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1

Manipulation of acute inflammatory lung disease  

Microsoft Academic Search

Inflammatory lung disease to innocuous antigens or infectious pathogens is a common occurrence and in some cases, life threatening. Often, the inflammatory infiltrate that accompanies these events contributes to pathology by deleterious effects on otherwise healthy tissue and by compromising lung function by consolidating (blocking) the airspaces. A fine balance, therefore, exists between a lung immune response and immune-mediated damage,

E L Wissinger; J Saldana; A Didierlaurent; T Hussell

2008-01-01

2

Proteomic Biomarkers for Acute Interstitial Lung Disease in Gefitinib-Treated Japanese Lung Cancer Patients  

PubMed Central

Interstitial lung disease (ILD) events have been reported in Japanese non-small-cell lung cancer (NSCLC) patients receiving EGFR tyrosine kinase inhibitors. We investigated proteomic biomarkers for mechanistic insights and improved prediction of ILD. Blood plasma was collected from 43 gefitinib-treated NSCLC patients developing acute ILD (confirmed by blinded diagnostic review) and 123 randomly selected controls in a nested case-control study within a pharmacoepidemiological cohort study in Japan. We generated ?7 million tandem mass spectrometry (MS/MS) measurements with extensive quality control and validation, producing one of the largest proteomic lung cancer datasets to date, incorporating rigorous study design, phenotype definition, and evaluation of sample processing. After alignment, scaling, and measurement batch adjustment, we identified 41 peptide peaks representing 29 proteins best predicting ILD. Multivariate peptide, protein, and pathway modeling achieved ILD prediction comparable to previously identified clinical variables; combining the two provided some improvement. The acute phase response pathway was strongly represented (17 of 29 proteins, p?=?1.0×10?25), suggesting a key role with potential utility as a marker for increased risk of acute ILD events. Validation by Western blotting showed correlation for identified proteins, confirming that robust results can be generated from an MS/MS platform implementing strict quality control. PMID:21799770

Kawakami, Takao; Nagasaka, Keiko; Takami, Sachiko; Wada, Kazuya; Tu, Hsiao-Kun; Otsuji, Makiko; Kyono, Yutaka; Dobashi, Tae; Komatsu, Yasuhiko; Kihara, Makoto; Akimoto, Shingo; Peers, Ian S.; South, Marie C.; Higenbottam, Tim; Fukuoka, Masahiro; Nakata, Koichiro; Ohe, Yuichiro; Kudoh, Shoji; Clausen, Ib Groth; Nishimura, Toshihide; Marko-Varga, Gyorgy; Kato, Harubumi

2011-01-01

3

Ulcerative colitis combined with acute interstitial lung disease and airway disease: A case report and literature review  

PubMed Central

The aim of this study was to investigate the clinical features of ulcerative colitis (UC) combined with acute interstitial lung disease (ILD). One case with acute UC combined with ILD and airway disease was reported, and the pathological diagnosis of previous cases of UC combined with ILD was retrospectively analyzed according to the corresponding literature. The present case concerned a male patient with UC who presented with dry cough and progressive dyspnea. The chest computed tomography (CT) images showed as normal on the seventh day; diffuse ground-glass shadows were observed on the 11th day and diffuse reticular, patchy, nodular shadows and lung cysts were observed on the 21st day. The results of an open lung biopsy on the 23rd day indicated pleural adhesions, and the pathologies were pulmonary fibrosis and airway inflammation. Glucocorticoid therapy was ineffective in the patient, but cyclophosphamide combined with ? globulin rapidly caused the disease to remit. A total of 24 cases with UC combined with ILD and two cases of UC combined with acute ILD were retrieved through PubMed. UC combined with acute ILD was rare in clinical practice. Patients with dry cough, progressive dyspnea and diffuse ground-glass shadows in pulmonary CT images should be closely monitored. Glucocorticoid therapy should be carefully selected and precautions should be taken against opportunistic infections of the lung. Cyclophosphamide combined with ? globulin may be an effective treatment strategy.

XU, LISHENG; XIAO, WEI; MA, DEDONG; ZHOU, SHENGYU; ZHANG, QINGHUI

2014-01-01

4

Acute lung injury review.  

PubMed

The first report of acute respiratory distress syndrome (ARDS) was published in 1967, and even now acute lung injury (ALI) and ARDS are severe forms of diffuse lung disease that impose a substantial health burden all over the world. Recent estimates indicate approximately 190,000 cases per year of ALI in the United States each year, with an associated 74,500 deaths per year. Common causes of ALI/ARDS are sepsis, pneumonia, trauma, aspiration pneumonia, pancreatitis, and so on. Several pathologic stages of ALI/ARDS have been described: acute inflammation with neutrophil infiltration, fibroproliferative phase with hyaline membranes, with varying degrees of interstitial fibrosis, and resolution phase. There has been intense investigation into the pathophysiologic events relevant to each stage of ALI/ARDS, and much has been learned in the alveolar epithelial, endobronchial homeostasis, and alveolar cell immune responses, especially neutrophils and alveolar macrophages in an animal model. However, these effective results in the animal models are not equally adoptive to those in randomized, controlled trials. The clinical course of ALI/ARDS is variable with the likely pathophysiologic complexity of human ALI/ARDS. In 1994, the definition was recommended by the American-European Consensus Conference Committee, which facilitated easy nomination of patients with ALI/ARDS for a randomized, clinical trial. Here, we review the recent randomized, clinical trials of ALI/ARDS. PMID:19420806

Tsushima, Kenji; King, Landon S; Aggarwal, Neil R; De Gorordo, Antonio; D'Alessio, Franco R; Kubo, Keishi

2009-01-01

5

Interstitial Lung Diseases  

MedlinePLUS

Interstitial lung disease is the name for a large group of diseases that inflame or scar the lungs. The inflammation ... air is responsible for some types of interstitial lung diseases. Specific types include Black lung disease among coal ...

6

Sex-specific Differences in Hyperoxic Lung Injury in Mice: Implications for Acute and Chronic Lung Disease in Humans  

PubMed Central

Sex-specific differences in pulmonary morbidity in humans are well documented. Hyperoxia contributes to lung injury in experimental animals and humans. The mechanisms responsible for sex differences in the susceptibility towards hyperoxic lung injury remain largely unknown. In this investigation, we tested the hypothesis that mice will display sex-specific differences in hyperoxic lung injury. Eight week-old male and female mice (C57BL/6J) were exposed to 72 h of hyperoxia (FiO2>0.95). After exposure to hyperoxia, lung injury, levels of 8-iso-prostaglandin F2 alpha (8-iso-PGF 2?) (LC-MS/MS), apoptosis (TUNEL) and inflammatory markers (suspension bead array) were determined. CytochromeP450 (CYP)1A expression in the lung was assessed using immunohistochemistry and western blotting. After exposure to hyperoxia, males showed greater lung injury, neutrophil infiltration and apoptosis, compared to air-breathing controls than females. Pulmonary 8-iso-PGF 2? levels were higher in males than females after hyperoxia exposure. Sexually dimorphic increases in levels of IL-6 (F>M) and VEGF (M>F) in the lungs were also observed. CYP1A1 expression in the lung was higher in female mice compared to males under hyperoxic conditions. Overall, our results support the hypothesis that male mice are more susceptible than females to hyperoxic lung injury and that differences in inflammatory and oxidative stress markers contribute to these sex-specific dimorphic effects. In conclusion, this paper describes the establishment of an animal model that shows sex differences in hyperoxic lung injury in a temporal manner and thus has important implications for lung diseases mediated by hyperoxia in humans. PMID:23792423

Lingappan, Krithika; Jiang, Weiwu; Wang, Lihua; Couroucli, Xanthi I.; Barrios, Roberto; Moorthy, Bhagavatula

2014-01-01

7

Childhood Interstitial Lung Disease  

MedlinePLUS

... page from the NHLBI on Twitter. What Is Childhood Interstitial Lung Disease? Childhood interstitial (in-ter-STISH-al) lung disease, or ... doctors better understand these diseases. Rate This Content: Childhood Interstitial Lung Disease Clinical Trials Clinical trials are ...

8

Interstitial Lung Disease  

MedlinePLUS

... MS Dept. of Medicine View full profile Interstitial Lung Disease (ILD): Overview Interstitial lung disease (ILD) is a ... they may make informed decisions Learn more. Interstitial Lung Disease Program As a center specializing in the care ...

