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Systemic Corticosteroid Therapy May Delay Viral Clearance in Patients with Middle East Respiratory Syndrome Coronavirus Infection.

Systemic Corticosteroid Therapy May Delay Viral Clearance in Patients with Middle East Respiratory Syndrome Coronavirus Infection.

Am J Respir Crit Care Med. 2017 Dec 11;:

Authors: Hui DS

PMID: 29227752 [PubMed - as supplied by publisher]




Recommendations for a Standardized Pulmonary Function Report. An Official American Thoracic Society Technical Statement.
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Recommendations for a Standardized Pulmonary Function Report. An Official American Thoracic Society Technical Statement.

Am J Respir Crit Care Med. 2017 Dec 01;196(11):1463-1472

Authors: Culver BH, Graham BL, Coates AL, Wanger J, Berry CE, Clarke PK, Hallstrand TS, Hankinson JL, Kaminsky DA, MacIntyre NR, McCormack MC, Rosenfeld M, Stanojevic S, Weiner DJ, ATS Committee on Proficiency Standards for Pulmonary Function Laboratories

Abstract
BACKGROUND: The American Thoracic Society committee on Proficiency Standards for Pulmonary Function Laboratories has recognized the need for a standardized reporting format for pulmonary function tests. Although prior documents have offered guidance on the reporting of test data, there is considerable variability in how these results are presented to end users, leading to potential confusion and miscommunication.
METHODS: A project task force, consisting of the committee as a whole, was approved to develop a new Technical Standard on reporting pulmonary function test results. Three working groups addressed the presentation format, the reference data supporting interpretation of results, and a system for grading quality of test efforts. Each group reviewed relevant literature and wrote drafts that were merged into the final document.
RESULTS: This document presents a reporting format in test-specific units for spirometry, lung volumes, and diffusing capacity that can be assembled into a report appropriate for a laboratory's practice. Recommended reference sources are updated with data for spirometry and diffusing capacity published since prior documents. A grading system is presented to encourage uniformity in the important function of test quality assessment.
CONCLUSIONS: The committee believes that wide adoption of these formats and their underlying principles by equipment manufacturers and pulmonary function laboratories can improve the interpretation, communication, and understanding of test results.

PMID: 29192835 [PubMed - indexed for MEDLINE]




Mepolizumab Attenuates Airway Eosinophil Numbers, but Not Their Functional Phenotype, in Asthma.
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Mepolizumab Attenuates Airway Eosinophil Numbers, but Not Their Functional Phenotype, in Asthma.

Am J Respir Crit Care Med. 2017 Dec 01;196(11):1385-1395

Authors: Kelly EA, Esnault S, Liu LY, Evans MD, Johansson MW, Mathur S, Mosher DF, Denlinger LC, Jarjour NN

Abstract
RATIONALE: Mepolizumab, an IL-5-blocking antibody, reduces exacerbations in patients with severe eosinophilic asthma. Mepolizumab arrests eosinophil maturation; however, the functional phenotype of eosinophils that persist in the blood and airway after administration of IL-5 neutralizing antibodies has not been reported.
OBJECTIVES: To determine the effect of anti-IL-5 antibody on the numbers and phenotypes of allergen-induced circulating and airway eosinophils.
METHODS: Airway inflammation was elicited in participants with mild allergic asthma by segmental allergen challenge before and 1 month after a single intravenous 750-mg dose of mepolizumab. Eosinophils were examined in blood, bronchoalveolar lavage, and endobronchial biopsies 48 hours after challenge.
MEASUREMENTS AND MAIN RESULTS: Segmental challenge without mepolizumab induced a rise in circulating eosinophils, bronchoalveolar lavage eosinophilia, and eosinophil peroxidase deposition in bronchial mucosa. IL-5 neutralization before allergen challenge abolished the allergen-induced rise in circulating eosinophils and expression of IL-3 receptors, whereas airway eosinophilia and eosinophil peroxidase deposition were blunted but not eliminated. Before mepolizumab treatment, bronchoalveolar lavage eosinophils had more surface IL-3 and granulocyte-monocyte colony-stimulating factor receptors, CD69, CD44, and CD23 and decreased IL-5 and eotaxin receptors than blood eosinophils. This activation phenotype indicated by bronchoalveolar lavage eosinophil surface markers, as well as the release of eosinophil peroxidase by eosinophils in the bronchial mucosa, was maintained after mepolizumab.
CONCLUSIONS: Mepolizumab reduced airway eosinophil numbers but had a limited effect on airway eosinophil activation markers, suggesting that these cells retain functionality. This observation may explain why IL-5 neutralization reduces but does not completely eradicate asthma exacerbations. Clinical trial registered with www.clinicaltrials.gov (NCT00802438).

