Search

Your search keyword '"Reed, Robert M."' showing total 611 results
Start Over Author "Reed, Robert M."
611 results on '"Reed, Robert M."'

2. Rare genetic variants explain missing heritability in smoking.

Author

Jang, Seon-Kyeong, Evans, Luke, Fialkowski, Allison, Arnett, Donna K, Ashley-Koch, Allison E, Barnes, Kathleen C, Becker, Diane M, Bis, Joshua C, Blangero, John, Bleecker, Eugene R, Boorgula, Meher Preethi, Bowden, Donald W, Brody, Jennifer A, Cade, Brian E, Jenkins, Brenda W Campbell, Carson, April P, Chavan, Sameer, Cupples, L Adrienne, Custer, Brian, Damrauer, Scott M, David, Sean P, de Andrade, Mariza, Dinardo, Carla L, Fingerlin, Tasha E, Fornage, Myriam, Freedman, Barry I, Garrett, Melanie E, Gharib, Sina A, Glahn, David C, Haessler, Jeffrey, Heckbert, Susan R, Hokanson, John E, Hou, Lifang, Hwang, Shih-Jen, Hyman, Matthew C, Judy, Renae, Justice, Anne E, Kaplan, Robert C, Kardia, Sharon LR, Kelly, Shannon, Kim, Wonji, Kooperberg, Charles, Levy, Daniel, Lloyd-Jones, Donald M, Loos, Ruth JF, Manichaikul, Ani W, Gladwin, Mark T, Martin, Lisa Warsinger, Nouraie, Mehdi, Melander, Olle, Meyers, Deborah A, Montgomery, Courtney G, North, Kari E, Oelsner, Elizabeth C, Palmer, Nicholette D, Payton, Marinelle, Peljto, Anna L, Peyser, Patricia A, Preuss, Michael, Psaty, Bruce M, Qiao, Dandi, Rader, Daniel J, Rafaels, Nicholas, Redline, Susan, Reed, Robert M, Reiner, Alexander P, Rich, Stephen S, Rotter, Jerome I, Schwartz, David A, Shadyab, Aladdin H, Silverman, Edwin K, Smith, Nicholas L, Smith, J Gustav, Smith, Albert V, Smith, Jennifer A, Tang, Weihong, Taylor, Kent D, Telen, Marilyn J, Vasan, Ramachandran S, Gordeuk, Victor R, Wang, Zhe, Wiggins, Kerri L, Yanek, Lisa R, Yang, Ivana V, Young, Kendra A, Young, Kristin L, Zhang, Yingze, Liu, Dajiang J, Keller, Matthew C, and Vrieze, Scott

Subjects
Smoking, Gene Frequency, Phenotype, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Tobacco, Genetics, Tobacco Smoke and Health, Human Genome, Cancer
Abstract

Common genetic variants explain less variation in complex phenotypes than inferred from family-based studies, and there is a debate on the source of this 'missing heritability'. We investigated the contribution of rare genetic variants to tobacco use with whole-genome sequences from up to 26,257 unrelated individuals of European ancestries and 11,743 individuals of African ancestries. Across four smoking traits, single-nucleotide-polymorphism-based heritability ([Formula: see text]) was estimated from 0.13 to 0.28 (s.e., 0.10-0.13) in European ancestries, with 35-74% of it attributable to rare variants with minor allele frequencies between 0.01% and 1%. These heritability estimates are 1.5-4 times higher than past estimates based on common variants alone and accounted for 60% to 100% of our pedigree-based estimates of narrow-sense heritability ([Formula: see text], 0.18-0.34). In the African ancestry samples, [Formula: see text] was estimated from 0.03 to 0.33 (s.e., 0.09-0.14) across the four smoking traits. These results suggest that rare variants are important contributors to the heritability of smoking.

Published
2022

6. Multiethnic genome-wide and HLA association study of total serum IgE level

Author

Daya, Michelle, Cox, Corey, Acevedo, Nathalie, Boorgula, Meher P, Campbell, Monica, Chavan, Sameer, Cho, Michael H, David, Gloria L, Kachroo, Priyadarshini, Lasky-Su, Jessica, Li, Xingnan, McHugh, Caitlin P, Qiao, Dandi, Rafaels, Nicholas, Beck, Lisa A, Bleecker, Eugene R, Caraballo, Luis, Cupples, Adrienne L, Figueiredo, Camila A, Gallo, Richard L, Hanifin, Jon, Hansel, Nadia N, Hata, Tissa R, Hersh, Craig P, Knight-Madden, Jennifer, Leung, Donald YM, Guttman-Yassky, Emma, Meyers, Deborah A, O’Connor, George, Ober, Carole, Ong, Peck Y, Ortega, Victor E, Paller, Amy S, Putcha, Nirupama, Reed, Robert M, Schneider, Lynda C, Silverman, Edwin K, Slifka, Mark K, Spergel, Jonathan M, Vasan, Ramachandran S, Viaud-Martinez, Karine A, Watson, Harold, Weiss, Scott T, Consortium, NHLBI Trans-Omics for Precision Medicine, Ruczinski, Ingo, Beaty, Terri H, Mathias, Rasika A, and Barnes, Kathleen C