9

Lung Disease  

MedlinePLUS

... can cause sudden death. Pulmonary hypertension. This is high blood pressure in the arteries that bring blood to the lungs. It can affect blood flow in the lungs and can reduce oxygen flow into the blood. Sarcoidosis and pulmonary fibrosis. ...

10

Lung Diseases  

MedlinePLUS

... or blockage of the airways resulting in poor air flow. Others, including pulmonary fibrosis http://www.nhlbi.nih.gov/health/health-topics/topics/ipf/ , ... produces a decrease in the total volume of air that the lungs are able to hold. Research ...

11

Genetics and Lung Disease  

MedlinePLUS

... Society What should I know about genetics and lung disease? If you compare the genes of a group ... your risk of getting asthma. For a few lung diseases, genes play a much bigger role. These are ...

12

Role of Extracellular Adenosine in Acute Lung Injury  

NSDL National Science Digital Library

Acute lung injury (ALI) is a lung disease characterized by pulmonary edema and severe hypoxia. The past decade hosted a search for endogenous mechanisms controlling lung inflammation and pulmonary edema during ALI. As such, recent evidence indicates extracellular adenosine in orchestrating the resolution of pulmonary edema and inflammation during ALI.

Tobias Eckle (University of Colorado Denver Anesthesiology, Mucosal Inflammation Program); Michael Koeppen (University of Colorado Denver Anesthesiology); Holger K. Eltzschig (University of Colorado Denver Anesthesiology)

2009-10-01

13

Microparticles and acute lung injury.  

PubMed

The pathophysiology of acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), is characterized by increased vascular and epithelial permeability, hypercoagulation and hypofibrinolysis, inflammation, and immune modulation. These detrimental changes are orchestrated by cross talk between a complex network of cells, mediators, and signaling pathways. A rapidly growing number of studies have reported the appearance of distinct populations of microparticles (MPs) in both the vascular and alveolar compartments in animal models of ALI/ARDS or respective patient populations, where they may serve as diagnostic and prognostic biomarkers. MPs are small cytosolic vesicles with an intact lipid bilayer that can be released by a variety of vascular, parenchymal, or blood cells and that contain membrane and cytosolic proteins, organelles, lipids, and RNA supplied from and characteristic for their respective parental cells. Owing to this endowment, MPs can effectively interact with other cell types via fusion, receptor-mediated interaction, uptake, or mediator release, thereby acting as intrinsic stimulators, modulators, or even attenuators in a variety of disease processes. This review summarizes current knowledge on the formation and potential functional role of different MPs in inflammatory diseases with a specific focus on ALI/ARDS. ALI has been associated with the formation of MPs from such diverse cellular origins as platelets, neutrophils, monocytes, lymphocytes, red blood cells, and endothelial and epithelial cells. Because of their considerable heterogeneity in terms of origin and functional properties, MPs may contribute via both harmful and beneficial effects to the characteristic pathological features of ALI/ARDS. A better understanding of the formation, function, and relevance of MPs may give rise to new promising therapeutic strategies to modulate coagulation, inflammation, endothelial function, and permeability either through removal or inhibition of "detrimental" MPs or through administration or stimulation of "favorable" MPs. PMID:22728467

McVey, Mark; Tabuchi, Arata; Kuebler, Wolfgang M

2012-09-01

14

Warning Signs of Lung Disease  

MedlinePLUS

... Warning Signs of Lung Disease Warning Signs of Lung Disease WARNING SIGNS If you have any of these ... production has lasted a month, this could indicate lung disease. Wheezing - Noisy breathing or wheezing is a sign ...

15

Flavorings-Related Lung Disease  

MedlinePLUS

... Safety & Health Topics NIOSH Share Compartir FLAVORINGS-RELATED LUNG DISEASE On this Page Background Flavorings-Related Lung Disease ... practices that place workers at risk. Flavorings-Related Lung Disease Microwave popcorn plant and flavoring plant workers have ...

16

Interstitial lung disease - adults - discharge  

MedlinePLUS

... your breathing problems that are caused by interstitial lung disease. This disease scars your lungs, which makes it ... Raghu G. Interstitial lung disease. In: Goldman L, Schafer AI. ... ed. Philadelphia, PA: Elsevier Saunders; 2011: chap 92. Selman M, ...

17

Scleroderma Lung Disease  

Microsoft Academic Search

Pulmonary involvement is second in frequency only to esophageal involvement as a visceral complication of systemic sclerosis\\u000a (SSc) and has surpassed renal involvement as the most common cause of death. Interstitial lung disease and pulmonary vascular\\u000a disease, particularly pulmonary arterial hypertension, are the most commonly encountered types of lung involvement. Chronic\\u000a aspiration, airway disease, neuromuscular weakness, extrinsic pulmonary restrictive pathology,

Jérôme Le Pavec; David Launay; Stephen C. Mathai; Paul M. Hassoun; Marc Humbert

2011-01-01

18

Lung disease in farmers.  

PubMed Central

Lung diseases in farmers attributable to their occupation include (a) farmer's lung, caused by exposure to mouldy hay, (b) the asthma caused by exposure to grain dust and (c) silo-filler's disease. Their prevalence in Canada is unknown. Farmer's lung results from inhalation of mould spores in hay; the mechanism is immunologic. The exact cause and mechanism of grain dust asthma are unknown but may be immunologic. Silo-filler's disease is caused by the toxic effects of inhaled nitrogen dioxide. PMID:321110

Warren, C. P.

1977-01-01

19

Interstitial lung disease  

MedlinePLUS

... to the chest Working with or around asbestos, coal dust, cotton dust, and silica dust (called occupational ... routinely screened for lung disease. These jobs include coal mining, sand blasting, and working on a ship.

20

Occupational Lung Diseases  

MedlinePLUS

... disease? Some dusts, such as asbestos, silica, and coal can cause serious scarring (fibrosis) in the lungs. ... Chlorine Gas Lun g Scarring Asbestos Silica Foundry Coal Dust Asbestos Shipyards Sandblasters Brake Manufacturers Latex Beryllium ...

21

16. Immunologic lung disease  

Microsoft Academic Search

This review summarizes the recent advances regarding pathogenesis, diagnosis, and treatment of immunological diseases of the lung. Rather than attempt a comprehensive analysis, we have focused on selected diseases that are of particular relevance to the practicing physician, and the material has been organized according to the dominant immunologic mechanisms underlying the disease. Because of the redundancy that characterizes the

Joseph E. Prince; Farrah Kheradmand; David B. Corry

2003-01-01

22

Adalimumab (Humira) induced acute lung injury  

PubMed Central

Patient: Male, 78 Final Diagnosis: Acute lung injury due to Adalimumab Symptoms: — Medication: Adalimumab Clinical Procedure: Intubated and put on mechanical ventilation Specialty: Pulmonology Objective: Unusual or unexpected effect of treatment Background: Adalimumab is a recombinant human monoclonal antibody that blocks the effects of tumor necrosis factor-alpha. Adalimumab related acute lung injury is a rare form of acute respiratory distress syndrome of possible immune etiology that develops immediately after an infusion. Case Report: We describe a 78 year old, male with no previous cardiac comorbidities, who developed acute lung injury (ALI) within one hour of administration of adalimumab. He was successfully treated with mechanical ventilatory support and adjuvant therapy. Conclusions: TNF? antagonists are a part of a new and revolutionary treatment for severe and difficult-to-treat autoimmune and inflammatory diseases. This report emphasizes that this fatal complication may occur with use of this drug. Clinicians need to be aware of this condition as prompt recognition and supportive management can prevent unwanted morbidity and mortality. PMID:23826460

Kohli, Ritesh; Namek, Karim

2013-01-01

23

Efferocytosis and lung disease.  