PMID: 28862877 [PubMed - indexed for MEDLINE]




Lung Endothelial MicroRNA-1 Regulates Tumor Growth and Angiogenesis.
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Lung Endothelial MicroRNA-1 Regulates Tumor Growth and Angiogenesis.

Am J Respir Crit Care Med. 2017 Dec 01;196(11):1443-1455

Authors: Korde A, Jin L, Zhang JG, Ramaswamy A, Hu B, Kolahian S, Guardela BJ, Herazo-Maya J, Siegfried JM, Stabile L, Pisani MA, Herbst RS, Kaminski N, Elias JA, Puchalski JT, Takyar SS

Abstract
RATIONALE: Vascular endothelial growth factor down-regulates microRNA-1 (miR-1) in the lung endothelium, and endothelial cells play a critical role in tumor progression and angiogenesis.
OBJECTIVES: To examine the clinical significance of miR-1 in non-small cell lung cancer (NSCLC) and its specific role in tumor endothelium.
METHODS: miR-1 levels were measured by Taqman assay. Endothelial cells were isolated by magnetic sorting. We used vascular endothelial cadherin promoter to create a vascular-specific miR-1 lentiviral vector and an inducible transgenic mouse. KRASG12D mut/Trp53-/- (KP) mice, lung-specific vascular endothelial growth factor transgenic mice, Lewis lung carcinoma xenografts, and primary endothelial cells were used to test the effects of miR-1.
MEASUREMENTS AND MAIN RESULTS: In two cohorts of patients with NSCLC, miR-1 levels were lower in tumors than the cancer-free tissue. Tumor miR-1 levels correlated with the overall survival of patients with NSCLC. miR-1 levels were also lower in endothelial cells isolated from NSCLC tumors and tumor-bearing lungs of KP mouse model. We examined the significance of lower miR-1 levels by testing the effects of vascular-specific miR-1 overexpression. Vector-mediated delivery or transgenic overexpression of miR-1 in endothelial cells decreased tumor burden in KP mice, reduced the growth and vascularity of Lewis lung carcinoma xenografts, and decreased tracheal angiogenesis in vascular endothelial growth factor transgenic mice. In endothelial cells, miR-1 level was regulated through phosphoinositide 3-kinase and specifically controlled proliferation, de novo DNA synthesis, and ERK1/2 activation. Myeloproliferative leukemia oncogene was targeted by miR-1 in the lung endothelium and regulated tumor growth and angiogenesis.
CONCLUSIONS: Endothelial miR-1 is down-regulated in NSCLC tumors and controls tumor progression and angiogenesis.

PMID: 28853613 [PubMed - indexed for MEDLINE]




MicroRNA-542 Promotes Mitochondrial Dysfunction and SMAD Activity and Is Elevated in Intensive Care Unit-acquired Weakness.
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MicroRNA-542 Promotes Mitochondrial Dysfunction and SMAD Activity and Is Elevated in Intensive Care Unit-acquired Weakness.

