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Novel Airway and Ventilator Management of Tracheobronchial Disruption After Blunt Trauma.
Mehdiratta N, Archer M, Stewart M, Dennis B, Grogan E
(2017) Ann Thorac Surg 104: e359-e361
MeSH Terms: Accidents, Traffic, Bronchi, Bronchoscopy, Combined Modality Therapy, Female, Follow-Up Studies, Humans, Injury Severity Score, Middle Aged, Multiple Trauma, Positive-Pressure Respiration, Radiography, Thoracic, Risk Assessment, Thoracic Injuries, Trachea, Trauma Centers, Treatment Outcome, Wounds, Nonpenetrating
Show Abstract · Added February 3, 2018
Tracheobronchial injuries can be difficult to diagnose and manage, especially in the presence of polytrauma. A 50-year-old woman presented as a Level I trauma activation after being struck by a motor vehicle. Initial evaluation demonstrated intracranial hemorrhage and multiple chest injuries, including multilevel bilateral rib fractures, pneumomediastinum, and concern for tracheobronchial injury. After initial stabilization, bronchoscopy was performed and demonstrated an injury to the carina. We report a novel airway and ventilation strategy in the setting of concomitant tracheobronchial injury after severe blunt chest trauma in which extracorporeal support is contraindicated.
Copyright © 2017 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.
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18 MeSH Terms
Beta-blockers and Traumatic Brain Injury: A Systematic Review, Meta-analysis, and Eastern Association for the Surgery of Trauma Guideline.
Alali AS, Mukherjee K, McCredie VA, Golan E, Shah PS, Bardes JM, Hamblin SE, Haut ER, Jackson JC, Khwaja K, Patel NJ, Raj SR, Wilson LD, Nathens AB, Patel MB
(2017) Ann Surg 266: 952-961
MeSH Terms: Adrenergic beta-Antagonists, Brain Injuries, Bronchial Spasm, Cardiovascular Diseases, Hospital Mortality, Humans, Quality of Life, Treatment Outcome
Show Abstract · Added June 26, 2018
OBJECTIVE - To determine if beta-(β)-blockers improve outcomes after acute traumatic brain injury (TBI).
BACKGROUND - There have been no new inpatient pharmacologic therapies to improve TBI outcomes in a half-century. Treatment of TBI patients with β-blockers offers a potentially beneficial approach.
METHODS - Using MEDLINE, EMBASE, and CENTRAL databases, eligible articles for our systematic review and meta-analysis (PROSPERO CRD42016048547) included adult (age ≥ 16 years) blunt trauma patients admitted with TBI. The exposure of interest was β-blocker administration initiated during the hospitalization. Outcomes were mortality, functional measures, quality of life, cardiopulmonary morbidity (e.g., hypotension, bradycardia, bronchospasm, and/or congestive heart failure). Data were analyzed using a random-effects model, and represented by pooled odds ratio (OR) with 95% confidence intervals (CI) and statistical heterogeneity (I).
RESULTS - Data were extracted from 9 included studies encompassing 2005 unique TBI patients with β-blocker treatment and 6240 unique controls. Exposure to β-blockers after TBI was associated with a reduction of in-hospital mortality (pooled OR 0.39, 95% CI: 0.27-0.56; I = 65%, P < 0.00001). None of the included studies examined functional outcome or quality of life measures, and cardiopulmonary adverse events were rarely reported. No clear evidence of reporting bias was identified.
CONCLUSIONS - In adults with acute TBI, observational studies reveal a significant mortality advantage with β-blockers; however, quality of evidence is very low. We conditionally recommend the use of in-hospital β-blockers. However, we recommend further high-quality trials to answer questions about the mechanisms of action, effectiveness on subgroups, dose-response, length of therapy, functional outcome, and quality of life after β-blocker use for TBI.
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MeSH Terms
The impact of temperature and relative humidity on spatiotemporal patterns of infant bronchiolitis epidemics in the contiguous United States.
Sloan C, Heaton M, Kang S, Berrett C, Wu P, Gebretsadik T, Sicignano N, Evans A, Lee R, Hartert T
(2017) Health Place 45: 46-54
MeSH Terms: Bronchiolitis, Epidemics, Humans, Humidity, Infant, Infant, Newborn, Respiratory Syncytial Virus, Human, Seasons, Spatial Analysis, Temperature, Time Factors, United States
Show Abstract · Added March 14, 2018
Infant bronchiolitis is primarily due to infection by respiratory syncytial virus (RSV), which is highly seasonal. The goal of the study is to understand how circulation of RSV is impacted by fluctuations in temperature and humidity in order to inform prevention efforts. Using data from the Military Health System (MHS) Data Repository (MDR), we calculated rates of infant bronchiolitis for the contiguous US from July 2004 to June 2013. Monthly temperature and relative humidity were extracted from the National Climate Data Center. Using a spatiotemporal generalized linear model for binomial data, we estimated bronchiolitis rates and the effects of temperature and relative humidity while allowing them to vary over location and time. Our results indicate a seasonal pattern that begins in the Southeast during November or December, then spreading in a Northwest direction. The relationships of temperature and humidity were spatially heterogeneous, and we find that climate can partially account for early onset or longer epidemic duration. Small changes in climate may be associated with larger fluctuations in epidemic duration.