PubMed

In healthy individuals, billions of cells die by apoptosis each day. Clearance of these apoptotic cells, termed "efferocytosis," must be efficient to prevent secondary necrosis and the release of proinflammatory cell contents that disrupt tissue homeostasis and potentially foster autoimmunity. During inflammation, most apoptotic cells are cleared by macrophages; the efferocytic process actively induces a macrophage phenotype that favors tissue repair and suppression of inflammation. Several chronic lung diseases, particularly airways diseases such as chronic obstructive lung disease, asthma, and cystic fibrosis, are characterized by an increased lung burden of uningested apoptotic cells. Alveolar macrophages from individuals with these chronic airways diseases have decreased efferocytosis relative to alveolar macrophages from healthy subjects. These two findings have led to the hypothesis that impaired apoptotic cell clearance may contribute causally to sustained lung inflammation and that therapies to enhance efferocytosis might be beneficial. This review of the English-language scientific literature (2006 to mid-2012) explains how such existing therapies as corticosteroids, statins, and macrolides may act in part by augmenting apoptotic cell clearance. However, efferocytosis can also impede host defenses against lung infection. Thus, determining whether novel therapies to augment efferocytosis should be developed and in whom they should be used lies at the heart of efforts to differentiate specific phenotypes within complex chronic lung diseases to provide appropriately personalized therapies. PMID:23732585

McCubbrey, Alexandra L; Curtis, Jeffrey L

2013-06-01

24

Lung Diseases and Conditions  

MedlinePLUS

... lead to a disease called COPD (chronic obstructive pulmonary disease). COPD prevents proper airflow in and out of ... surgery can cause a blood clot called a pulmonary embolism (PE) to block a lung artery. A PE can reduce or block the flow of blood in the ... July 17, 2012 The ...

25

NOD-Like Receptors in Lung Diseases  

PubMed Central

The lung is a particularly vulnerable organ at the interface of the body and the exterior environment. It is constantly exposed to microbes and particles by inhalation. The innate immune system needs to react promptly and adequately to potential dangers posed by these microbes and particles, while at the same time avoiding extensive tissue damage. Nucleotide-binding oligomerization domain-like receptors (NLRs) represent a group of key sensors for microbes and damage in the lung. As such they are important players in various infectious as well as acute and chronic sterile inflammatory diseases, such as pneumonia, chronic obstructive pulmonary disease (COPD), acute lung injury/acute respiratory distress syndrome, pneumoconiosis, and asthma. Activation of most known NLRs leads to the production and release of pro-inflammatory cytokines, and/or to the induction of cell death. We will review NLR functions in the lung during infection and sterile inflammation. PMID:24312100

Chaput, Catherine; Sander, Leif Erik; Suttorp, Norbert; Opitz, Bastian

2013-01-01

26

Occupational lung diseases.  

PubMed

Chest radiography and high-resolution computed tomography are indispensable tools in the detection, classification and characterization of occupational lung diseases that are caused by inhaling mineral particles such as asbestos, silicon-containing rock dust and other tissue-damaging antigens, nanomaterials and toxins. Radiographic evidence of occupational lung disease is interpreted with a patient's clinical signs and symptoms and a detailed occupational history in mind because of high variability in radiographic findings. This Directed Reading reviews the history, epidemiology, functional anatomy, pathobiology and medical diagnostic imaging of occupational lung diseases associated with inhalation of fine particulates in the workplace. This article is a Directed Reading. Your access to Directed Reading quizzes for continuing education credit is determined by your CE preference. For access to other quizzes, go to www.asrt.org/store. PMID:21771937

Furlow, Bryant

2011-01-01

27

Lung function in children and adolescents with antecedents of acute rheumatic fever  

Microsoft Academic Search

Static lung volumes, CO-lung transfer, airway resistance, maximal expiratory flows and lung elastic properties were studied in 29 children and adolescents 1–10 years after recovery from acute rheumatic fever. There were essentially no changes in lung function even in the subjects with a residual valvular disease. The only abnormality was a tendency for the elastic lung recoil at TLC to

A. Noseda; J. C. Yernault; P. Viart; D. Baran

1985-01-01

28

Interstitial Lung Disease (ILD): Treatment  

MedlinePLUS

... MS Dept. of Medicine View full profile Interstitial Lung Disease (ILD): Treatment Treatment for ILD is based upon ... they may make informed decisions Learn more. Interstitial Lung Disease Program As a center specializing in the care ...

29

Subclinical Interstitial Lung Disease  

PubMed Central

The widespread use of high-resolution computed tomography in clinical and research settings has increased the detection of interstitial lung abnormalities (ILA) in asymptomatic and undiagnosed individuals. We reported that in smokers, ILA were present in about 1 of every 12 high-resolution computed tomographic scans; however, the long-term significance of these subclinical changes remains unclear. Studies in families affected with pulmonary fibrosis, smokers with chronic obstructive pulmonary disease, and patients with inflammatory lung disease have shown that asymptomatic and undiagnosed individuals with ILA have reductions in lung volume, functional limitations, increased pulmonary symptoms, histopathologic changes, and molecular profiles similar to those observed in patients with clinically significant interstitial lung disease (ILD). These findings suggest that, in select at-risk populations, ILA may represent early stages of pulmonary fibrosis or subclinical ILD. The growing interest surrounding this topic is motivated by our poor understanding of the inciting events and natural history of ILD, coupled with a lack of effective therapies. In this perspective, we outline past and current research focused on validating radiologic, physiological, and molecular methods to detect subclinical ILD. We discuss the limitations of the available cross-sectional studies and the need for future longitudinal studies to determine the prognostic and therapeutic implications of subclinical ILD in populations at risk of developing clinically significant ILD. PMID:22366047

Doyle, Tracy J.; Hunninghake, Gary M.

2012-01-01

30

Animal models of fibrotic lung disease.  

PubMed

Interstitial lung fibrosis can develop as a consequence of occupational or medical exposure, as a result of genetic defects, and after trauma or acute lung injury leading to fibroproliferative acute respiratory distress syndrome, or it can develop in an idiopathic manner. The pathogenesis of each form of lung fibrosis remains poorly understood. They each result in a progressive loss of lung function with increasing dyspnea, and most forms ultimately result in mortality. To better understand the pathogenesis of lung fibrotic disorders, multiple animal models have been developed. This review summarizes the common and emerging models of lung fibrosis to highlight their usefulness in understanding the cell-cell and soluble mediator interactions that drive fibrotic responses. Recent advances have allowed for the development of models to study targeted injuries of Type II alveolar epithelial cells, fibroblastic autonomous effects, and targeted genetic defects. Repetitive dosing in some models has more closely mimicked the pathology of human fibrotic lung disease. We also have a much better understanding of the fact that the aged lung has increased susceptibility to fibrosis. Each of the models reviewed in this report offers a powerful tool for studying some aspect of fibrotic lung disease. PMID:23526222

B Moore, Bethany; Lawson, William E; Oury, Tim D; Sisson, Thomas H; Raghavendran, Krishnan; Hogaboam, Cory M

2013-08-01

31

Ultrastructure of the lung in a murine model of malaria-associated acute lung injury/acute respiratory distress syndrome  

PubMed Central

Background The mechanisms through which infection with Plasmodium spp. result in lung disease are largely unknown. Recently a number of mouse models have been developed to research malaria-associated lung injury but no detailed ultrastructure studies of the disease in its terminal stages in a murine model have yet been published. The goal was to perform an ultrastructural analysis of the lungs of mice that died with malaria-associated acute lung injury/acute respiratory distress syndrome to better determine the relevancy of the murine models and investigate the mechanism of disease. Methods DBA/2 mice were infected with Plasmodium berghei strain ANKA. Mice had their lungs removed immediately after death, processed using standard methods and viewed by transmission electron microscopy (TEM). Results Infected red blood cell:endothelium contact, swollen endothelium with distended cytoplasmic extensions and thickening of endothelium basement membrane were observed. Septa were thick and filled with congested capillaries and leukocytes and the alveolar spaces contained blood cells, oedema and cell debris. Conclusion Results show that the lung ultrastructure of P. berghei ANKA-infected mice has similar features to what has been described in post-mortem TEM studies of lungs from individuals infected with Plasmodium falciparum. These data support the use of murine models to study malaria-associated acute lung injury. PMID:24927627

2014-01-01

32

Pneumoproteins in interstitial lung diseases.  