Am J Respir Crit Care Med. 2017 Dec 01;196(11):1422-1433

Authors: Garros RF, Paul R, Connolly M, Lewis A, Garfield BE, Natanek SA, Bloch S, Mouly V, Griffiths MJ, Polkey MI, Kemp PR

Abstract
RATIONALE: Loss of skeletal muscle mass and function is a common consequence of critical illness and a range of chronic diseases, but the mechanisms by which this occurs are unclear.
OBJECTIVES: To identify microRNAs (miRNAs) that were increased in the quadriceps of patients with muscle wasting and to determine the molecular pathways by which they contributed to muscle dysfunction.
METHODS: miRNA-542-3p/5p (miR-542-3p/5p) were quantified in the quadriceps of patients with chronic obstructive pulmonary disease and intensive care unit-acquired weakness (ICUAW). The effect of miR-542-3p/5p was determined on mitochondrial function and transforming growth factor-β signaling in vitro and in vivo.
MEASUREMENTS AND MAIN RESULTS: miR-542-3p/5p were elevated in patients with chronic obstructive pulmonary disease but more markedly in patients with ICUAW. In vitro, miR-542-3p suppressed the expression of the mitochondrial ribosomal protein MRPS10 and reduced 12S ribosomal RNA (rRNA) expression, suggesting mitochondrial ribosomal stress. miR-542-5p increased nuclear phospho-SMAD2/3 and suppressed expression of SMAD7, SMURF1, and PPP2CA, proteins that inhibit or reduce SMAD2/3 phosphorylation, suggesting that miR-542-5p increased transforming growth factor-β signaling. In mice, miR-542 overexpression caused muscle wasting, and reduced mitochondrial function, 12S rRNA expression, and SMAD7 expression, consistent with the effects of the miRNAs in vitro. Similarly, in patients with ICUAW, the expression of 12S rRNA and of the inhibitors of SMAD2/3 phosphorylation were reduced, indicative of mitochondrial ribosomal stress and increased transforming growth factor-β signaling. In patients undergoing aortic surgery, preoperative levels of miR-542-3p/5p were positively correlated with muscle loss after surgery.
CONCLUSIONS: Elevated miR-542-3p/5p may cause muscle atrophy in intensive care unit patients through the promotion of mitochondrial dysfunction and activation of SMAD2/3 phosphorylation.

PMID: 28809518 [PubMed - indexed for MEDLINE]




Adverse Heart-Lung Interactions in Ventilator-induced Lung Injury.
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Adverse Heart-Lung Interactions in Ventilator-induced Lung Injury.

Am J Respir Crit Care Med. 2017 Dec 01;196(11):1411-1421

Authors: Katira BH, Giesinger RE, Engelberts D, Zabini D, Kornecki A, Otulakowski G, Yoshida T, Kuebler WM, McNamara PJ, Connelly KA, Kavanagh BP

Abstract
RATIONALE: In the original 1974 in vivo study of ventilator-induced lung injury, Webb and Tierney reported that high Vt with zero positive end-expiratory pressure caused overwhelming lung injury, subsequently shown by others to be due to lung shear stress.
OBJECTIVES: To reproduce the lung injury and edema examined in the Webb and Tierney study and to investigate the underlying mechanism thereof.
METHODS: Sprague-Dawley rats weighing approximately 400 g received mechanical ventilation for 60 minutes according to the protocol of Webb and Tierney (airway pressures of 14/0, 30/0, 45/10, 45/0 cm H2O). Additional series of experiments (20 min in duration to ensure all animals survived) were studied to assess permeability (n = 4 per group), echocardiography (n = 4 per group), and right and left ventricular pressure (n = 5 and n = 4 per group, respectively).
MEASUREMENTS AND MAIN RESULTS: The original Webb and Tierney results were replicated in terms of lung/body weight ratio (45/0 > 45/10 ≈ 30/0 ≈ 14/0; P < 0.05) and histology. In 45/0, pulmonary edema was overt and rapid, with survival less than 30 minutes. In 45/0 (but not 45/10), there was an increase in microvascular permeability, cyclical abolition of preload, and progressive dilation of the right ventricle. Although left ventricular end-diastolic pressure decreased in 45/10, it increased in 45/0.
CONCLUSIONS: In a classic model of ventilator-induced lung injury, high peak pressure (and zero positive end-expiratory pressure) causes respiratory swings (obliteration during inspiration) in right ventricular filling and pulmonary perfusion, ultimately resulting in right ventricular failure and dilation. Pulmonary edema was due to increased permeability, which was augmented by a modest (approximately 40%) increase in hydrostatic pressure. The lung injury and acute cor pulmonale is likely due to pulmonary microvascular injury, the mechanism of which is uncertain, but which may be due to cyclic interruption and exaggeration of pulmonary blood flow.