Subjects
Clinical Research, Genetics, Lung, Asthma, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Good Health and Well Being, Adolescent, Adult, Aged, Child, Child, Preschool, Dermatitis, Atopic, Ethnicity, Female, Gene Frequency, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, HLA-A2 Antigen, HLA-DQ beta-Chains, Humans, Immunoglobulin E, Male, Middle Aged, National Heart, Lung, and Blood Institute (U.S.), United States, Whole Genome Sequencing, Young Adult, Total serum IgE, human leukocyte antigen, genome-wide association study, atopic dermatitis, asthma, multiethnic, NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium, Immunology, Allergy
Abstract

BackgroundTotal serum IgE (tIgE) is an important intermediate phenotype of allergic disease. Whole genome genetic association studies across ancestries may identify important determinants of IgE.ObjectiveWe aimed to increase understanding of genetic variants affecting tIgE production across the ancestry and allergic disease spectrum by leveraging data from the National Heart, Lung and Blood Institute Trans-Omics for Precision Medicine program; the Consortium on Asthma among African-ancestry Populations in the Americas (CAAPA); and the Atopic Dermatitis Research Network (N = 21,901).MethodsWe performed genome-wide association within strata of study, disease, and ancestry groups, and we combined results via a meta-regression approach that models heterogeneity attributable to ancestry. We also tested for association between HLA alleles called from whole genome sequence data and tIgE, assessing replication of associations in HLA alleles called from genotype array data.ResultsWe identified 6 loci at genome-wide significance (P < 5 × 10-9), including 4 loci previously reported as genome-wide significant for tIgE, as well as new regions in chr11q13.5 and chr15q22.2, which were also identified in prior genome-wide association studies of atopic dermatitis and asthma. In the HLA allele association study, HLA-A∗02:01 was associated with decreased tIgE level (Pdiscovery = 2 × 10-4; Preplication = 5 × 10-4; Pdiscovery+replication = 4 × 10-7), and HLA-DQB1∗03:02 was strongly associated with decreased tIgE level in Hispanic/Latino ancestry populations (PHispanic/Latino discovery+replication = 8 × 10-8).ConclusionWe performed the largest genome-wide association study and HLA association study of tIgE focused on ancestrally diverse populations and found several known tIgE and allergic disease loci that are relevant in non-European ancestry populations.

Published
2021

7. Epigenetic marker of telomeric age is associated with exacerbations and hospitalizations in chronic obstructive pulmonary disease

Author

Hernández Cordero, Ana I, Yang, Chen Xi, Li, Xuan, Milne, Stephen, Chen, Virginia, Hollander, Zsuzsanna, Ng, Raymond, Criner, Gerard J, Woodruff, Prescott G, Lazarus, Stephen C, Connett, John E, Han, MeiLan K, Martinez, Fernando J, Reed, Robert M, Man, SF Paul, Leung, Janice M, and Sin, Don D

Subjects
Chronic Obstructive Pulmonary Disease, Lung, Genetics, Clinical Research, Prevention, Respiratory, Adult, Aged, Anti-Bacterial Agents, Azithromycin, Biomarkers, DNA Methylation, Disease Progression, Female, Follow-Up Studies, Hospitalization, Humans, Incidence, Male, Middle Aged, Pulmonary Disease, Chronic Obstructive, Quality of Life, Retrospective Studies, Surveys and Questionnaires, Telomere, Time Factors, United States, COPD, Telomeres, AECOPD, Epigenetics, DNA methylation, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Respiratory System
Abstract