E-print Network

??The interstitial lung diseases (ILD)s are a diverse group of pulmonary disorders that are classified together because of similar clinical, roentgenographic, physiologic, or pathologic manifestations,… (more)

Janssen, Rob

2006-01-01

33

Metal-Induced Lung Disease. Lessons from Japan's Experience  

Microsoft Academic Search

Abstract: Metal-Induced Lung Disease: Lessons from Japan’s Experience: Yukinori K USAKA, et al. Department of Environmental Health, School of Medicine, Fukui Medical University— Metals inducing occupational respiratory diseases, e.g. metal fever, acute and chronic pneumonia, asthma, bronchitis, chronic obstructive lung disease, pulmonary fibrosis and lung cancer are described. The metals mentioned are the following: aluminum, antimony, arsenic, barium, beryllium, cadmium,

Yukinori KUSAKA; Kazuhiro SATO; Narufumi SUGANUMA; Yutaka HOSODA

2001-01-01

34

Risk of acute urinary retention associated with inhaled anticholinergics in patients with chronic obstructive lung disease: systematic review.  

PubMed

Inhaled anticholinergics (ipratropium bromide and tiotropium bromide) are widely used as maintenance treatment in chronic obstructive pulmonary disease. Previous studies have reported on their cardiovascular effects but relatively little is known about their effects on the bladder. Acute urinary retention is a medical emergency which can be associated with serious complications. Our objective was to evaluate the existing literature regarding the effects of inhaled anticholinergics on urinary retention among patients with chronic obstructive pulmonary disease. We searched PubMed and the United States Food and Drug Administration (FDA) adverse events database for case reports, observational studies, randomized controlled trials (or meta-analyses of such trials) that reported on the outcome of urinary retention with inhaled anticholinergics (ipratropium or tiotropium). We checked 27 published articles and identified relevant papers including two case reports, three pooled analyses, two observational studies and one randomized controlled trial. Two of the observational studies and a pooled analysis of randomized controlled trials reported a significant increase in the risk of acute urinary retention with inhaled anticholinergics. Older patients with benign prostatic hyperplasia seem to be at the highest risk of this adverse effect which tends to occur soon after treatment initiation. Although all the links in the chain have yet to be fully elucidated, the preponderance of evidence suggests the possibility of a causal relationship between inhaled anticholinergics and urinary retention. Clinicians should carefully balance these and other adverse effects of inhaled anticholinergics against their known symptomatic benefits on exacerbations, after eliciting patient preferences for various outcomes in a shared decision-making context. PMID:25083248

Loke, Yoon K; Singh, Sonal

2013-02-01

35

Lung pathology of fatal severe acute respiratory syndrome  

Microsoft Academic Search

1 Summary Background Severe acute respiratory syndrome (SARS) is a novel infectious disease with global impact. A virus from the family Coronaviridae has been identified as the cause, but the pathogenesis is still unclear. Methods Post-mortem tissue samples from six patients who died from SARS in February and March, 2003, and an open lung biopsy from one of these patients

John M Nicholls; Leo L M Poon; Kam C Lee; Wai F Ng; Sik T Lai; Chung Y Leung; Chung M Chu; Pak K Hui; Kong L Mak; Wilina Lim; Kin W Yan; Kwok H Chan; Ngai C Tsang; Yi Guan; Kwok Y Yuen; J S Malik Peiris

2003-01-01

36

Occupational Interstitial Lung Disease Update  

Microsoft Academic Search

Overview Occupational exposures produce a wide range of interstitial lung disorders. Occupational etiologies account for a significant portion of all interstitial lung disease (ILD), and new causes continue to be described. All of these disorders are preventable with the reduction or elimination of workplace exposure. This chapter highlights the common, persistent diseases that continue to plague workers globally, as well

Lee S. Newman

37

Acute Exacerbation of Chronic Obstructive Pulmonary Disease: Cardiovascular Links  

PubMed Central

Chronic obstructive pulmonary disease (COPD) is a chronic, progressive lung disease resulting from exposure to cigarette smoke, noxious gases, particulate matter, and air pollutants. COPD is exacerbated by acute inflammatory insults such as lung infections (viral and bacterial) and air pollutants which further accelerate the steady decline in lung function. The chronic inflammatory process in the lung contributes to the extrapulmonary manifestations of COPD which are predominantly cardiovascular in nature. Here we review the significant burden of cardiovascular disease in COPD and discuss the clinical and pathological links between acute exacerbations of COPD and cardiovascular disease. PMID:24724085

Laratta, Cheryl R.; van Eeden, Stephan

2014-01-01

38

Pathogenesis of indirect (secondary) acute lung injury  

PubMed Central

At present, therapeutic interventions to treat acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) remain largely limited to lung-protective strategies, as no real molecular–pathophysiologic-driven therapeutic intervention has yet become available. This is in part the result of the heterogeneous nature of the etiological processes that contribute to the state of ALI/ARDS. This article sets out to understand the development of ALI resulting from indirect pulmonary insults, such as extrapulmonary sepsis and trauma, shock, burn injury or mass transfusion, as opposed to direct pulmonary challenges, such as pneumonia, aspiration or lung contusion. Here, we consider not only the experimental and clinical data concerning the roles of various immune (neutrophil, macrophage, lymphocyte and dendritic) as well as nonimmune (epithelial and endothelial) cells in orchestrating the development of ALI resulting from indirect pulmonary stimuli, but also how these cell populations might be targeted therapeutically. PMID:21348592

Perl, Mario; Lomas-Neira, Joanne; Venet, Fabienne; Chung, Chun-Shiang; Ayala, Alfred

2011-01-01

39

[Interstitial lung diseases : The pattern is important].  

PubMed

Interstitial lung diseases (ILDs) comprise a number of rare entities with an estimated incidence of 10-25 per 100,000 inhabitants but the incidence greatly increases beyond the age of 65 years. The prognosis depends on the underlying cause. The fibrotic disorders show a set of radiological and histopathological patterns that are distinct but not entirely specific. In the absence of a clear clinical picture and consistent high resolution computed tomography (HRCT) findings, patients are advised to undergo surgical lung biopsies from two or three lung lobes (or transbronchial biopsies) to determine the histopathological pattern. The ILDs are differentiated into disorders of known causes (e.g. collagen vascular disease, drug-related), idiopathic interstitial pneumonia (IIP), granulomatous ILDs (e.g. sarcoidosis) and other forms of ILD (e.g. Langerhans' cell histiocytosis). The IIPs encompass idiopathic pulmonary fibrosis (IPF), non-specific interstitial pneumonia, desquamative interstitial pneumonia, respiratory bronchiolitis-interstitial lung disease, cryptogen organizing pneumonia, lymphocytic interstitial pneumonia and acute interstitial pneumonia. Additionally, a category of unclassified interstitial pneumonia exists. The pathologist has to recognize and address the histopathological pattern. In a multidisciplinary discussion the disorder is allocated to a clinicopathological entity and the histopathological pattern plays a major role in the classification of the entity. Recognition of the underlying pattern and the respective histopathological differential diagnoses is important as the therapy varies depending on the cause and ranges from elimination of the stimulus (if possible) to antifibrotic drug therapy up to preparation for lung transplantation. PMID:25319226

Fink, L

2014-11-01

40

Diverse macrophage populations mediate acute lung inflammation and resolution.  

PubMed

Acute respiratory distress syndrome (ARDS) is a devastating disease with distinct pathological stages. Fundamental to ARDS is the acute onset of lung inflammation as a part of the body's immune response to a variety of local and systemic stimuli. In patients surviving the inflammatory and subsequent fibroproliferative stages, transition from injury to resolution and recovery is an active process dependent on a series of highly coordinated events regulated by the immune system. Experimental animal models of acute lung injury (ALI) reproduce key components of the injury and resolution phases of human ARDS and provide a methodology to explore mechanisms and potential new therapies. Macrophages are essential to innate immunity and host defense, playing a featured role in the lung and alveolar space. Key aspects of their biological response, including differentiation, phenotype, function, and cellular interactions, are determined in large part by the presence, severity, and chronicity of local inflammation. Studies support the importance of macrophages to initiate and maintain the inflammatory response, as well as a determinant of resolution of lung inflammation and repair. We will discuss distinct roles for lung macrophages during early inflammatory and late resolution phases of ARDS using experimental animal models. In addition, each section will highlight human studies that relate to the diverse role of macrophages in initiation and resolution of ALI and ARDS. PMID:24508730

Aggarwal, Neil R; King, Landon S; D'Alessio, Franco R

2014-04-15

41

Work-related lung diseases.  