PMID: 28795839 [PubMed - indexed for MEDLINE]




Fifty Years of Research in ARDS. Long-Term Follow-up after Acute Respiratory Distress Syndrome. Insights for Managing Medical Complexity after Critical Illness.
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Fifty Years of Research in ARDS. Long-Term Follow-up after Acute Respiratory Distress Syndrome. Insights for Managing Medical Complexity after Critical Illness.

Am J Respir Crit Care Med. 2017 Dec 01;196(11):1380-1384

Authors: Herridge MS

Abstract
Critical illness is not a discrete disease state or syndrome. It is the culmination of a multiplicity of heterogeneous disease states and their varied health trajectories leading to extreme illness that requires advanced life support in a distinct geographic location in the hospital. It is a marker of newly acquired or worsened medical complexity and multimorbidities. Fifty years ago, distinguished critical care colleagues identified a syndrome of severe lung injury that united a group of patients with disparate admitting diagnoses. Acute respiratory distress syndrome continues to represent an important, incremental insult and risk modifier of acute and longer-term outcome, but it does not solely define our patients or their outcomes in isolation. Over the next 50 years, our research and clinical agenda needs to sharpen our lens on the fundamental importance of our patients' pre-critical illness health status, their intrinsic susceptibilities to tissue injury, and their innate and varied resiliencies. We need to take responsibility for the contribution that we make to morbidity through our practice in the intensive care unit each day. Engagement in frank and transparent communication with our patients and their caregivers about the very real and morbid consequences of being this sick is essential. We must enforce explicit consent about the morbidity of innovative, experimental, or high-risk medical and surgical procedures and ensure that our ongoing level of treatment aligns with patients' and caregivers' goals and values. Interprofessional and multidisciplinary collaboration is crucial to modify existing complex care pathways for our patients and their families to foster optimal rehabilitation and reintegration into the workplace and community.

PMID: 28767270 [PubMed - indexed for MEDLINE]




Effect of Obstructive Sleep Apnea Treatment on Renal Function in Patients with Cardiovascular Disease.
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Effect of Obstructive Sleep Apnea Treatment on Renal Function in Patients with Cardiovascular Disease.

Am J Respir Crit Care Med. 2017 Dec 01;196(11):1456-1462

Authors: Loffler KA, Heeley E, Freed R, Anderson CS, Brockway B, Corbett A, Chang CL, Douglas JA, Ferrier K, Graham N, Hamilton GS, Hlavac M, McArdle N, McLachlan J, Mukherjee S, Naughton MT, Thien F, Young A, Grunstein RR, Palmer LJ, Woodman RJ, Hanly PJ, McEvoy RD, SAVE (Sleep Apnea Cardiovascular Endpoints) Investigators

Abstract
RATIONALE: Obstructive sleep apnea (OSA) is associated with impaired renal function, but uncertainty exists over whether OSA treatment can influence renal outcomes.
OBJECTIVES: To determine the effects of continuous positive airway pressure (CPAP) on renal function in subjects with coexisting OSA and cardiovascular disease.
METHODS: This was a substudy of the international SAVE (Sleep Apnea Cardiovascular Endpoints) trial, in which 2,717 patients with moderate to severe OSA and established coronary or cerebrovascular disease were randomized to receive either CPAP plus usual care or usual care alone. Renal function and adverse renal events were compared between the CPAP (n = 102) and usual care (n = 98) groups. Glomerular filtration rate was estimated at randomization and at the end of follow-up, and the urinary albumin-to-creatinine ratio was measured at study exit.
MEASUREMENTS AND MAIN RESULTS: In 200 substudy participants (mean age, 64 yr; median, 4% oxygen desaturation index; 20 events/h; mean estimated glomerular filtration rate at baseline, 82 ml/min/1.73 m2), the median (interquartile range) changes in estimated glomerular filtration rate (ml/min/1.73 m2/yr) were -1.64 (-3.45 to -0.740) in the CPAP group and -2.30 (-4.53 to -0.71) in the usual care group (P = 0.21) after a median of 4.4 years. There were no between-group differences in end-of-study urinary albumin-to-creatinine ratio or in the occurrence of serious renal or urinary adverse events during the trial. The level of CPAP adherence did not influence the findings.
CONCLUSIONS: CPAP treatment of OSA in patients with cardiovascular disease does not alter renal function or the occurrence of renal adverse events. Clinical trial registered with www.clinicaltrials.gov (NCT00738179).

