. Make, Douglas Stinson, Stephanie A. Santorico, Richard Rosiello, Neil R. MacIntyre, David A. Lynch, Tanya Mann, Deborah L. Thompson, Joel L. Weissfeld, J. Michael Wells, William Lunn, Jeffrey L. Curtis, Edwin J R van Beek, Dawn L. DeMeo, Francine L. Jacobson, Antara Mallampalli, Matthew J. Budoff, Philip Alapat, Robert O. Crapo, Raúl San José Estépar, Carlos Orozco, Geoffrey McLennan, Nan M. Laird, Iuliana Ionita, Barbara J. Klanderman, Harvey O. Coxson, Peter Bercz, Craig P. Hersh, George R. Washko, H. Page McAdams, Paul Ferguson, R. Graham Barr, Robert M. Steiner, Anastasia Rodionova, Elizabeth Guy, Amir Sharafkhaneh, Dennis E. Niewoehner, Hans Fischer, Victor Kim, Hrudaya Nath, Kathryn L. Rice, John P. Reilly, Charles Trinh, John H. M. Austin, Douglas Everett, C. Santiago Restrepo, Joseph H. Tashjian, John E. Hokanson, Richard Casaburi, Robert L. Jensen, Fernando J. Martinez, Mark T. Dransfield, James Murphy, Antonio Anzueto, Jessica Bon, Gloria Westney, Terri H. Beaty, Lynn B. Gerald, Nicola A. Hanania, Chandra Dass, Alejandro P. Comellas, Alex Kluiber, Xavier Soler, Joe W. Ramsdell, Frank C. Sciurba, Philip F. Judy, Elizabeth A. Regan, Jordan A. Zach, Jonathan M. Samet, MeiLan K. Han, Janos Porszasz, Eric Hoff Man, Andre Williams, Mustafa A. Atik, Gerard J. Criner, Paul A. Friedman, Carl R. Fuhrman, Marilyn G. Foreman, Timothy Bresnahan, Nadia N. Hansel, Amy Willis, Sandra G. Adams, Eleonora Meoni, William C. Bailey, A. James Mamary, Carla Wilson, Christoph Lange, James D. Crapo, Christine H. Wendt, Eugene Berkowitz, Russell P. Bowler, Amy L Mumbower, Charlene McEvoy, Robert A. Wise, Venkata Bandi, Ella A. Kazerooni, Nathaniel Marchetti, Homayoon Farzadegan, Aditi Satti, and Byron Thomashow
- Subjects
Male ,Pulmonary and Respiratory Medicine ,Chronic Obstructive ,medicine.medical_specialty ,Exacerbation ,Chronic Obstructive Pulmonary Disease ,Respiratory Tract Diseases ,Clinical Sciences ,Respiratory System ,Critical Care and Intensive Care Medicine ,Pulmonary Disease ,Pulmonary Disease, Chronic Obstructive ,Risk Factors ,Clinical Research ,Internal medicine ,medicine ,Humans ,Longitudinal Studies ,Intensive care medicine ,Lung ,Original Research ,Proportional Hazards Models ,Aged ,First episode ,COPD ,Framingham Risk Score ,Proportional hazards model ,business.industry ,Incidence ,Smoking ,Hazard ratio ,Respiratory disease ,Middle Aged ,medicine.disease ,United States ,respiratory tract diseases ,Hospitalization ,Good Health and Well Being ,Acute Disease ,Cohort ,Quality of Life ,Respiratory ,Female ,Cardiology and Cardiovascular Medicine ,business ,Follow-Up Studies - Abstract
BACKGROUND The risk factors for acute episodes of respiratory disease in current and former smokers who do not have COPD are unknown. METHODS Eight thousand two hundred forty-six non-Hispanic white and black current and former smokers in the Genetic Epidemiology of COPD (COPDGene) cohort had longitudinal follow-up (LFU) every 6 months to determine acute respiratory episodes requiring antibiotics or systemic corticosteroids, an ED visit, or hospitalization. Negative binomial regression was used to determine the factors associated with acute respiratory episodes. A Cox proportional hazards model was used to determine adjusted hazard ratios (HRs) for time to first episode and an acute episode of respiratory disease risk score. RESULTS At enrollment, 4,442 subjects did not have COPD, 658 had mild COPD, and 3,146 had moderate or worse COPD. Nine thousand three hundred three acute episodes of respiratory disease and 2,707 hospitalizations were reported in LFU (3,044 acute episodes of respiratory disease and 827 hospitalizations in those without COPD). Major predictors included acute episodes of respiratory disease in year prior to enrollment (HR, 1.20; 95% CI, 1.15-1.24 per exacerbation), airflow obstruction (HR, 0.94; 95% CI, 0.91-0.96 per 10% change in % predicted FEV 1 ), and poor health-related quality of life (HR, 1.07; 95% CI, 1.06-1.08 for each 4-unit increase in St. George's Respiratory Questionnaire score). Risks were similar for those with and without COPD. CONCLUSIONS Although acute episode of respiratory disease rates are higher in subjects with COPD, risk factors are similar, and at a population level, there are more episodes in smokers without COPD.
- Published
- 2014
14. Preventing Acute Exacerbations and Hospital Admissions in COPD
- Author
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Nathaniel Marchetti, Gerard J. Criner, and Richard K. Albert
- Subjects
Pulmonary and Respiratory Medicine ,medicine.medical_specialty ,medicine.medical_treatment ,Muscarinic Antagonists ,Lung volume reduction surgery ,Critical Care and Intensive Care Medicine ,Pulmonary Disease, Chronic Obstructive ,Pneumonectomy ,Quality of life ,Adrenal Cortex Hormones ,Humans ,Medicine ,Pulmonary rehabilitation ,Disease management (health) ,Intensive care medicine ,Cause of death ,COPD ,business.industry ,Disease progression ,Disease Management ,Adrenergic beta-Agonists ,medicine.disease ,Hospitalization ,Disease Progression ,Cardiology and Cardiovascular Medicine ,business - Abstract
COPD is a leading cause of morbidity and mortality worldwide and is now the third leading cause of death in the United States. Acute exacerbations of COPD (AECOPDs) are common events that often lead to hospitalization, and their frequency worsens with disease progression. AECOPDs are associated with worsened quality of life, increased health-care costs, and increased mortality. Accordingly, there is great interest in preventing AECOPDs to improve outcomes. Both pharmacologic and nonpharmacologic interventions alter the frequency of AECOPDs and COPD-related hospitalizations. To examine the best available evidence, we restricted this review to include studies that used randomized controlled designs lasting at least 6 months. Pharmacologic interventions discussed include inhaled corticosteroids, long-acting β-agonists, long-acting antimuscarinic agents, macrolide antibiotics, and phosphodiesterase-4 inhibitors. The nonpharmacologic interventions discussed include lung volume reduction surgery, pulmonary rehabilitation, and disease management programs.
- Published
- 2013
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