Database : MEDLINE
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[PMID]: 29522352
[Au] Autor:Petersen H; Vazquez Guillamet R; Meek P; Sood A; Tesfaigzi Y
[Ad] Address:Lovelace Respiratory Research Institute, Health and Environmental Epidemiology Program, Albuquerque, New Mexico, United States.
[Ti] Title:Early Endotyping - A Chance for Intervention in COPD.
[So] Source:Am J Respir Cell Mol Biol;, 2018 Mar 09.
[Is] ISSN:1535-4989
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Chronic obstructive pulmonary disease (COPD) is a syndrome that comprises several lung pathologies, but subphenotyping the various disease subtypes has been difficult. One reason may be that current efforts which are focused on studying COPD once it has occurred do not allow to trace back the different origins of disease. This prespective proposes that emphysema originates when susceptible airway, endothelial, and/or hematopoietic cells are exposed to environmental toxins, such as cigarette smoke, biomass fuel, or traffic emissions. These susceptible cell types may initiate different distinct pathobiological mechanisms ("COPD endotypes") that ultimately manifest the emphysematous destruction of the lung. Based on evidence from the "Airway" endotype, we suggest that grading these endotypes by severity may allow to better diagnose disease at early stages when intervention can be designed based on the mechanisms involved. Therefore, genomic, proteomic, and metabolomic studies on at risk patients will be important to identify biomarkers that help designate each endotype. Together with understanding of the involved molecular pathways that lead to disease manifestation, these efforts may provide intervention strategies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1165/rcmb.2018-0002PS

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[PMID]: 29381718
[Au] Autor:Sasaki M; Chubachi S; Kameyama N; Sato M; Haraguchi M; Miyazaki M; Takahashi S; Nakano T; Kuroda Y; Betsuyaku T; Matsuo K
[Ad] Address:Division of Pulmonary Medicine, Keio University School of Medicine, Tokyo, Japan.
[Ti] Title:Effects of long-term cigarette smoke exposure on bone metabolism, structure, and quality in a mouse model of emphysema.
[So] Source:PLoS One;13(1):e0191611, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Smoking is a common risk factor for both chronic obstructive pulmonary disease (COPD) and osteoporosis. In patients with COPD, severe emphysema is a risk factor for vertebral fracture; however, the effects of smoking or emphysema on bone health remain largely unknown. We report bone deterioration in a mouse model of emphysema induced by nose-only cigarette smoke (CS) exposure. Unexpectedly, short-term exposure for 4-weeks decreased bone turnover and increased bone volume in mice. However, prolonged exposure for 20- and 40-weeks reversed the effects from suppression to promotion of bone resorption. This long-term CS exposure increased osteoclast number and impaired bone growth, while it increased bone volume. Strikingly, long-term CS exposure deteriorated bone quality of the lumbar vertebrae as illustrated by disorientation of collagen fibers and the biological apatite c-axis. This animal model may provide a better understanding of the mechanisms underlying the deterioration of bone quality in pulmonary emphysema caused by smoking.
[Mh] MeSH terms primary: Bone and Bones/metabolism
Disease Models, Animal
Emphysema/metabolism
Smoke
Tobacco Products
[Mh] MeSH terms secundary: Animals
Bone Remodeling
Mice
Mice, Inbred C57BL
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Smoke)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180131
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191611