PMID: 28743190 [PubMed - indexed for MEDLINE]




Signs of Gas Trapping in Normal Lung Density Regions in Smokers.
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Signs of Gas Trapping in Normal Lung Density Regions in Smokers.

Am J Respir Crit Care Med. 2017 Dec 01;196(11):1404-1410

Authors: Bodduluri S, Reinhardt JM, Hoffman EA, Newell JD, Nath H, Dransfield MT, Bhatt SP, COPDGene Investigators

Abstract
RATIONALE: A substantial proportion of subjects without overt airflow obstruction have significant respiratory morbidity and structural abnormalities as visualized by computed tomography. Whether regions of the lung that appear normal using traditional computed tomography criteria have mild disease is not known.
OBJECTIVES: To identify subthreshold structural disease in normal-appearing lung regions in smokers.
METHODS: We analyzed 8,034 subjects with complete inspiratory and expiratory computed tomographic data participating in the COPDGene Study, including 103 lifetime nonsmokers. The ratio of the mean lung density at end expiration (E) to end inspiration (I) was calculated in lung regions with normal density (ND) by traditional thresholds for mild emphysema (-910 Hounsfield units) and gas trapping (-856 Hounsfield units) to derive the ND-E/I ratio. Multivariable regression analysis was used to measure the associations between ND-E/I, lung function, and respiratory morbidity.
MEASUREMENTS AND MAIN RESULTS: The ND-E/I ratio was greater in smokers than in nonsmokers, and it progressively increased from mild to severe chronic obstructive pulmonary disease severity. A proportion of 26.3% of smokers without airflow obstruction had ND-E/I greater than the 90th percentile of normal. ND-E/I was independently associated with FEV1 (adjusted β = -0.020; 95% confidence interval [CI], -0.032 to -0.007; P = 0.001), St. George's Respiratory Questionnaire scores (adjusted β = 0.952; 95% CI, 0.529 to 1.374; P < 0.001), 6-minute-walk distance (adjusted β = -10.412; 95% CI, -12.267 to -8.556; P < 0.001), and body mass index, airflow obstruction, dyspnea, and exercise capacity index (adjusted β = 0.169; 95% CI, 0.148 to 0.190; P < 0.001), and also with FEV1 change at follow-up (adjusted β = -3.013; 95% CI, -4.478 to -1.548; P = 0.001).
CONCLUSIONS: Subthreshold gas trapping representing mild small airway disease is prevalent in normal-appearing lung regions in smokers without airflow obstruction, and it is associated with respiratory morbidity. Clinical trial registered with www.clinicaltrials.gov (NCT00608764).

PMID: 28707983 [PubMed - indexed for MEDLINE]




Prenatal Nitrate Exposure and Childhood Asthma. Influence of Maternal Prenatal Stress and Fetal Sex.
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Prenatal Nitrate Exposure and Childhood Asthma. Influence of Maternal Prenatal Stress and Fetal Sex.

Am J Respir Crit Care Med. 2017 Dec 01;196(11):1396-1403

Authors: Bose S, Chiu YM, Hsu HL, Di Q, Rosa MJ, Lee A, Kloog I, Wilson A, Schwartz J, Wright RO, Cohen S, Coull BA, Wright RJ