Copyright © 2017 Elsevier Ltd. All rights reserved.
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12 MeSH Terms
The airway epithelium undergoes metabolic reprogramming in individuals at high risk for lung cancer.
Rahman SMJ, Ji X, Zimmerman LJ, Li M, Harris BK, Hoeksema MD, Trenary IA, Zou Y, Qian J, Slebos RJ, Beane J, Spira A, Shyr Y, Eisenberg R, Liebler DC, Young JD, Massion PP
(2016) JCI Insight 1: e88814
MeSH Terms: Bronchi, Cell Line, Epithelial Cells, Gene Expression Profiling, Humans, Lipid Metabolism, Lung Neoplasms, Metabolomics, Proteome, Respiratory Mucosa, Smoke, Smoking
Show Abstract · Added April 27, 2017
The molecular determinants of lung cancer risk remain largely unknown. Airway epithelial cells are prone to assault by risk factors and are considered to be the primary cell type involved in the field of cancerization. To investigate risk-associated changes in the bronchial epithelium proteome that may offer new insights into the molecular pathogenesis of lung cancer, proteins were identified in the airway epithelial cells of bronchial brushing specimens from risk-stratified individuals by shotgun proteomics. Differential expression of selected proteins was validated by parallel reaction monitoring mass spectrometry in an independent set of individual bronchial brushings. We identified 2,869 proteins, of which 312 proteins demonstrated a trend in expression. Pathway analysis revealed enrichment of carbohydrate metabolic enzymes in high-risk individuals. Glucose consumption and lactate production were increased in human bronchial epithelial BEAS2B cells treated with cigarette smoke condensate for 7 months. Increased lipid biosynthetic capacity and net reductive carboxylation were revealed by metabolic flux analyses of [U-C] glutamine in this in vitro model, suggesting profound metabolic reprogramming in the airway epithelium of high-risk individuals. These results provide a rationale for the development of potentially new chemopreventive strategies and selection of patients for surveillance programs.
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12 MeSH Terms
The intersection between asthma and acute chest syndrome in children with sickle-cell anaemia.
DeBaun MR, Strunk RC
(2016) Lancet 387: 2545-53
MeSH Terms: Acute Chest Syndrome, Adolescent, Age Distribution, Anemia, Sickle Cell, Anti-Bacterial Agents, Asthma, Bronchial Hyperreactivity, Child, Child, Preschool, Female, Humans, Infant, Infant, Newborn, Male, Risk Factors, Young Adult
Show Abstract · Added July 20, 2016
Acute chest syndrome is a frequent cause of acute lung disease in children with sickle-cell disease. Asthma is common in children with sickle-cell disease and is associated with increased incidence of vaso-occlusive pain events, acute chest syndrome episodes, and earlier death. Risk factors for asthma exacerbation and an acute chest syndrome episode are similar, and both can present with shortness of breath, chest pain, cough, and wheezing. Despite overlapping risk factors and symptoms, an acute exacerbation of asthma or an episode of acute chest syndrome are two distinct entities that need disease-specific management strategies. Although understanding has increased about asthma as a comorbidity in sickle-cell disease and its effects on morbidity, substantial gaps remain in knowledge about best management.
Copyright © 2016 Elsevier Ltd. All rights reserved.
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16 MeSH Terms
Transbronchial Cryobiopsy Can Diagnose Constrictive Bronchiolitis in Veterans of Recent Conflicts in the Middle East.
Lentz RJ, Fessel JP, Johnson JE, Maldonado F, Miller RF, Rickman OB
(2016) Am J Respir Crit Care Med 193: 806-8
MeSH Terms: Adult, Afghan Campaign 2001-, Biopsy, Bronchiolitis Obliterans, Bronchoscopy, Cryosurgery, Humans, Iraq War, 2003-2011, Male, Middle Aged, Retrospective Studies, Veterans Health
Added April 25, 2016
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12 MeSH Terms
p73 Is Required for Multiciliogenesis and Regulates the Foxj1-Associated Gene Network.