  3 / 27941 MEDLINE  
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[PMID]: 29272750
[Au] Autor:Galibert M; Wartenberg M; Lecaille F; Saidi A; Mavel S; Joulin-Giet A; Korkmaz B; Brömme D; Aucagne V; Delmas AF; Lalmanach G
[Ad] Address:CNRS UPR 4301, Centre de Biophysique Moléculaire, Rue Charles Sadron, Orléans, France.
[Ti] Title:Substrate-derived triazolo- and azapeptides as inhibitors of cathepsins K and S.
[So] Source:Eur J Med Chem;144:201-210, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Cathepsin (Cat) K is a critical bone-resorbing protease and is a relevant target for the treatment of osteoporosis and bone metastasis, while CatS is an attractive target for drugs in autoimmune diseases (e.g. rheumatoid arthritis), emphysema or neuropathic pain. Despite major achievements, current pharmacological inhibitors are still lacking in safety and may have damaging side effects. A promising strategy for developing safer reversible and competitive inhibitors as new lead compounds could be to insert non-cleavable bonds at the scissile P1-P1' position of selective substrates of CatS and CatK. Accordingly, we introduced a 1,4-disubstituted 1,2,3-triazole heterocycle that mimics most of the features of a trans-amide bond, or we incorporated a semicarbazide bond (azaGly residue) by replacing the α-carbon of the glycyl residue at P1 by a nitrogen atom. AzaGly-containing peptidomimetics inhibited powerfully their respective target proteases in the nM range, while triazolopeptides were weaker inhibitors (Ki in the µM range). The selectivity of the azaGly CatS inhibitor (1b) was confirmed by using spleen lysates from wild-type vs CatS-deficient mice. Alternatively, the azaGly bradykinin-derived CatK inhibitor (2b) potently inhibited CatK (Ki = 9 nM) and impaired its kininase activity in vitro. Molecular modeling studies support that the semicarbazide bond of 2b is more favorable than the 1,2,3-triazole linkage of the bradykinin-derived pseudopeptide 2a to preserve an effective affinity towards CatK, its protease target.
[Mh] MeSH terms primary: Cathepsin K/antagonists & inhibitors
Cathepsins/antagonists & inhibitors
Protease Inhibitors/chemistry
Protease Inhibitors/pharmacology
Triazoles/chemistry
Triazoles/pharmacology
[Mh] MeSH terms secundary: Amino Acid Sequence
Animals
Cathepsin K/metabolism
Cathepsins/metabolism
Humans
Mice, Inbred C57BL
Molecular Docking Simulation
Peptides/chemistry
Peptides/pharmacology
Peptidomimetics/chemistry
Peptidomimetics/pharmacology
Structure-Activity Relationship
Substrate Specificity
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Peptides); 0 (Peptidomimetics); 0 (Protease Inhibitors); 0 (Triazoles); EC 3.4.- (Cathepsins); EC 3.4.22.27 (cathepsin S); EC 3.4.22.38 (Cathepsin K)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:171223
[St] Status:MEDLINE

  4 / 27941 MEDLINE  
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[PMID]: 29521765
[Au] Autor:Aubin-Lemay C; Acar P; Alnaif N; Alamri A; Azzi AJ; Cugno S
[Ad] Address:Division of Plastic and Reconstructive Surgery, Montreal Children's Hospital, McGill University, Montreal.
[Ti] Title:An Extremely Rare Cause of Orbital Emphysema in a Child.
[So] Source:J Craniofac Surg;, 2018 Mar 08.
[Is] ISSN:1536-3732
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The authors present a rare case of nontraumatic medial orbital wall fracture in an 11-year-old girl. Fractures of the orbital wall secondary to nose blowing have not been previously described in the pediatric population. The patient reported a history of chronic forceful nose blowing, followed by periorbital swelling after an episode of vigorous nose blowing. Erroneous diagnoses of sinusitis and periorbital cellulitis lead to unnecessary antibiotic treatment. The authors hypothesize that repeated and aggressive nose blowing is analogous to stress fractures, leading to weakening and eventual fracture of the medial orbital wall.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1097/SCS.0000000000004465

  5 / 27941 MEDLINE  
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[PMID]: 29485901
[Au] Autor:Han MK; Tayob N; Murray S; Woodruff PG; Curtis JL; Kim V; Criner G; Galban CJ; Ross BD; Hoffman EA; Lynch DA; Kazerooni E; Martinez FJ; COPDGene and SPIROMICS Investigators
[Ad] Address:University of Michigan, Pulmonary & Critical Care, Ann Arbor, Michigan, United States ; mrking@umich.edu.
[Ti] Title:Association between Emphysema and COPD Outcomes in COPDGene and SPIROMICS Cohorts.
[So] Source:Am J Respir Crit Care Med;, 2018 Feb 27.
[Is] ISSN:1535-4970
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1164/rccm.201801-0051LE