Abstract
RATIONALE: Impact of ambient pollution upon children's asthma may differ by sex, and exposure dose and timing. Psychosocial stress can also modify pollutant effects. These associations have not been examined for in utero ambient nitrate exposure.
OBJECTIVES: We implemented Bayesian-distributed lag interaction models to identify sensitive prenatal windows for the influence of nitrate (NO3-) on child asthma, accounting for effect modification by sex and stress.
METHODS: Analyses included 752 mother-child dyads. Daily ambient NO3- exposure during pregnancy was derived using a hybrid chemical transport (Geos-Chem)/land-use regression model and natural log transformed. Prenatal maternal stress was indexed by a negative life events score (high [>2] vs. low [≤2]). The outcome was clinician-diagnosed asthma by age 6 years.
MEASUREMENTS AND MAIN RESULTS: Most mothers were Hispanic (54%) or black (29%), had a high school education or less (66%), never smoked (80%), and reported low prenatal stress (58%); 15% of children developed asthma. BDILMs adjusted for maternal age, race, education, prepregnancy obesity, atopy, and smoking status identified two sensitive windows (7-19 and 33-40 wk gestation), during which increased NO3- was associated with greater odds of asthma, specifically among boys born to mothers reporting high prenatal stress. Cumulative effects of NO3- across pregnancy were also significant in this subgroup (odds ratio = 2.64, 95% confidence interval = 1.27-5.39; per interquartile range increase in ln NO3-).
CONCLUSIONS: Prenatal NO3- exposure during distinct sensitive windows was associated with incident asthma in boys concurrently exposed to high prenatal stress.

PMID: 28661182 [PubMed - indexed for MEDLINE]




High-Attenuation Areas on Chest Computed Tomography and Clinical Respiratory Outcomes in Community-Dwelling Adults.
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High-Attenuation Areas on Chest Computed Tomography and Clinical Respiratory Outcomes in Community-Dwelling Adults.

Am J Respir Crit Care Med. 2017 Dec 01;196(11):1434-1442

Authors: Podolanczuk AJ, Oelsner EC, Barr RG, Bernstein EJ, Hoffman EA, Easthausen IJ, Stukovsky KH, RoyChoudhury A, Michos ED, Raghu G, Kawut SM, Lederer DJ

Abstract
RATIONALE: Areas of increased lung attenuation visualized by computed tomography are associated with all-cause mortality in the general population. It is uncertain whether this association is attributable to interstitial lung disease (ILD).
OBJECTIVES: To determine whether high-attenuation areas are associated with the risk of ILD hospitalization and mortality in the general population.
METHODS: We performed a cohort study of 6,808 adults aged 45-84 years sampled from six communities in the United States. High-attenuation areas were defined as the percentage of imaged lung volume with attenuation values between -600 and -250 Hounsfield units. An adjudication panel determined ILD hospitalization and death.
MEASUREMENTS AND MAIN RESULTS: After adjudication, 52 participants had a diagnosis of ILD during 75,232 person-years (median, 12.2 yr) of follow-up. There were 48 hospitalizations attributable to ILD (crude rate, 6.4 per 10,000 person-years). Twenty participants died as a result of ILD (crude rate, 2.7 per 10,000 person-years). High-attenuation areas were associated with an increased rate of ILD hospitalization (adjusted hazard ratio, 2.6 per 1-SD increment in high-attenuation areas; 95% confidence interval, 1.9-3.5; P < 0.001), a finding that was stronger among men, African Americans, and Hispanics. High-attenuation areas were also associated with an increased rate of ILD-specific death (adjusted hazard ratio, 2.3; 95% confidence interval, 1.7-3.0; P < 0.001). Our findings were consistent among both smokers and nonsmokers.
CONCLUSIONS: Areas of increased lung attenuation are a novel risk factor for ILD hospitalization and mortality. Measurement of high-attenuation areas by screening and diagnostic computed tomography may be warranted in at-risk adults.

PMID: 28613921 [PubMed - indexed for MEDLINE]




How Did Nurses and Physicians Assess Breathlessness? The Devil Is in the Details.
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How Did Nurses and Physicians Assess Breathlessness? The Devil Is in the Details.

Am J Respir Crit Care Med. 2016 06 15;193(12):1439

Authors: Tulaimat A

PMID: 27304249 [PubMed - indexed for MEDLINE]




Reply: Assessment of Intensive Care Unit Patients' Experience of Breathlessness.
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Reply: Assessment of Intensive Care Unit Patients' Experience of Breathlessness.