BackgroundChronic obstructive pulmonary disease (COPD) is an age-related condition that has been associated with early telomere attrition; the clinical implications of telomere shortening in COPD are not well known. In this study we aimed to determine the relationship of the epigenetic regulation of telomeric length in peripheral blood with the risk of exacerbations and hospitalization in patients with COPD.MethodsBlood DNA methylation profiles were obtained from 292 patients with COPD enrolled in the placebo arm of the Macrolide Azithromycin to Prevent Rapid Worsening of Symptoms Associated with Chronic Obstructive Pulmonary Disease (MACRO) Study and who were followed for 1-year. We calculated telomere length based on DNA methylation markers (DNAmTL) and related this biomarker to the risk of exacerbation and hospitalization and health status (St. George Respiratory Questionnaire [SGRQ]) score over time using a Cox proportional hazards model. We also used linear models to investigate the associations of DNAmTL with the rates of exacerbation and hospitalization (adjusted for chronological age, lung function, race, sex, smoking, body mass index and cell composition).ResultsParticipants with short DNAmTL demonstrated increased risk of exacerbation (P = 0.02) and hospitalization (P = 0.03) compared to those with longer DNAmTL. DNAmTL age acceleration was associated with higher rates of exacerbation (P = 1.35 × 10-04) and hospitalization (P = 5.21 × 10-03) and poor health status (lower SGRQ scores) independent of chronological age (P = 0.03).ConclusionTelomeric age based on blood DNA methylation is associated with COPD exacerbation and hospitalization and thus a promising biomarker for poor outcomes in COPD.

Published
2021

11. Whole genome sequence analysis of pulmonary function and COPD in 19,996 multi-ethnic participants.

Author

Zhao, Xutong, Qiao, Dandi, Yang, Chaojie, Kasela, Silva, Kim, Wonji, Ma, Yanlin, Shrine, Nick, Batini, Chiara, Sofer, Tamar, Taliun, Sarah A Gagliano, Sakornsakolpat, Phuwanat, Balte, Pallavi P, Prokopenko, Dmitry, Yu, Bing, Lange, Leslie A, Dupuis, Josée, Cade, Brian E, Lee, Jiwon, Gharib, Sina A, Daya, Michelle, Laurie, Cecelia A, Ruczinski, Ingo, Cupples, L Adrienne, Loehr, Laura R, Bartz, Traci M, Morrison, Alanna C, Psaty, Bruce M, Vasan, Ramachandran S, Wilson, James G, Taylor, Kent D, Durda, Peter, Johnson, W Craig, Cornell, Elaine, Guo, Xiuqing, Liu, Yongmei, Tracy, Russell P, Ardlie, Kristin G, Aguet, François, VanDenBerg, David J, Papanicolaou, George J, Rotter, Jerome I, Barnes, Kathleen C, Jain, Deepti, Nickerson, Deborah A, Muzny, Donna M, Metcalf, Ginger A, Doddapaneni, Harshavardhan, Dugan-Perez, Shannon, Gupta, Namrata, Gabriel, Stacey, Rich, Stephen S, O'Connor, George T, Redline, Susan, Reed, Robert M, Laurie, Cathy C, Daviglus, Martha L, Preudhomme, Liana K, Burkart, Kristin M, Kaplan, Robert C, Wain, Louise V, Tobin, Martin D, London, Stephanie J, Lappalainen, Tuuli, Oelsner, Elizabeth C, Abecasis, Goncalo R, Silverman, Edwin K, Barr, R Graham, NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium, TOPMed Lung Working Group, Cho, Michael H, and Manichaikul, Ani

Subjects
NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium, TOPMed Lung Working Group, Lung, Humans, Pulmonary Disease, Chronic Obstructive, Genetic Predisposition to Disease, Intracellular Signaling Peptides and Proteins, Calcium-Binding Proteins, Small Ubiquitin-Related Modifier Proteins, Follow-Up Studies, Feasibility Studies, Polymorphism, Single Nucleotide, Adult, Aged, Aged, 80 and over, Middle Aged, African Americans, Female, Male, Protein Inhibitors of Activated STAT, Respiratory Physiological Phenomena, Genome-Wide Association Study, Genetic Loci, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Whole Genome Sequencing, and over, Polymorphism, Single Nucleotide, Pulmonary Disease, Chronic Obstructive
Abstract

Chronic obstructive pulmonary disease (COPD), diagnosed by reduced lung function, is a leading cause of morbidity and mortality. We performed whole genome sequence (WGS) analysis of lung function and COPD in a multi-ethnic sample of 11,497 participants from population- and family-based studies, and 8499 individuals from COPD-enriched studies in the NHLBI Trans-Omics for Precision Medicine (TOPMed) Program. We identify at genome-wide significance 10 known GWAS loci and 22 distinct, previously unreported loci, including two common variant signals from stratified analysis of African Americans. Four novel common variants within the regions of PIAS1, RGN (two variants) and FTO show evidence of replication in the UK Biobank (European ancestry n ~ 320,000), while colocalization analyses leveraging multi-omic data from GTEx and TOPMed identify potential molecular mechanisms underlying four of the 22 novel loci. Our study demonstrates the value of performing WGS analyses and multi-omic follow-up in cohorts of diverse ancestry.