Marshall CB, Mays DJ, Beeler JS, Rosenbluth JM, Boyd KL, Santos Guasch GL, Shaver TM, Tang LJ, Liu Q, Shyr Y, Venters BJ, Magnuson MA, Pietenpol JA
(2016) Cell Rep 14: 2289-300
MeSH Terms: Animals, Bronchioles, Cell Differentiation, Cells, Cultured, Cilia, Epithelial Cells, Epithelium, Female, Forkhead Transcription Factors, Gene Regulatory Networks, Lung, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Phosphoproteins, RNA Interference, Sequence Analysis, RNA, Trachea, Trans-Activators, Transcriptome, Tumor Protein p73
Show Abstract · Added March 17, 2016
We report that p73 is expressed in multiciliated cells (MCCs), is required for MCC differentiation, and directly regulates transcriptional modulators of multiciliogenesis. Loss of ciliary biogenesis provides a unifying mechanism for many phenotypes observed in p73 knockout mice including hydrocephalus; hippocampal dysgenesis; sterility; and chronic inflammation/infection of lung, middle ear, and sinus. Through p73 and p63 ChIP-seq using murine tracheal cells, we identified over 100 putative p73 target genes that regulate MCC differentiation and homeostasis. We validated Foxj1, a transcriptional regulator of multiciliogenesis, and many other cilia-associated genes as direct target genes of p73 and p63. We show p73 and p63 are co-expressed in a subset of basal cells and suggest that p73 marks these cells for MCC differentiation. In summary, p73 is essential for MCC differentiation, functions as a critical regulator of a transcriptome required for MCC differentiation, and, like p63, has an essential role in development of tissues.
Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.
3 Communities
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23 MeSH Terms
Lung cancer risk test trial: study design, participant baseline characteristics, bronchoscopy safety, and establishment of a biospecimen repository.
Crawford EL, Levin A, Safi F, Lu M, Baugh A, Zhang X, Yeo J, Khuder SA, Boulos AM, Nana-Sinkam P, Massion PP, Arenberg DA, Midthun D, Mazzone PJ, Nathan SD, Wainz R, Silvestri G, Tita J, Willey JC
(2016) BMC Pulm Med 16: 16
MeSH Terms: Aged, Aged, 80 and over, Agriculture, Asbestos, Biological Specimen Banks, Bronchi, Bronchoscopy, Cohort Studies, Early Detection of Cancer, Epithelial Cells, Female, Forced Expiratory Volume, Genetic Predisposition to Disease, Humans, Incidence, Lung Diseases, Obstructive, Lung Neoplasms, Male, Middle Aged, Occupational Exposure, Prospective Studies, Respiratory Mucosa, Risk Assessment, Smoking, Tomography, Spiral Computed, Vital Capacity
Show Abstract · Added February 16, 2016
BACKGROUND - The Lung Cancer Risk Test (LCRT) trial is a prospective cohort study comparing lung cancer incidence among persons with a positive or negative value for the LCRT, a 15 gene test measured in normal bronchial epithelial cells (NBEC). The purpose of this article is to describe the study design, primary endpoint, and safety; baseline characteristics of enrolled individuals; and establishment of a bio-specimen repository.
METHODS/DESIGN - Eligible participants were aged 50-90 years, current or former smokers with 20 pack-years or more cigarette smoking history, free of lung cancer, and willing to undergo bronchoscopic brush biopsy for NBEC sample collection. NBEC, peripheral blood samples, baseline CT, and medical and demographic data were collected from each subject.
DISCUSSION - Over a two-year span (2010-2012), 403 subjects were enrolled at 12 sites. At baseline 384 subjects remained in study and mean age and smoking history were 62.9 years and 50.4 pack-years respectively, with 34% current smokers. Obstructive lung disease (FEV1/FVC <0.7) was present in 157 (54%). No severe adverse events were associated with bronchoscopic brushing. An NBEC and matched peripheral blood bio-specimen repository was established. The demographic composition of the enrolled group is representative of the population for which the LCRT is intended. Specifically, based on baseline population characteristics we expect lung cancer incidence in this cohort to be representative of the population eligible for low-dose Computed Tomography (LDCT) lung cancer screening. Collection of NBEC by bronchial brush biopsy/bronchoscopy was safe and well-tolerated in this population. These findings support the feasibility of testing LCRT clinical utility in this prospective study. If validated, the LCRT has the potential to significantly narrow the population of individuals requiring annual low-dose helical CT screening for early detection of lung cancer and delay the onset of screening for individuals with results indicating low lung cancer risk. For these individuals, the small risk incurred by undergoing once in a lifetime bronchoscopic sample collection for LCRT may be offset by a reduction in their CT-related risks. The LCRT biospecimen repository will enable additional studies of genetic basis for COPD and/or lung cancer risk.