Am J Respir Crit Care Med. 2016 06 15;193(12):1439-41

Authors: Haugdahl HS, Storli SL, Meland B, Dybwik K, Romild U, Klepstad P

PMID: 27304248 [PubMed - indexed for MEDLINE]




At the Critical Time of Deciding on Extubation, It Is Too Late to Assess Patient Breathlessness.
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At the Critical Time of Deciding on Extubation, It Is Too Late to Assess Patient Breathlessness.

Am J Respir Crit Care Med. 2016 06 15;193(12):1438-9

Authors: Thille AW, Boissier F

PMID: 27304247 [PubMed - indexed for MEDLINE]




Reply: Oral Treprostinil Combination Trials Post Hoc Secondary Analyses: A Step toward Verifying Its Efficacy.
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Reply: Oral Treprostinil Combination Trials Post Hoc Secondary Analyses: A Step toward Verifying Its Efficacy.

Am J Respir Crit Care Med. 2016 06 15;193(12):1437-8

Authors: Fares WH

PMID: 27304246 [PubMed - indexed for MEDLINE]




Novel Analysis of the Oral Treprostinil Combination Therapy Trial Data.
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Novel Analysis of the Oral Treprostinil Combination Therapy Trial Data.

Am J Respir Crit Care Med. 2016 06 15;193(12):1434-6

Authors: White RJ, Rao Y

PMID: 27304245 [PubMed - indexed for MEDLINE]




Diagnosis of Latent Tuberculosis Infection in HIV-infected Pregnant Women. "Baby Steps" toward Better Tuberculosis Control in Pregnancy.
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Diagnosis of Latent Tuberculosis Infection in HIV-infected Pregnant Women. "Baby Steps" toward Better Tuberculosis Control in Pregnancy.

Am J Respir Crit Care Med. 2016 06 15;193(12):1332-3

Authors: Zenner D, Ashkin D

PMID: 27304241 [PubMed - indexed for MEDLINE]




Shear Stress Maladaptation in Pulmonary Arterial Hypertension. An Ageless Concept.
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Shear Stress Maladaptation in Pulmonary Arterial Hypertension. An Ageless Concept.

Am J Respir Crit Care Med. 2016 06 15;193(12):1331-2

Authors: Bonnet S, Provencher S

PMID: 27304240 [PubMed - indexed for MEDLINE]




When Do Coughs and Sneezes Cause Diseases?
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When Do Coughs and Sneezes Cause Diseases?

Am J Respir Crit Care Med. 2016 06 15;193(12):1329-30

Authors: Gordon S, Ferreira DM

PMID: 27304239 [PubMed - indexed for MEDLINE]




Ozone-induced Metabolic Effects in Humans. Ieiunium, Conviviorum, aut Timor? (Fasting, Feasting, or Fear?).
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Ozone-induced Metabolic Effects in Humans. Ieiunium, Conviviorum, aut Timor? (Fasting, Feasting, or Fear?).

Am J Respir Crit Care Med. 2016 06 15;193(12):1327-9

Authors: Rajagopalan S, Brook RD

PMID: 27304238 [PubMed - indexed for MEDLINE]




Critical Illness-related Post-traumatic Stress. An Important Message.
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Critical Illness-related Post-traumatic Stress. An Important Message.

Am J Respir Crit Care Med. 2016 06 15;193(12):1326-7

Authors: Bienvenu OJ

PMID: 27304237 [PubMed - indexed for MEDLINE]




A Cough Is a Cough, Is It Not? Neurophenotypes Define Patients with Chronic Cough.
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A Cough Is a Cough, Is It Not? Neurophenotypes Define Patients with Chronic Cough.

Am J Respir Crit Care Med. 2016 06 15;193(12):1324-6

Authors: Mazzone SB

PMID: 27304236 [PubMed - indexed for MEDLINE]




The Advent of High-Throughput Sequencing Studies of Chronic Obstructive Pulmonary Disease.
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The Advent of High-Throughput Sequencing Studies of Chronic Obstructive Pulmonary Disease.