Published
2020

13. Genetic diversity fuels gene discovery for tobacco and alcohol use

Author

Saunders, Gretchen R. B., Wang, Xingyan, Chen, Fang, Jang, Seon-Kyeong, Liu, Mengzhen, Wang, Chen, Gao, Shuang, Jiang, Yu, Khunsriraksakul, Chachrit, Otto, Jacqueline M., Addison, Clifton, Akiyama, Masato, Albert, Christine M., Aliev, Fazil, Alonso, Alvaro, Arnett, Donna K., Ashley-Koch, Allison E., Ashrani, Aneel A., Barnes, Kathleen C., Barr, R. Graham, Bartz, Traci M., Becker, Diane M., Bielak, Lawrence F., Benjamin, Emelia J., Bis, Joshua C., Bjornsdottir, Gyda, Blangero, John, Bleecker, Eugene R., Boardman, Jason D., Boerwinkle, Eric, Boomsma, Dorret I., Boorgula, Meher Preethi, Bowden, Donald W., Brody, Jennifer A., Cade, Brian E., Chasman, Daniel I., Chavan, Sameer, Chen, Yii-Der Ida, Chen, Zhengming, Cheng, Iona, Cho, Michael H., Choquet, Hélène, Cole, John W., Cornelis, Marilyn C., Cucca, Francesco, Curran, Joanne E., de Andrade, Mariza, Dick, Danielle M., Docherty, Anna R., Duggirala, Ravindranath, Eaton, Charles B., Ehringer, Marissa A., Esko, Tõnu, Faul, Jessica D., Silva, Lilian Fernandes, Fiorillo, Edoardo, Fornage, Myriam, Freedman, Barry I., Gabrielsen, Maiken E., Garrett, Melanie E., Gharib, Sina A., Gieger, Christian, Gillespie, Nathan, Glahn, David C., Gordon, Scott D., Gu, Charles C., Gu, Dongfeng, Gudbjartsson, Daniel F., Guo, Xiuqing, Haessler, Jeffrey, Hall, Michael E., Haller, Toomas, Harris, Kathleen Mullan, He, Jiang, Herd, Pamela, Hewitt, John K., Hickie, Ian, Hidalgo, Bertha, Hokanson, John E., Hopfer, Christian, Hottenga, JoukeJan, Hou, Lifang, Huang, Hongyan, Hung, Yi-Jen, Hunter, David J., Hveem, Kristian, Hwang, Shih-Jen, Hwu, Chii-Min, Iacono, William, Irvin, Marguerite R., Jee, Yon Ho, Johnson, Eric O., Joo, Yoonjung Y., Jorgenson, Eric, Justice, Anne E., Kamatani, Yoichiro, Kaplan, Robert C., Kaprio, Jaakko, Kardia, Sharon L. R., Keller, Matthew C., Kelly, Tanika N., Kooperberg, Charles, Korhonen, Tellervo, Kraft, Peter, Krauter, Kenneth, Kuusisto, Johanna, Laakso, Markku, Lasky-Su, Jessica, Lee, Wen-Jane, Lee, James J., Levy, Daniel, Li, Liming, Li, Kevin, Li, Yuqing, Lin, Kuang, Lind, Penelope A., Liu, Chunyu, Lloyd-Jones, Donald M., Lutz, Sharon M., Ma, Jiantao, Mägi, Reedik, Manichaikul, Ani, Martin, Nicholas G., Mathur, Ravi, Matoba, Nana, McArdle, Patrick F., McGue, Matt, McQueen, Matthew B., Medland, Sarah E., Metspalu, Andres, Meyers, Deborah A., Millwood, Iona Y., Mitchell, Braxton D., Mohlke, Karen L., Moll, Matthew, Montasser, May E., Morrison, Alanna C., Mulas, Antonella, Nielsen, Jonas B., North, Kari E., Oelsner, Elizabeth C., Okada, Yukinori, Orrù, Valeria, Palmer, Nicholette D., Palviainen, Teemu, Pandit, Anita, Park, S. Lani, Peters, Ulrike, Peters, Annette, Peyser, Patricia A., Polderman, Tinca J. C., Rafaels, Nicholas, Redline, Susan, Reed, Robert M., Reiner, Alex P., Rice, John P., Rich, Stephen S., Richmond, Nicole E., Roan, Carol, Rotter, Jerome I., Rueschman, Michael N., Runarsdottir, Valgerdur, Saccone, Nancy L., Schwartz, David A., Shadyab, Aladdin H., Shi, Jingchunzi, Shringarpure, Suyash S., Sicinski, Kamil, Skogholt, Anne Heidi, Smith, Jennifer A., Smith, Nicholas L., Sotoodehnia, Nona, Stallings, Michael C., Stefansson, Hreinn, Stefansson, Kari, Stitzel, Jerry A., Sun, Xiao, Syed, Moin, Tal-Singer, Ruth, Taylor, Amy E., Taylor, Kent D., Telen, Marilyn J., Thai, Khanh K., Tiwari, Hemant, Turman, Constance, Tyrfingsson, Thorarinn, Wall, Tamara L., Walters, Robin G., Weir, David R., Weiss, Scott T., White, Wendy B., Whitfield, John B., Wiggins, Kerri L., Willemsen, Gonneke, Willer, Cristen J., Winsvold, Bendik S., Xu, Huichun, Yanek, Lisa R., Yin, Jie, Young, Kristin L., Young, Kendra A., Yu, Bing, Zhao, Wei, Zhou, Wei, Zöllner, Sebastian, Zuccolo, Luisa, Batini, Chiara, Bergen, Andrew W., Bierut, Laura J., David, Sean P., Gagliano Taliun, Sarah A., Hancock, Dana B., Jiang, Bibo, Munafò, Marcus R., Thorgeirsson, Thorgeir E., Liu, Dajiang J., and Vrieze, Scott