TRIAL REGISTRATION - The LCRT Study, NCT 01130285, was registered with Clinicaltrials.gov on May 24, 2010.
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26 MeSH Terms
Human Metapneumovirus Is Capable of Entering Cells by Fusion with Endosomal Membranes.
Cox RG, Mainou BA, Johnson M, Hastings AK, Schuster JE, Dermody TS, Williams JV
(2015) PLoS Pathog 11: e1005303
MeSH Terms: Bronchi, Cell Line, Endosomes, Flow Cytometry, Humans, Metapneumovirus, Microscopy, Confocal, Paramyxoviridae Infections, RNA, Small Interfering, Respiratory Mucosa, Transfection, Viral Fusion Proteins, Virus Internalization
Show Abstract · Added February 4, 2016
Human metapneumovirus (HMPV), a member of the Paramyxoviridae family, is a leading cause of lower respiratory illness. Although receptor binding is thought to initiate fusion at the plasma membrane for paramyxoviruses, the entry mechanism for HMPV is largely uncharacterized. Here we sought to determine whether HMPV initiates fusion at the plasma membrane or following internalization. To study the HMPV entry process in human bronchial epithelial (BEAS-2B) cells, we used fluorescence microscopy, an R18-dequenching fusion assay, and developed a quantitative, fluorescence microscopy assay to follow virus binding, internalization, membrane fusion, and visualize the cellular site of HMPV fusion. We found that HMPV particles are internalized into human bronchial epithelial cells before fusing with endosomes. Using chemical inhibitors and RNA interference, we determined that HMPV particles are internalized via clathrin-mediated endocytosis in a dynamin-dependent manner. HMPV fusion and productive infection are promoted by RGD-binding integrin engagement, internalization, actin polymerization, and dynamin. Further, HMPV fusion is pH-independent, although infection with rare strains is modestly inhibited by RNA interference or chemical inhibition of endosomal acidification. Thus, HMPV can enter via endocytosis, but the viral fusion machinery is not triggered by low pH. Together, our results indicate that HMPV is capable of entering host cells by multiple pathways, including membrane fusion from endosomal compartments.
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13 MeSH Terms
Highly differentiated human airway epithelial cells: a model to study host cell-parasite interactions in pertussis.
Guevara C, Zhang C, Gaddy JA, Iqbal J, Guerra J, Greenberg DP, Decker MD, Carbonetti N, Starner TD, McCray PB, Mooi FR, Gómez-Duarte OG
(2016) Infect Dis (Lond) 48: 177-88
MeSH Terms: Animals, Antigens, Bacterial, Bacterial Adhesion, Bordetella pertussis, Bronchi, Epithelial Cells, Fimbriae Proteins, Host-Pathogen Interactions, Humans, Mice, Models, Biological, Primary Cell Culture, Respiratory Mucosa, Virulence Factors, Bordetella, Whooping Cough
Show Abstract · Added April 26, 2017
BACKGROUND - Bordetella pertussis colonizes the human respiratory mucosa. Most studies on B. pertussis adherence have relied on cultured mammalian cells that lack key features present in differentiated human airway cells or on animal models that are not natural hosts of B. pertussis. The objectives of this work were to evaluate B. pertussis infection in highly differentiated human airway cells in vitro and to show the role of B. pertussis fimbriae in cell adherence.
METHODS - Primary human airway epithelial (PHAE) cells from human bronchi and a human bronchial epithelial (HBE) cell line were grown in vitro under air-liquid interface conditions.
RESULTS - PHAE and HBE cells infected with B. pertussis wild-type strain revealed bacterial adherence to the apical surface of cells, bacteria-induced cytoskeleton changes, and cell detachment. Mutations in the major fimbrial subunits Fim2/3 or in the minor fimbrial adhesin subunit FimD affected B. pertussis adherence to predominantly HBE cells. This cell model recapitulates the morphologic features of the human airway infected by B. pertussis and confirms the role of fimbriae in B. pertussis adherence. Furthermore, HBE cells show that fimbrial subunits, and specifically FimD adhesin, are critical in B. pertussis adherence to airway cells.
CONCLUSIONS - The relevance of this model to study host-parasite interaction in pertussis lies in the striking physiologic and morphologic similarity between the PHAE and HBE cells and the human airway ciliated and goblet cells in vivo. These cells can proliferate in vitro, differentiate, and express the same genetic profile as human respiratory cells in vivo.
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15 MeSH Terms