PubMed

Work-related respiratory diseases affect people in every industrial sector, constituting approximately 60% of all disease and injury mortality and 70% of all occupational disease mortality. There are two basic types: interstitial lung diseases, that is the pneumoconioses (asbestosis, byssinosis, chronic beryllium disease, coal workers' pneumoconiosis (CWP), silicosis, flock workers' lung, and farmers' lung disease), and airways diseases, such as work-related or exacerbated asthma, chronic obstructive pulmonary disease and bronchiolitis obliterans (a disease that was recognized in the production of certain foods only 10 years ago). Common factors in the development of these diseases are exposures to dusts, metals, allergens and other toxins, which frequently cause oxidative damage. In response, the body reacts by activating primary immune response genes (i.e. cytokines that often lead to further oxidative damage), growth factors and tissue remodelling proteins. Frequently, complex imbalances in these processes contribute to the development of disease. For example, tissue matrix metalloproteases can cause the degradation of tissue, as in the development of CWP small profusions, but usually overexpression of matrix metalloproteases is controlled by serum protein inhibitors. Thus, disruption of such a balance can lead to adverse tissue damage. Susceptibility to these types of lung disease has been investigated largely through candidate gene studies, which have been characteristically small, often providing findings that have been difficult to corroborate. An important exception to this has been the finding that the HLA-DPB11(E69) allele is closely associated with chronic beryllium disease and beryllium sensitivity. Although chronic beryllium disease is only caused by exposure to beryllium, inheritance of HLA-DPB1(E69) carries an increased risk of between two- and 30-fold in beryllium exposed workers. Most, if not all, of these occupationally related diseases are preventable; therefore, it is disturbing that rates of CWP, for example, are again increasing in the United States in the 21st century. PMID:22997873

Weston, Ainsley

2011-01-01

42

Aspiration-related lung diseases.  

PubMed

Aspiration is a common but underrecognized clinicopathologic entity, with varied radiographic manifestations. Aspiration represents a spectrum of diseases, including diffuse aspiration bronchiolitis, aspiration pneumonitis, airway obstruction by foreign body, exogenous lipoid pneumonia, interstitial fibrosis, and aspiration pneumonia with or without lung abscess formation. Many patients who aspirate do not present with disease, suggesting that pathophysiology is related to a variety of factors, including decreased levels of consciousness, dysphagia, impaired mucociliary clearance, composition of aspirate, and impaired host defenses. In this pictorial essay, we will review the different types of aspiration lung diseases, focusing on their imaging features and differential diagnosis. PMID:24911122

Prather, Andrew D; Smith, Tristan R; Poletto, Dana M; Tavora, Fabio; Chung, Jonathan H; Nallamshetty, Leelakrishna; Hazelton, Todd R; Rojas, Carlos A

2014-09-01

43

Sleep in patients with restrictive lung disease.  

PubMed

Restrictive lung disease leads to ventilatory defects and diffusion impairments. These changes may contribute to abnormal nocturnal pathophysiology, including sleep architecture disruption and impaired ventilation and oxygenation. Patients with restrictive lung disease may suffer significant daytime fatigue and dysfunction. Hypercarbia and hypoxemia during sleep may impact progression of lung disease and related symptoms. Little is known about the impact of treatment of sleep disruption on sleep quality and overall prognosis in restrictive lung disease. This review discusses the pathophysiology of sleep and comorbid sleep disorders in restrictive lung diseases including interstitial lung disease, neuromuscular disease, and obesity hypoventilation syndrome. PMID:25156766

Won, Christine H J; Kryger, Meir

2014-09-01

44

Asbestos-related lung disease.  

PubMed

The inhalation of asbestos fibers may lead to a number of respiratory diseases, including lung cancer, asbestosis, pleural plaques, benign pleural effusion, and malignant mesothelioma. Although exposure is now regulated, patients continue to present with these diseases because of the long latent period between exposure and clinical disease. Presenting signs and symptoms tend to be nonspecific; thus, the occupational history helps guide clinical suspicion. High-risk populations include persons in construction trades, boilermakers, shipyard workers, railroad workers, and U.S. Navy veterans. Every effort should be made to minimize ongoing exposure. Patients with a history of significant asbestos exposure may warrant diagnostic testing and follow-up assessment, although it is unclear whether this improves outcomes. Patients with significant exposure and dyspnea should have chest radiography and spirometry. The prognosis depends on the specific disease entity. Asbestosis generally progresses slowly, whereas malignant mesothelioma has an extremely poor prognosis. The treatment of patients with asbestos exposure and lung cancer is identical to that of any patient with lung cancer. Because exposure to cigarette smoke increases the risk of developing lung cancer in patients with a history of asbestos exposure, smoking cessation is essential. Patients with asbestosis or lung cancer should receive influenza and pneumococcal vaccinations. PMID:17375514

O'Reilly, Katherine M A; Mclaughlin, Anne Marie; Beckett, William S; Sime, Patricia J

2007-03-01

45

Occupational lung disease in China.  

PubMed

Occupational lung disease has been a major public health problem in China. The recently transformed industrial structure and expansion of the industrial labor force, accompanying the rapid industrialization and economic growth, pose both tremendous challenges and opportunities for occupational health policy and research. New occupational health problems are emerging, while the traditional occupational lung disease continued to occur. Simultaneously, relevant scientific research and professional activities have accelerated notably. The progress and achievement in occupational health research are creating more powerful forces in eliminating industrial hazards and protecting workers' health in China. PMID:14664484

Wang, Xiao-Rong; Christiani, David C

2003-01-01

46

Acute Amiodarone Pulmonary Toxicity Following Lung Resection  

PubMed Central

Amiodarone is one of the most frequently prescribed antiarrhythmic agents. Despite its widespread use, it is associated with systemic side effects. Pulmonary toxicity, the most severe adverse effect of amiodarone, has usually been described in the context of chronic amiodarone use. We report a case of an 80-year-old male presenting acutely following right upper lung lobe resection for stage 1b adenocarcinoma. He developed atrial fibrillation on postoperative day four and received 12.5 g of amiodarone within a 12 day period. On presentation, he had new bilateral lung opacities and a 35% absolute decline in the predicted diffusion capacity for carbon monoxide. Pulmonary embolism was ruled out on chest computed tomography. Amiodarone was discontinued and prednisone was initiated. Despite initial improvement, he suffered from multiple hypoxemic episodes until his death in the fourth month. In a subset of patients undergoing thoracic surgery who are intubated and require high levels of oxygen, the risk of amiodarone lung toxicity increases and patients may present acutely.

Fadahunsi, Opeyemi; Krol, Ronald

2014-01-01

47

Acute amiodarone pulmonary toxicity following lung resection.  

PubMed

Amiodarone is one of the most frequently prescribed antiarrhythmic agents. Despite its widespread use, it is associated with systemic side effects. Pulmonary toxicity, the most severe adverse effect of amiodarone, has usually been described in the context of chronic amiodarone use. We report a case of an 80-year-old male presenting acutely following right upper lung lobe resection for stage 1b adenocarcinoma. He developed atrial fibrillation on postoperative day four and received 12.5 g of amiodarone within a 12 day period. On presentation, he had new bilateral lung opacities and a 35% absolute decline in the predicted diffusion capacity for carbon monoxide. Pulmonary embolism was ruled out on chest computed tomography. Amiodarone was discontinued and prednisone was initiated. Despite initial improvement, he suffered from multiple hypoxemic episodes until his death in the fourth month. In a subset of patients undergoing thoracic surgery who are intubated and require high levels of oxygen, the risk of amiodarone lung toxicity increases and patients may present acutely. PMID:25324704

Fadahunsi, Opeyemi; Krol, Ronald

2014-09-01

48

Transfusion-Related Acute Lung Injury: The Work of DAMPs*  

PubMed Central

Current notions in immunology hold that not only pathogen-mediated tissue injury but any injury activates the innate immune system. In principle, this evolutionarily highly conserved, rapid first-line defense system responds to pathogen-induced injury with the creation of infectious inflammation, and non-pathogen-induced tissue injury with ‘sterile’ tissue inflammation. In this review, evidence has been collected in support of the notion that the transfusion-related acute lung injury induces a ‘sterile’ inflammation in the lung of transfused patients in terms of an acute innate inflammatory disease. The inflammatory response is mediated by the patient's innate immune cells including lung-passing neutrophils and pulmonary endothelial cells, which are equipped with pattern recognition receptors. These receptors are able to sense injury-induced, damage-associated molecular patterns (DAMPs) generated during collection, processing, and storage of blood/blood components. The recognition process leads to activation of these innate cells. A critical role for a protein complex known as the NLRP3 inflammasome has been suggested to be at the center of such a scenario. This complex undergoes an initial ‘priming’ step mediated by 1 class of DAMPs and then an ‘activating’ step mediated by another class of DAMPs to activate interleukin-1beta and interleukin-18. These 2 cytokines then promote, via transactivation, the formation of lung inflammation. PMID:23637644

Land, Walter G.