Am J Respir Crit Care Med. 2016 06 15;193(12):1323-4

Authors: Ortega VE, Celedón JC

PMID: 27304235 [PubMed - indexed for MEDLINE]




Reply: Apneic Oxygenation Has Not Been Disproven.
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Reply: Apneic Oxygenation Has Not Been Disproven.

Am J Respir Crit Care Med. 2016 06 01;193(11):1316-7

Authors: Semler MW, Janz DR, Rice TW

PMID: 27248595 [PubMed - indexed for MEDLINE]




Apneic Oxygenation Has Not Been Disproven.
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Apneic Oxygenation Has Not Been Disproven.

Am J Respir Crit Care Med. 2016 06 01;193(11):1316

Authors: Pavlov I

PMID: 27248594 [PubMed - indexed for MEDLINE]




Reply: Different Definitions of Lung Recruitment by Computed Tomography Scan.
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Reply: Different Definitions of Lung Recruitment by Computed Tomography Scan.

Am J Respir Crit Care Med. 2016 06 01;193(11):1315-6

Authors: Gattinoni L, Carlesso E, Chiumello D, Cressoni M

PMID: 27248593 [PubMed - indexed for MEDLINE]




Different Definitions of Lung Recruitment by Computed Tomography Scan.
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Different Definitions of Lung Recruitment by Computed Tomography Scan.

Am J Respir Crit Care Med. 2016 06 01;193(11):1314-5

Authors: Chen L, Sklar M, Dres M, Goligher EC

PMID: 27248592 [PubMed - indexed for MEDLINE]




Sarcoidosis and T-Helper Cells. Th1, Th17, or Th17.1?
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Sarcoidosis and T-Helper Cells. Th1, Th17, or Th17.1?

Am J Respir Crit Care Med. 2016 06 01;193(11):1198-200

Authors: Georas SN, Chapman TJ, Crouser ED

PMID: 27248588 [PubMed - indexed for MEDLINE]




Nature versus Nurture: Does Genetic Ancestry Alter the Effect of Air Pollution in Children with Asthma?
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Nature versus Nurture: Does Genetic Ancestry Alter the Effect of Air Pollution in Children with Asthma?

Am J Respir Crit Care Med. 2016 06 01;193(11):1196-8

Authors: Sack CS, Goss CH

PMID: 27248587 [PubMed - indexed for MEDLINE]




Clarifying Sepsis Management.
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Clarifying Sepsis Management.

Am J Respir Crit Care Med. 2016 06 01;193(11):1195-6

Authors: Levy MM

PMID: 27248586 [PubMed - indexed for MEDLINE]




Recognizing the Many Faces of Chronic Obstructive Pulmonary Disease.
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Recognizing the Many Faces of Chronic Obstructive Pulmonary Disease.

Am J Respir Crit Care Med. 2016 06 01;193(11):1190-2

Authors: Castaldi PJ, Vachani A

PMID: 27248584 [PubMed - indexed for MEDLINE]




Could Protecting the Immunoproteasome Reduce Exacerbations in Chronic Obstructive Pulmonary Disease?
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Could Protecting the Immunoproteasome Reduce Exacerbations in Chronic Obstructive Pulmonary Disease?

Am J Respir Crit Care Med. 2016 06 01;193(11):1188-90

Authors: Donnelly LE

PMID: 27248583 [PubMed - indexed for MEDLINE]




Can Alveolar Macrophages Made from Stem Cells Achieve Functional Rescue of Lung Diseases?
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Can Alveolar Macrophages Made from Stem Cells Achieve Functional Rescue of Lung Diseases?

Am J Respir Crit Care Med. 2016 06 01;193(11):1187-8

Authors: Jakubzick CV, Warburton D

PMID: 27248582 [PubMed - indexed for MEDLINE]




Reply: The Impact of Septic Liver Dysfunction on Long-Term Mortality Must Not Be Neglected.
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Reply: The Impact of Septic Liver Dysfunction on Long-Term Mortality Must Not Be Neglected.

Am J Respir Crit Care Med. 2016 05 15;193(10):1184

Authors: Nesseler N, Launey Y, Aninat C, White J, Corlu A, Pieper K, Mallédant Y, Seguin P

PMID: 27174485 [PubMed - indexed for MEDLINE]




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