Published
2022
Full Text
View/download PDF

14. Metoprolol for the Prevention of Acute Exacerbations of COPD

Author

Dransfield, Mark T, Voelker, Helen, Bhatt, Surya P, Brenner, Keith, Casaburi, Richard, Come, Carolyn E, Cooper, J Allen D, Criner, Gerard J, Curtis, Jeffrey L, Han, MeiLan K, Hatipoğlu, Umur, Helgeson, Erika S, Jain, Vipul V, Kalhan, Ravi, Kaminsky, David, Kaner, Robert, Kunisaki, Ken M, Lambert, Allison A, Lammi, Matthew R, Lindberg, Sarah, Make, Barry J, Martinez, Fernando J, McEvoy, Charlene, Panos, Ralph J, Reed, Robert M, Scanlon, Paul D, Sciurba, Frank C, Smith, Anthony, Sriram, Peruvemba S, Stringer, William W, Weingarten, Jeremy A, Wells, J Michael, Westfall, Elizabeth, Lazarus, Stephen C, and Connett, John E

Subjects
Clinical Trials and Supportive Activities, Chronic Obstructive Pulmonary Disease, Lung, Clinical Research, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Respiratory, Adrenergic beta-1 Receptor Antagonists, Aged, Aged, 80 and over, Disease Progression, Female, Forced Expiratory Volume, Hospitalization, Humans, Kaplan-Meier Estimate, Male, Metoprolol, Middle Aged, Prospective Studies, Pulmonary Disease, Chronic Obstructive, Treatment Failure, BLOCK COPD Trial Group, Medical and Health Sciences, General & Internal Medicine
Abstract

BackgroundObservational studies suggest that beta-blockers may reduce the risk of exacerbations and death in patients with moderate or severe chronic obstructive pulmonary disease (COPD), but these findings have not been confirmed in randomized trials.MethodsIn this prospective, randomized trial, we assigned patients between the ages of 40 and 85 years who had COPD to receive either a beta-blocker (extended-release metoprolol) or placebo. All the patients had a clinical history of COPD, along with moderate airflow limitation and an increased risk of exacerbations, as evidenced by a history of exacerbations during the previous year or the prescribed use of supplemental oxygen. We excluded patients who were already taking a beta-blocker or who had an established indication for the use of such drugs. The primary end point was the time until the first exacerbation of COPD during the treatment period, which ranged from 336 to 350 days, depending on the adjusted dose of metoprolol.ResultsA total of 532 patients underwent randomization. The mean (±SD) age of the patients was 65.0±7.8 years; the mean forced expiratory volume in 1 second (FEV1) was 41.1±16.3% of the predicted value. The trial was stopped early because of futility with respect to the primary end point and safety concerns. There was no significant between-group difference in the median time until the first exacerbation, which was 202 days in the metoprolol group and 222 days in the placebo group (hazard ratio for metoprolol vs. placebo, 1.05; 95% confidence interval [CI], 0.84 to 1.32; P = 0.66). Metoprolol was associated with a higher risk of exacerbation leading to hospitalization (hazard ratio, 1.91; 95% CI, 1.29 to 2.83). The frequency of side effects that were possibly related to metoprolol was similar in the two groups, as was the overall rate of nonrespiratory serious adverse events. During the treatment period, there were 11 deaths in the metoprolol group and 5 in the placebo group.ConclusionsAmong patients with moderate or severe COPD who did not have an established indication for beta-blocker use, the time until the first COPD exacerbation was similar in the metoprolol group and the placebo group. Hospitalization for exacerbation was more common among the patients treated with metoprolol. (Funded by the Department of Defense; BLOCK COPD ClinicalTrials.gov number, NCT02587351.).