2013-01-01

49

Genetically manipulated mouse models of lung disease: potential and pitfalls  

PubMed Central

Gene targeting in mice (transgenic and knockout) has provided investigators with an unparalleled armamentarium in recent decades to dissect the cellular and molecular basis of critical pathophysiological states. Fruitful information has been derived from studies using these genetically engineered mice with significant impact on our understanding, not only of specific biological processes spanning cell proliferation to cell death, but also of critical molecular events involved in the pathogenesis of human disease. This review will focus on the use of gene-targeted mice to study various models of lung disease including airways diseases such as asthma and chronic obstructive pulmonary disease, and parenchymal lung diseases including idiopathic pulmonary fibrosis, pulmonary hypertension, pneumonia, and acute lung injury. We will attempt to review the current technological approaches of generating gene-targeted mice and the enormous dataset derived from these studies, providing a template for lung investigators. PMID:22198907

Choi, Alexander J. S.; Owen, Caroline A.; Choi, Augustine M. K.

2012-01-01

50

Psychiatric aspects of chronic lung disease  

Microsoft Academic Search

Chronic lung diseases continue to be common and cause significant morbidity and mortality. There is a complex interplay between\\u000a psychiatric issues and pulmonary diseases. This review aims to summarize the recent literature and advances involving psychiatric\\u000a aspects of lung diseases, including chronic obstructive pulmonary disease, asthma, restrictive lung disease, and cystic fibrosis.\\u000a The authors include the latest findings in epidemiology,

Abhishek Jain; Sermsak Lolak

2009-01-01

51

Chronic lung disease in the Papua New Guinea Highlands.  

PubMed Central

In the Eastern Highlands of Papua New Guinea 46 men and 24 women with chronic lung disease underwent clinical and lung function investigations. In all cases the sole or predominant abnormality was irreversible airways obstruction, probably from chronic bronchitis with variable amounts of acompanying emphysema. There were close similarities to chronic obstructife lung disease in European populations in terms of symptoms, airways obstruction, transfer factor, and radiographic emphysema and inflammatory changes. Bronchiectasis and local fibrosis were present in a few subjects, but previous reports that pulmonary and pleural fibrosis are features of the disease were not confirmed. Possibly environmental and genetic factors may increase the associated blood gas disturbances leading to pulmonary hypertension. Unlike chronic obstructive lung disease in European populations, tobacco smoking is not an important aetiological factor. Although there is no direct evidence, the most likely possibilities are domestic wood smoke and acute chest infections. PMID:515985

Anderson, H R

1979-01-01

52

Pathology Case Study: Lung and Liver Disease  

NSDL National Science Digital Library

The University of Pittsburgh School of Medicine's Department of Pathology has compiled a series of case studies to help both students and instructors in the health sciences field. The patient in this case is a 24 year-old man âÂÂadmitted for acute worsening of his respiratory status and liver failure.â The patientâÂÂs history includes end-stage restrictive lung disease and end-stage liver disease. The âÂÂGross Descriptionâ and âÂÂMicroscopic Descriptionâ sections provide key information and images that contributed to the patientâÂÂs diagnosis. Clicking on the âÂÂFinal Diagnosisâ provides a thorough explanation of the diagnosis and illness from the contributing doctors.

Johnson, Douglas R.

2009-08-20

53

Exploring lung physiology in health and disease with lung slices  

PubMed Central

The development of therapeutic approaches to treat lung disease requires an understanding of both the normal and disease physiology of the lung. Although traditional experimental approaches only address either organ or cellular physiology, the use of lung slice preparations provides a unique approach to investigate integrated physiology that links the cellular and organ responses. Living lung slices are robust and can be prepared from a variety of species, including humans, and they retain many aspects of the cellular and structural organization of the lung. Functional portions of intrapulmonary airways, arterioles and veins are present within the alveoli parenchyma. The dynamics of macroscopic changes of contraction and relaxation associated with the airways and vessels are readily observed with conventional low-magnification microscopy. The microscopic changes associated with cellular events, that determine the macroscopic responses, can be observed with confocal or two-photon microscopy. To investigate disease processes, lung slices can either be prepared from animal models of disease or animals exposed to disease invoking conditions. Alternatively, the lung slices themselves can be experimentally manipulated. Because of the ability to observe changes in cell physiology and how these responses manifest themselves at the level of the organ, lung slices have become a standard tool for the investigation of lung disease. PMID:21600999

Sanderson, Michael J.

2011-01-01

54

Radiographic measurement of total lung capacity in acute asthma  

Microsoft Academic Search

The thoracic cage appears to be large during attacks of asthma. Lung volume measurements by body plethysmography and helium dilution have suggested that total lung capacity may be increased during an acute attack of asthma, but doubt has been cast on the accuracy of these measurements in the presence of airflow obstruction. The change in total lung capacity has therefore

M S Rothstein; M N Zelefsky; P Q Eichacker; D J Rudolph; M H Williams

1989-01-01

55

Apoptosis in Lung Injury and Disease  

Microsoft Academic Search

Pulmonary cell death may contribute significantly to acute and chronic lung injuries caused by various adverse environmental\\u000a agents. Pulmonary cells may die by necrosis, apoptosis, and other forms of regulated cell death. Apoptosis exerts a homeostatic\\u000a function in lung defense and development, through the removal of dysfunctional cells and by regulating cellular proliferation.\\u000a Lung cell apoptosis can occur as a

Stefan W. Ryter; Hong Pyo Kim; Augustine M. K. Choi

56

Interstitial lung diseases in children  

PubMed Central

Interstitial lung disease (ILD) in infants and children comprises a large spectrum of rare respiratory disorders that are mostly chronic and associated with high morbidity and mortality. These disorders are characterized by inflammatory and fibrotic changes that affect alveolar walls. Typical features of ILD include dyspnea, diffuse infiltrates on chest radiographs, and abnormal pulmonary function tests with restrictive ventilatory defect and/or impaired gas exchange. Many pathological situations can impair gas exchange and, therefore, may contribute to progressive lung damage and ILD. Consequently, diagnosis approach needs to be structured with a clinical evaluation requiring a careful history paying attention to exposures and systemic diseases. Several classifications for ILD have been proposed but none is entirely satisfactory especially in children. The present article reviews current concepts of pathophysiological mechanisms, etiology and diagnostic approaches, as well as therapeutic strategies. The following diagnostic grouping is used to discuss the various causes of pediatric ILD: 1) exposure-related ILD; 2) systemic disease-associated ILD; 3) alveolar structure disorder-associated ILD; and 4) ILD specific to infancy. Therapeutic options include mainly anti-inflammatory, immunosuppressive, and/or anti-fibrotic drugs. The outcome is highly variable with a mortality rate around 15%. An overall favorable response to corticosteroid therapy is observed in around 50% of cases, often associated with sequelae such as limited exercise tolerance or the need for long-term oxygen therapy. PMID:20727133

2010-01-01

57

Prevention of chronic lung disease  

PubMed Central

Considerable effort has been devoted to the development of strategies to reduce the incidence of chronic lung disease, including use of medications, nutritional therapies, and respiratory care practices. Unfortunately, most of these strategies have not been successful. To date, the only two treatments developed specifically to prevent CLD whose efficacy is supported by evidence from randomized, controlled trials are the parenteral administration of vitamin A and corticosteroids. Two other therapies, the use of caffeine for the treatment of apnea of prematurity and aggressive phototherapy for the treatment of hyperbilirubinemia were evaluated for the improvement of other outcomes and found to reduce CLD. Cohort studies suggest that the use of CPAP as a strategy for avoiding mechanical ventilation might also be beneficial. Other therapies reduce lung injury in animal models but do not appear to reduce CLD in humans. The benefits of the efficacious therapies have been modest, with an absolute risk reduction in the 7–11% range. Further preventive strategies are needed to reduce the burden of this disease. However, each will need to be tested in randomized, controlled trials, and the expectations of new therapies should be modest reductions of the incidence of the disease. PMID:19736053