  6 / 27941 MEDLINE  
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[PMID]: 29415880
[Au] Autor:Houssaini A; Breau M; Kebe K; Abid S; Marcos E; Lipskaia L; Rideau D; Parpaleix A; Huang J; Amsellem V; Vienney N; Validire P; Maitre B; Attwe A; Lukas C; Vindrieux D; Boczkowski J; Derumeaux G; Pende M; Bernard D; Meiners S; Adnot S
[Ad] Address:INSERM U955, Département de Physiologie-Explorations Fonctionnelles, and DHU A-TVB Hôpital Henri Mondor, AP-HP, Créteil, France.
[Ti] Title:mTOR pathway activation drives lung cell senescence and emphysema.
[So] Source:JCI Insight;3(3), 2018 Feb 08.
[Is] ISSN:2379-3708
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Chronic obstructive pulmonary disease (COPD) is a highly prevalent and devastating condition for which no curative treatment is available. Exaggerated lung cell senescence may be a major pathogenic factor. Here, we investigated the potential role for mTOR signaling in lung cell senescence and alterations in COPD using lung tissue and derived cultured cells from patients with COPD and from age- and sex-matched control smokers. Cell senescence in COPD was linked to mTOR activation, and mTOR inhibition by low-dose rapamycin prevented cell senescence and inhibited the proinflammatory senescence-associated secretory phenotype. To explore whether mTOR activation was a causal pathogenic factor, we developed transgenic mice exhibiting mTOR overactivity in lung vascular cells or alveolar epithelial cells. In this model, mTOR activation was sufficient to induce lung cell senescence and to mimic COPD lung alterations, with the rapid development of lung emphysema, pulmonary hypertension, and inflammation. These findings support a causal relationship between mTOR activation, lung cell senescence, and lung alterations in COPD, thereby identifying the mTOR pathway as a potentially new therapeutic target in COPD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  7 / 27941 MEDLINE  
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[PMID]: 29411159
[Au] Autor:Maeda R; Funasaki A; Motono N; Sekimura A; Usuda K; Uramoto H
[Ad] Address:Department of Thoracic and Breast Surgery, Faculty of Medicine, University of Miyazaki, Kihara 5200, Kiyotake, Miyazaki, 889-1692, Japan. ryo_maeda@med.miyazaki-u.ac.jp.
[Ti] Title:Combined pulmonary fibrosis and emphysema predicts recurrence following surgery in patients with stage I non-small cell lung cancer.
[So] Source:Med Oncol;35(3):31, 2018 Feb 06.
[Is] ISSN:1559-131X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The purpose of this study was to clarify the clinicopathologic characteristics of non-small cell lung cancer (NSCLC) patients with combined pulmonary fibrosis and emphysema (CPFE). We investigated the association between CPFE, the cancer survival, and the pathological features of clinical stage I NSCLC patients. Between 2005 and 2014, 218 consecutive patients with clinical stage I NSCLC underwent complete resection with systematic lymph node dissection. A univariate analysis by log-rank tests was performed to determine the risk factors for recurrence, and the Cox proportional hazards regression model was used to identify potential independent predictors. The 5-year recurrence-free proportion of patients with CPFE was 36%, which was significantly lower than in those without CPFE (82%; p < 0.001). On multivariate analysis, the presence of CPFE was one of the statistically significant independent predictors for tumor recurrence (p = 0.005). Postoperative pathological prognostic factors, including moderate or poor histological differentiation, lymphatic permeation, intratumoral vascular invasion, and lymph node metastasis, were detected more often in patients with CPFE. NSCLC patients with CPFE have histologically more invasive tumors than those without CPFE. In patients with clinical stage I NSCLC, the presence of CPFE was a statistically significant predictor of recurrence.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.1007/s12032-018-1091-x