Published
2019

17. Serum IgG subclass levels and risk of exacerbations and hospitalizations in patients with COPD

Author

Leitao Filho, Fernando Sergio, Ra, Seung Won, Mattman, Andre, Schellenberg, Robert S, Criner, Gerard J, Woodruff, Prescott G, Lazarus, Stephen C, Albert, Richard, Connett, John E, Han, Meilan K, Martinez, Fernando J, Leung, Janice M, Paul Man, SF, Aaron, Shawn D, Reed, Robert M, Sin, Don D, and for the Canadian Respiratory Research Network (CRRN)

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Trials and Supportive Activities, Prevention, Clinical Research, Lung, Chronic Obstructive Pulmonary Disease, Respiratory, Aged, Biomarkers, Double-Blind Method, Female, Hospitalization, Humans, IgG Deficiency, Immunoglobulin G, Male, Middle Aged, Pulmonary Disease, Chronic Obstructive, Retrospective Studies, Risk Factors, IgG, IgG subclass deficiency, COPD, Exacerbation, Canadian Respiratory Research Network, Cardiorespiratory Medicine and Haematology, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract

BackgroundThe literature is scarce regarding the prevalence and clinical impact of IgG subclass deficiency in COPD. We investigated the prevalence of IgG subclass deficiencies and their association with exacerbations and hospitalizations using subjects from two COPD cohorts.MethodsWe measured IgG subclass levels using immunonephelometry in serum samples from participants enrolled in two previous COPD trials: Macrolide Azithromycin for Prevention of Exacerbations of COPD (MACRO; n = 976) and Simvastatin for the Prevention of Exacerbations in Moderate-to-Severe COPD (STATCOPE; n = 653). All samples were collected from clinically stable participants upon entry into both studies. IgG subclass deficiency was diagnosed when IgG subclass levels were below their respective lower limit of normal: IgG1

Published
2018

19. Azithromycin and risk of COPD exacerbations in patients with and without Helicobacter pylori

Author

Ra, Seung Won, Sze, Marc A, Lee, Eun Chong, Tam, Sheena, Oh, Yeni, Fishbane, Nick, Criner, Gerard J, Woodruff, Prescott G, Lazarus, Stephen C, Albert, Richard, Connett, John E, Han, Meilan K, Martinez, Fernando J, Aaron, Shawn D, Reed, Robert M, Man, SF Paul, Sin, Don D, and on behalf of the Canadian Respiratory Research Network

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Research, Lung, Chronic Obstructive Pulmonary Disease, Respiratory, Aged, Anti-Bacterial Agents, Antibodies, Bacterial, Azithromycin, Biomarkers, C-Reactive Protein, Disease Progression, Disease-Free Survival, Female, Helicobacter Infections, Helicobacter pylori, Humans, Kaplan-Meier Estimate, Male, Middle Aged, Proportional Hazards Models, Pulmonary Disease, Chronic Obstructive, Receptors, Tumor Necrosis Factor, Type II, Risk Factors, Serologic Tests, Time Factors, Treatment Outcome, COPD, Exacerbation, Canadian Respiratory Research Network, Cardiorespiratory Medicine and Haematology, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract

BackgroundHelicobacter pylori (HP) infection is associated with reduced lung function and systemic inflammation in chronic obstructive pulmonary disease (COPD) patients. Azithromycin (AZ) is active against HP and reduces the risk of COPD exacerbation. We determined whether HP infection status modifies the effects of AZ in COPD patients.MethodsPlasma samples from 1018 subjects with COPD who participated in the Macrolide Azithromycin (MACRO) in COPD Study were used to determine the HP infection status at baseline and 12 months of follow-up using a serologic assay. Based on HP infection status and randomization to either AZ or placebo (PL), the subjects were divided into 4 groups: HP+/AZ, HP-/AZ, HP+/PL, and HP-/PL. Time to first exacerbation was compared across the 4 groups using Kaplan-Meier survival analysis and a Cox proportional hazards model. The rates of exacerbation were compared using both the Kruskal-Wallis test and negative binomial analysis. Blood biomarkers at enrolment and at follow-up visits 3, 12, and 13 (1 month after treatment was stopped) months were measured.ResultsOne hundred eighty one (17.8%) patients were seropositive to HP. Non-Caucasian participants were nearly three times more likely to be HP seropositive than Caucasian participants (37.4% vs 13.6%; p

Published
2017

20. Effect of beta-blockers on exacerbation rate and lung function in chronic obstructive pulmonary disease (COPD)

Author

Duffy, Sean, Marron, Robert, Voelker, Helen, Albert, Richard, Connett, John, Bailey, William, Casaburi, Richard, Cooper, J Allen, Curtis, Jeffrey L, Dransfield, Mark, Han, MeiLan K, Make, Barry, Marchetti, Nathaniel, Martinez, Fernando, Lazarus, Stephen, Niewoehner, Dennis, Scanlon, Paul D, Sciurba, Frank, Scharf, Steven, Reed, Robert M, Washko, George, Woodruff, Prescott, McEvoy, Charlene, Aaron, Shawn, Sin, Don, Criner, Gerard J, and the NIH COPD Clinical Research Network and the Canadian Institutes of Health Research

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Chronic Obstructive Pulmonary Disease, Clinical Trials and Supportive Activities, Clinical Research, Heart Disease, Lung, Cardiovascular, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Respiratory, Adrenergic beta-Antagonists, Aged, Cohort Studies, Female, Follow-Up Studies, Humans, Male, Middle Aged, Pulmonary Disease, Chronic Obstructive, Respiratory Function Tests, Retrospective Studies, Treatment Outcome, COPD, Exacerbation, Beta-blocker, NIH COPD Clinical Research Network and the Canadian Institutes of Health Research, Cardiorespiratory Medicine and Haematology, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract

BackgroundBeta-blockers are commonly prescribed for patients with cardiovascular disease. Providers have been wary of treating chronic obstructive pulmonary disease (COPD) patients with beta-blockers due to concern for bronchospasm, but retrospective studies have shown that cardio-selective beta-blockers are safe in COPD and possibly beneficial. However, these benefits may reflect symptom improvements due to the cardiac effects of the medication. The purpose of this study is to evaluate associations between beta-blocker use and both exacerbation rates and longitudinal measures of lung function in two well-characterized COPD cohorts.MethodsWe retrospectively analyzed 1219 participants with over 180 days of follow up from the STATCOPE trial, which excluded most cardiac comorbidities, and from the placebo arm of the MACRO trial. Primary endpoints were exacerbation rates per person-year and change in spirometry over time in association with beta blocker use.ResultsOverall 13.9% (170/1219) of participants reported taking beta-blockers at enrollment. We found no statistically significant differences in exacerbation rates with respect to beta-blocker use regardless of the prevalence of cardiac comorbidities. In the MACRO cohort, patients taking beta-blockers had an exacerbation rate of 1.72/person-year versus a rate of 1.71/person-year in patients not taking beta-blockers. In the STATCOPE cohort, patients taking beta-blockers had an exacerbation rate of 1.14/person-year. Patients without beta-blockers had an exacerbation rate of 1.34/person-year. We found no detrimental effect of beta blockers with respect to change in lung function over time.ConclusionWe found no evidence that beta-blocker use was unsafe or associated with worse pulmonary outcomes in study participants with moderate to severe COPD.

Published
2017

25. Serum IgG Levels and Risk of COPD Hospitalization: A Pooled Meta-analysis

Author

Leitao Filho, Fernando Sergio, Mattman, Andre, Schellenberg, Robert, Criner, Gerard J., Woodruff, Prescott, Lazarus, Stephen C., Albert, Richard K., Connett, John, Han, Meilan K., Gay, Steven E., Martinez, Fernando J., Fuhlbrigge, Anne L., Stoller, James K., MacIntyre, Neil R., Casaburi, Richard, Diaz, Philip, Panos, Ralph J., Cooper, J. Allen, Jr., Bailey, William C., LaFon, David C., Sciurba, Frank C., Kanner, Richard E., Yusen, Roger D., Au, David H., Pike, Kenneth C., Fan, Vincent S., Leung, Janice M., Man, Shu-Fan Paul, Aaron, Shawn D., Reed, Robert M., and Sin, Don D.