Laughon, Matthew M.; Smith, P. Brian; Bose, Carl

2010-01-01

58

Lung Cancer and Interstitial Lung Diseases: A Systematic Review  

PubMed Central

Interstitial lung diseases (ILDs) represent a heterogeneous group of more than two hundred diseases of either known or unknown etiology with different pathogenesis and prognosis. Lung cancer, which is the major cause of cancer death in the developed countries, is mainly attributed to cigarette smoking and exposure to inhaled carcinogens. Different studies suggest a link between ILDs and lung cancer, through different pathogenetic mechanisms, such as inflammation, coagulation, dysregulated apoptosis, focal hypoxia, activation, and accumulation of myofibroblasts as well as extracellular matrix accumulation. This paper reviews current evidence on the association between lung cancer and interstitial lung diseases such as idiopathic pulmonary fibrosis, sarcoidosis, systemic sclerosis, dermatomyositis/polymyositis, rheumatoid arthritis, systemic lupus erythematosus, and pneumoconiosis. PMID:22900168

Archontogeorgis, Kostas; Steiropoulos, Paschalis; Tzouvelekis, Argyris; Nena, Evangelia; Bouros, Demosthenes

2012-01-01

59

Cell Therapy Approaches for Lung Diseases: Current Status  

PubMed Central

Summary and recent advances Recent findings suggest that embryonic stem cells and stem cells derived from adult tissues, including bone marrow and umbilical cord blood, could be utilized in repair and regeneration of injured or diseased lungs. This is an exciting and rapidly moving field that holds promise as a therapeutic approach for variety of lung diseases. Although initial emphasis was on engraftment of stem cells in lung, more, recent studies demonstrate that mesenchymal stem cells (MSCs) can modulate local inflammatory and immune responses in mouse lung disease models including acute lung injury and pulmonary fibrosis. Further, based on initial reports of safety and efficacy following allogeneic administration of MSCs to patients with Crohn’s disease or with graft-versus-host disease, a recent trial has been initiated to study the effect of MSCs in patients with chronic obstructive pulmonary disease. Notably, several recent clinical trials have demonstrated potential benefit of autologous stem cell administration in patient with pulmonary hypertension. In this review, we will describe recent advances in cell therapy with the focus on MSCs and their potential roles in lung development and repair. PMID:19349209

Sueblinvong, Viranuj; Weiss, Daniel J.

2013-01-01

60

Pulmonary nuclear medicine: Techniques in diagnosis of lung disease  

SciTech Connect

This book presents papers on the application of nuclear medicine to the diagnosis of lung diseases. Topics considered include lung physiology and anatomy, radiopharmaceuticals in pulmonary medicine, pulmonary embolism, obstructive pulmonary disease, diffuse infiltrative lung disease, pneumoconioses, tumor localization scans in primary lung tumors, the interactions of heart diseases and lung diseases on radionuclide tests of lung anatomy and function, radionuclide imaging in pediatric lung diseases, and future possibilities in pulmonary nuclear medicine.

Atkins, H.L.

1984-01-01

61

A Case of IgG4-Related Lung Disease Presenting as Interstitial Lung Disease  

PubMed Central

Intrathoracic involvement of immunoglobulin G4 (IgG4)-related disease has recently been reported. However, a subset of the disease presenting as interstitial lung disease is rare. Here, we report a case of a 35-year-old man with IgG4-related lung disease with manifestations similar to those of interstitial lung disease. Chest computed tomography showed diffuse ground glass opacities and rapidly progressive pleural and subpleural fibrosis in both upper lobes. Histological findings showed diffuse interstitial lymphoplasmacytic infiltration with an increased number of IgG4-positive plasma cells. Serum levels of IgG and IgG4 were also increased. The patient was diagnosed with IgG4-related lung disease, treated with anti-inflammatory agents, and showed improvement. Lung involvement of IgG4-related disease can present as interstitial lung disease and, therefore, should be differentiated when evaluating interstitial lung disease.

Ahn, Jee Hwan; Hong, Sun In; Cho, Dong Hui; Chae, Eun Jin; Song, Joon Seon

2014-01-01

62

Rheumatoid lung disease, pneumothorax, and eosinophilia.  

PubMed Central

Four cases of the triad of rheumatoid lung disease, spontaneous pneumothorax, and peripheral blood eosinophilia are reported. Cavitation of a rheumatoid lung nodule caused the pneumothorax in at least 1 case. The significance of eosinophilia and its value as a marker of extra-articular manifestations of rheumatoid disease are discussed. Images PMID:7073341

Crisp, A J; Armstrong, R D; Grahame, R; Dussek, J E

1982-01-01

63

Corticosteroids in infant chronic lung disease  

Microsoft Academic Search

Corticosteroids in infant chronic lung disease. C. May, A. Greenough. Chronic lung disease (CLD), defined as chronic oxygen dependency at 36 weeks postmenstrual age, is increasing and associated with chronic respiratory morbidity and high health care utilisation at follow up. Many strategies, tested in randomised trials, have failed to reduce CLD. In contrast, corticosteroids if given systemically within the first

A. Greenough; Lung Biology; Anne Greenough

64

Human Epidermal Growth Factor Receptor Signaling in Acute Lung Injury  

PubMed Central

Acute lung injury (ALI) is a syndrome marked by increased permeability across the pulmonary epithelium resulting in pulmonary edema. Recent evidence suggests that members of the human epidermal growth factor receptor (HER) family are activated in alveolar epithelial cells during ALI and regulate alveolar epithelial barrier function. These tyrosine kinase receptors, which also participate in the pathophysiology of pulmonary epithelial malignancies, regulate cell growth, differentiation, and migration as well as cell–cell adhesion, all processes that influence epithelial injury and repair. In this review we outline mechanisms of epithelial injury and repair in ALI, activation patterns of this receptor family in pulmonary epithelial cells as a consequence injury, how receptor activation alters alveolar permeability, and the possible intracellular signaling pathways involved. Finally, we propose a theoretical model for how HER-mediated modulation of alveolar permeability might affect lung injury and repair. Understanding how these receptors signal has direct therapeutic implications in lung injury and other diseases characterized by altered epithelial barrier function. PMID:22652197

Downey, Gregory P.; Kern, Jeffrey A.

2012-01-01

65

Krypton-81m ventilation scanning: acute respiratory disease  

SciTech Connect

From experience with 700 patients undergoing ventilation and perfusion lung scanning with krypton-81m/technetium-99m technique, 34 patients suffering from nonembolic acute respiratory disease were selected for review. In 16 patients with pneumonia, all had defects of ventilation corresponding to, or larger than, the radiologic consolidation. In 13 patients there was some preservation of perfusion in the consolidated region. In two of the three patients with matched defects, the pneumonia was of long standing. In seven patients with collapse or atelectasis and in 11 patients with acute reversible bronchial obstruction and normal volume lungs, a similar pattern or ventillation and perfusion was observed.

Lavender, J.P. (Royal Postgraduate Medical School, London, England); Irving, H.; Armstrong, J.D. II

1981-02-01

66

Mesenchymal stem cell therapy in lung disorders: pathogenesis of lung diseases and mechanism of action of mesenchymal stem cell.  

PubMed

Lung disorders such as asthma, acute respiratory distress syndrome (ARDS), chronic obstructive lung disease (COPD), and interstitial lung disease (ILD) show a few common threads of pathogenic mechanisms: inflammation, aberrant immune activity, infection, and fibrosis. Currently no modes of effective treatment are available for ILD or emphysema. Being anti-inflammatory, immunomodulatory, and regenerative in nature, the administration of mesenchymal stem cells (MSCs) has shown the capacity to control immune dysfunction and inflammation in the lung. The intravenous infusion of MSCs, the common mode of delivery, is followed by their entrapment in lung vasculature before MSCs reach to other organ systems thus indicating the feasible and promising approach of MSCs therapy for lung diseases. In this review, we discuss the mechanistic basis for MSCs therapy for asthma, ARDS, COPD, and ILD. PMID:23992090

Inamdar, Ajinkya C; Inamdar, Arati A

2013-10-01

67

Imaging of occupational and environmental lung diseases  

SciTech Connect

The chest radiograph is the basic tool for identifying occupational and environmental lung diseases; however, its sensitivity and specificity for the diagnosis of occupational and environmental lung diseases are low. High-resolution CT is the optimal method of recognizing parenchymal abnormalities in occupational and environmental disease. With the exception of pleural plaques, the CT findings of occupational and environmental lung diseases are nonspecific. Therefore, correlation of imaging features with history of exposure, other clinical features, and sometimes pathology is needed for the diagnosis of pneumoconiosis.