  8 / 27941 MEDLINE  
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[PMID]: 29298081
[Au] Autor:Copeland CR; Nath H; Terry NLJ; Wilson CG; Kim YI; Lynch DA; Bodduluri S; Wells JM; Dransfield MT; Díaz AA; Washko GR; Foreman MG; Bhatt SP; Genetic Epidemiology of COPD (COPDGene) Investigators
[Ad] Address:University of Alabama at Birmingham, Pulmonary, Allergy and Critical Care Medicine, Birmingham, Alabama, United States ; crutherford@uabmc.edu.
[Ti] Title:Paratracheal Paraseptal Emphysema and Expiratory Central Airway Collapse in Smokers.
[So] Source:Ann Am Thorac Soc;, 2018 Jan 03.
[Is] ISSN:2325-6621
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: Expiratory central airway collapse (ECAC) is associated with respiratory morbidity independent of underlying lung disease. However, not all smokers develop ECAC and the etiology of ECAC in adult smokers is unclear. Paraseptal emphysema in the paratracheal location, by untethering airway walls, may predispose smokers to developing ECAC. OBJECTIVE: To evaluate whether paratracheal paraseptal emphysema (paratracheal PSE) is associated with ECAC. METHODS: We analyzed paired inspiratory and expiratory computed tomography scans from participants enrolled in a multicenter study (COPDGene) of smokers aged 45-80 years. ECAC was defined as >50% reduction in cross sectional area of the trachea during expiration. In a nested case-control design, participants with and without ECAC were included in a 1:2 fashion, and inspiratory scans were further analyzed using the Fleischner Society criteria for presence of centrilobular emphysema, paraseptal emphysema, airway wall thickening, and paratracheal PSE (maximal diameter > 0.5 cm). RESULTS: 1320 patients were included, 440 with and 880 without ECAC. Those with ECAC were older, had higher BMI, and were less likely to be male or current smokers. Paratracheal PSE was more frequent in those with ECAC than controls (16.6% vs. 11.8%; p=0.016), and after adjustment for age, race, sex, body-mass-index, smoking pack-years, and FEV1, paratracheal PSE was independently associated with ECAC (adjusted OR 1.53, 95%CI 1.18 to 1.98; p=0.001). Further, increasing size of paratracheal PSE (maximal diameter of at least 1 cm and 1.5 cm) was associated with greater odds of ECAC (adjusted OR 1.63, 95%CI 1.18 to 2.25; p=0.003 and 1.77, 95%CI 1.19 to 2.64; p=0.005, respectively). CONCLUSION: Paraseptal emphysema adjacent to the trachea is associated with ECAC. The identification of this risk factor on inspiratory scans should prompt further evaluation for ECAC. Clinical trial registered with ClinicalTrials.gov (NCT00608764).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Cl] Clinical Trial:ClinicalTrial
[St] Status:Publisher
[do] DOI:10.1513/AnnalsATS.201709-713OC

  9 / 27941 MEDLINE  
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[PMID]: 29294041
[Au] Autor:Moya CM; Zaballos MA; Garzón L; Luna C; Simón R; Yaffe MB; Gallego E; Santisteban P; Moreno JC
[Ad] Address:Thyroid Molecular Laboratory, Institute for Medical and Molecular Genetics, La Paz University Hospital, Madrid, Spain.
[Ti] Title:TAZ/WWTR1 Mediates the Pulmonary Effects of NKX2-1 Mutations in Brain-Lung-Thyroid Syndrome.
[So] Source:J Clin Endocrinol Metab;103(3):839-852, 2018 Mar 01.
[Is] ISSN:1945-7197
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Context: Identification of a frameshift heterozygous mutation in the transcription factor NKX2-1 in a patient with brain-lung-thyroid syndrome (BLTS) and life-threatening lung emphysema. Objective: To study the genetic defect that causes this complex phenotype and dissect the molecular mechanism underlying this syndrome through functional analysis. Methods: Mutational study by DNA sequencing, generation of expression vectors, site-directed mutagenesis, protein-DNA-binding assays, luciferase reporter gene assays, confocal microscopy, coimmunoprecipitation, and bioinformatics analysis. Results: We identified a mutation [p.(Val75Glyfs*334)] in the amino-terminal domain of the NKX2-1 gene, which was functionally compared with a previously identified mutation [p.(Ala276Argfs*75)] in the carboxy-terminal domain in other patients with BLTS but without signs of respiratory distress. Both mutations showed similar protein expression profiles, subcellular localization, and deleterious effects on thyroid-, brain-, and lung-specific promoter activity. Coexpression of the coactivator TAZ/WWTR1 (transcriptional coactivator with PDZ-binding motif/WW domain-containing transcription regulator protein 1) restored the transactivation properties of p.(Ala276Argfs*75) but not p.(Val75Glyfs*334) NKX2-1 on a lung-specific promoter, although both NKX2-1 mutants could interact equally with TAZ/WWTR1. The retention of residual transcriptional activity in the carboxy-terminal mutant, which was absent in the amino-terminal mutant, allowed the functional rescue by TAZ/WWTR1. Conclusions: Our results support a mechanistic model involving TAZ/WWTR1 in the development of human congenital emphysema, suggesting that this protein could be a transcriptional modifier of the lung phenotype in BLTS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1210/jc.2017-01241