Published
2020
Full Text
View/download PDF

26. Lobar lung transplantation from deceased donors: A systematic review.

Author

Eberlein, Michael, Reed, Robert M, Chahla, Mayy, Bolukbas, Servet, Blevins, Amy, Van Raemdonck, Dirk, Stanzi, Alessia, Inci, Ilhan, Marasco, Silvana, Shigemura, Norihisa, Aigner, Clemens, and Deuse, Tobias

Subjects
Cadaveric lobar lung transplantation, Lobar lung transplantation from deceased donors, Lung size matching, Primary graft dysfunction, Survival
Abstract

AimTo systematically review reports on deceased-donor-lobar lung transplantation (ddLLTx) and uniformly describe size matching using the donor-to-recipient predicted-total lung-capacity (pTLC) ratio.MethodsWe set out to systematically review reports on ddLLTx and uniformly describe size matching using the donor-to-recipient pTLC ratio and to summarize reported one-year survival data of ddLLTx and conventional-LTx. We searched in PubMed, CINAHL via EBSCO, Cochrane Database of Systematic Reviews via Wiley (CDSR), Database of Abstracts of Reviews of Effects via Wiley (DARE), Cochrane Central Register of Controlled Trials via Wiley (CENTRAL), Scopus (which includes EMBASE abstracts), and Web of Science for original reports on ddLLTx.ResultsNine observational cohort studies reporting on 301 ddLLTx met our inclusion criteria for systematic review of size matching, and eight for describing one-year-survival. The ddLLTx-group was often characterized by high acuity; however there was heterogeneity in transplant indications and pre-operative characteristics between studies. Data to calculate the pTLC ratio was available for 242 ddLLTx (80%). The mean pTLCratio before lobar resection was 1.25 ± 0.3 and the transplanted pTLCratio after lobar resection was 0.76 ± 0.2. One-year survival in the ddLLTx-group ranged from 50%-100%, compared to 72%-88% in the conventional-LTx group. In the largest study ddLLTx (n = 138) was associated with a lower one-year-survival compared to conventional-LTx (n = 539) (65.1% vs 84.1%, P < 0.001).ConclusionFurther investigations of optimal donor-to-recipient size matching parameters for ddLLTx could improve outcomes of this important surgical option.

Published
2017

27. β-Blocker Use and Clinical Outcomes in Patients With COPD Following Acute Myocardial Infarction

Author

LaFon, David C., primary, Helgeson, Erika S., additional, Lindberg, Sarah, additional, Voelker, Helen, additional, Bhatt, Surya P., additional, Casaburi, Richard, additional, Cassady, Steven J., additional, Connett, John, additional, Criner, Gerard J., additional, Hatipoglu, Umur, additional, Kaminsky, David A., additional, Kunisaki, Ken M., additional, Lazarus, Stephen C., additional, McEvoy, Charlene E., additional, Reed, Robert M., additional, Sciurba, Frank C., additional, Stringer, William, additional, and Dransfield, Mark T., additional

Published
2024
Full Text
View/download PDF

45. Associations Between Coronary Artery Calcium Score and Exacerbation Risk in BLOCK-COPD

Author

Wade, R. Chad, primary, Ling, Sharon X., additional, Helgeson, Erika S., additional, Voelker, Helen, additional, Labaki, Wassim W., additional, Meza, Daniel, additional, O’Corragain, Oisin, additional, So, Jennifer Y., additional, Criner, Gerard J., additional, Han, MeiLan K., additional, Kalhan, Ravi, additional, Reed, Robert M., additional, Dransfield, Mark T., additional, and Wells, J. Michael, additional

Published
2023
Full Text
View/download PDF

47. Successful lung transplantation using an allograft from a COVID-19–recovered donor: a potential role for subgenomic RNA to guide organ utilization

Author

Saharia, Kapil K., primary, Ramelli, Sabrina C., additional, Stein, Sydney R., additional, Roder, Allison E., additional, Kreitman, Allie, additional, Banakis, Stephanie, additional, Chung, Joon-Yong, additional, Burbelo, Peter D., additional, Singh, Manmeet, additional, Reed, Robert M., additional, Patel, Vipul, additional, Rabin, Joseph, additional, Krupnick, Alexander S., additional, Cohen, Jeffrey I., additional, de Wit, Emmie, additional, Ghedin, Elodie, additional, Hewitt, Stephen M., additional, Vannella, Kevin M., additional, Chertow, Daniel S., additional, and Grazioli, Alison, additional

Published
2023
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results