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[PMID]: 29197547
[Au] Autor:Gelb AF; Yamamoto A; Verbeken EK; Schein MJ; Moridzadeh R; Tran D; Fraser C; Barbers R; Elatre W; Koss MN; Glassy EF; Nadel JA
[Ad] Address:Pulmonary Division, Department of Medicine, Lakewood Regional Medical Center (LRMC), Lakewood, CA; Geffen School of Medicine at UCLA Medical Center, Los Angeles, CA. Electronic address: afgelb@msn.com.
[Ti] Title:Further Studies of Unsuspected Emphysema in Nonsmoking Patients With Asthma With Persistent Expiratory Airflow Obstruction.
[So] Source:Chest;153(3):618-629, 2018 Mar.
[Is] ISSN:1931-3543
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Previously, we and other investigators have described reversible loss of lung elastic recoil in patients with acute and persistent, moderate-to-severe, chronic, treated asthma who never smoked, and its adverse effect on maximal expiratory airflow. In four consecutive autopsies, we reported the pathophysiologic mechanism(s) has been unsuspected mild, diffuse, middle and upper lobe centrilobular emphysema. METHODS: We performed prospective studies (5 to 22 years) in 25 patients (12 female) with chronic asthma, age 55 ± 15 years, who never smoked, with persistent moderate-to-severe expiratory obstruction. Studies included measuring blood eosinophils, IgE, total exhaled nitric oxide (NO), central airway NO flux, peripheral airway/alveolar NO concentration, impulse oscillometry, heliox curves, lung elastic recoil, and high-resolution thin-section (1 mm) lung CT imaging at full inspiration with voxel quantification. RESULTS: In 25 patients with stable asthma with varying type 2 phenotype, after 270 µg of aerosolized albuterol sulfate had been administered with a metered dose inhaler with space chamber, FVC was 3.1 ± 1.0 L (83% ± 13% predicted) (mean ± SD), FEV was 1.8 ± 0.6 L (59% ± 11%), the FEV /FVC ratio was 59% ± 10%, and the ratio of single-breath diffusing capacity of the lung for carbon monoxide to alveolar volume was 4.8 ± 1.1 mL/min/mm Hg/L (120% ± 26%). All 25 patients with asthma had loss of static lung elastic recoil pressure, which contributed equally to decreased intrinsic airway conductance in limiting expiratory airflow. Lung CT scanning detected none or mild emphysema. In all four autopsied asthmatic lungs previously reported and one unreported explanted lung, microscopy revealed unsuspected mild, diffuse centrilobular emphysema in the upper and middle lung fields, and asthma-related remodeling in airways. In eight cases, during asthma remission, there were increases in measured static lung elastic recoil pressure-calculated intrinsic airway conductance, and measured maximal expiratory airflow at effort-independent lung volumes. CONCLUSIONS: As documented now in five cases, unsuspected microscopic mild centrilobular emphysema is the sentinel cause of loss of lung elastic recoil. This contributes significantly to expiratory airflow obstruction in never-smoking patients with asthma, with normal diffusing capacity and near-normal lung CT scan results. TRIAL REGISTRY: Protocol No. 20070934 and Study No. 1090472, Western Institutional Review Board, Olympia, WA; ClinicalTrials.gov; No. NCT00576069; URL: www.clinicaltrials.gov.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Cl] Clinical Trial:ClinicalTrial
[St] Status:In-Data-Review


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