Akira, M. [Kinki Cuo Chest Medical Center, Osaka (Japan)

2008-03-15

68

A Reconsideration of Acute Beryllium Disease  

PubMed Central

Context Although chronic beryllium disease (CBD) is clearly an immune-mediated granulomatous reaction to beryllium, acute beryllium disease (ABD) is commonly considered an irritative chemical phenomenon related to high exposures. Given reported new cases of ABD and projected increased demand for beryllium, we aimed to reevaluate the patho physiologic associations between ABD and CBD using two cases identified from a survey of beryllium production facility workers. Case Presentation Within weeks after exposure to beryllium fluoride began, two workers had systemic illness characterized by dermal and respiratory symptoms and precipitous declines in pulmonary function. Symptoms and pulmonary function abnormalities improved with cessation of exposure and, in one worker, recurred with repeat exposure. Bronchoalveolar lavage fluid analyses and blood beryllium lymphocyte proliferation tests revealed lymphocytic alveolitis and cellular immune recognition of beryllium. None of the measured air samples exceeded 100 ?g/m3, and most were < 10 ?g/m3, lower than usually described. In both cases, lung biopsy about 18 months after acute illness revealed noncaseating granulomas. Years after first exposure, the workers left employment because of CBD. Discussion Contrary to common understanding, these cases suggest that ABD and CBD represent a continuum of disease, and both involve hypersensitivity reactions to beryllium. Differences in disease presentation and progression are likely influenced by the solubility of the beryllium compound involved. Relevance to Practice ABD may occur after exposures lower than the high concentrations commonly described. Prudence dictates limitation of further beryllium exposure in both ABD and CBD. PMID:19672405

Cummings, Kristin J.; Stefaniak, Aleksandr B.; Virji, M. Abbas; Kreiss, Kathleen

2009-01-01

69

Asbestos-induced lung disease.  

PubMed Central

This review attempts to deal with two major questions concerning asbestos-induced lung disease: How does inhaled asbestos cause cell proliferation and fibrosis? and Will there continue to be risk from exposure to asbestos in schools and public buildings? The first is a scientific question that has spawned many interesting new experiments over the past 10 years, and there appear to be two hypothetical schemes which could explain, at least in part, the fibroproliferative effects of asbestos fibers. One supports the view that toxic oxygen radicals generated on fiber surfaces and/or intracellularly are the central mediators of disease. The second hypothesis is not mutually exclusive of the first, but, in my opinion, may be integral to it, i.e., the cellular injury induced by oxygen radicals stimulates the elaboration of multiple varieties of growth factors and cytokines that mediate the pathogenesis of asbestosis. There is increasing evidence that molecules such as platelet-derived growth factor and transforming growth factor beta, both synthesized and secreted by activated lung macrophages, are responsible, respectively, for the increased interstitial cell populations and extracellular matrix proteins that are the hallmarks of asbestos-induced fibrosis. The challenge today is to establish which combinations of the many factors released actually are playing a role in disease pathogenesis. The issue of continued risk currently is more a question of policy and perception than science because a sufficient database has not yet been established to allow full knowledge of the circumstances under which asbestos in buildings constitutes an ongoing health hazard. The litigious nature of this question does not help its resolution. In as much as public policy statements and risk assessment are not within my purview, I have focused on the state-of-the-art of asbestos as a complete carcinogen. It appears to be generally nongenotoxic, but all asbestos fiber types can induce chromosomal mutations and aneuploidy, perhaps through their ability to disrupt normal chromosome segregation. Images FIGURE 1. 1a FIGURE 1. 1b FIGURE 2. FIGURE 3. FIGURE 4. 4a FIGURE 4. 4b FIGURE 5. 5a FIGURE 5. 5b FIGURE 6. PMID:8354168

Brody, A R

1993-01-01

70

Imaging of Childhood Interstitial Lung Disease  

PubMed Central

The aphorism that children are not little adults certainly applies for the imaging of interstitial lung disease. Acquiring motion-free images of fine pulmonary structures at desired lung volumes is much more difficult in children than in adults. Several forms of interstitial lung disease are unique to children, and some forms of interstitial lung disease encountered in adults rarely, if ever, occur in children. Meticulous attention to imaging technique and specialized knowledge are required to properly perform and interpret chest imaging studies obtained for the evaluation of childhood interstitial lung disease (chILD). This review will address technique recommendations for imaging chILD, the salient imaging findings in various forms of chILD, and the efficacy of imaging in the diagnosis and management of chILD. PMID:22332031

2010-01-01

71

Prolonged acute kidney injury exacerbates lung inflammation at 7 days post-acute kidney injury  

PubMed Central

Abstract Patients with acute kidney injury (AKI) have increased mortality; data suggest that the duration, not just severity, of AKI predicts increased mortality. Animal models suggest that AKI is a multisystem disease that deleteriously affects the lungs, heart, brain, intestine, and liver; notably, these effects have only been examined within 48 h, and longer term effects are unknown. In this study, we examined the longer term systemic effects of AKI, with a focus on lung injury. Mice were studied 7 days after an episode of ischemic AKI (22 min of renal pedicle clamping and then reperfusion) and numerous derangements were present including (1) lung inflammation; (2) increased serum proinflammatory cytokines; (3) liver injury; and (4) increased muscle catabolism. Since fluid overload may cause respiratory complications post?AKI and fluid management is a critical component of post?AKI care, we investigated various fluid administration strategies in the development of lung inflammation post?AKI. Four different fluid strategies were tested – 100, 500, 1000, or 2000 ?L of saline administered subcutaneously daily for 7 days. Interestingly, at 7 days post?AKI, the 1000 and 2000 ?L fluid groups had less severe AKI and less severe lung inflammation versus the 100 and 500 ?L groups. In summary, our data demonstrate that appropriate fluid management after an episode of ischemic AKI led to both (1) faster recovery of kidney function and (2) significantly reduced lung inflammation, consistent with the notion that interventions to shorten AKI duration have the potential to reduce complications and improve patient outcomes. PMID:25052489

Andres-Hernando, Ana; Altmann, Christopher; Bhargava, Rhea; Okamura, Kayo; Bacalja, Jasna; Hunter, Brandi; Ahuja, Nilesh; Soranno, Danielle; Faubel, Sarah

2014-01-01

72

Management of acute gallbladder disease in England  

Microsoft Academic Search

Background: Recent literature suggests that early laparoscopic cholecystectomy for acute gallbladder disease is safe and efficacious, but few data are available on the management of acute gallbladder disease in England. Methods: Hospital Episode Statistics data for the years 2003-2005 were obtained from the Department of Health. All patients admitted as an emergency with acute gallbladder disease during the period from

G. G. David; A. A. Al-Sarira; S. Willmott; M. Deakin; D. J. Corless; J. P. Slavin

2008-01-01

73

Acute graft versus host disease  

PubMed Central

Acute graft-versus-host disease (GVHD) occurs after allogeneic hematopoietic stem cell transplant and is a reaction of donor immune cells against host tissues. Activated donor T cells damage host epithelial cells after an inflammatory cascade that begins with the preparative regimen. About 35%–50% of hematopoietic stem cell transplant (HSCT) recipients will develop acute GVHD. The exact risk is dependent on the stem cell source, age of the patient, conditioning, and GVHD prophylaxis used. Given the number of transplants performed, we can expect about 5500 patients/year to develop acute GVHD. Patients can have involvement of three organs: skin (rash/dermatitis), liver (hepatitis/jaundice), and gastrointestinal tract (abdominal pain/diarrhea). One or more organs may be involved. GVHD is a clinical diagnosis that may be supported with appropriate biopsies. The reason to pursue a tissue biopsy is to help differentiate from other diagnoses which may mimic GVHD, such as viral infection (hepatitis, colitis) or drug reaction (causing skin rash). Acute GVHD is staged and graded (grade 0-IV) by the number and extent of organ involvement. Patients with grade III/IV acute GVHD tend to have a poor outcome. Generally the patient is treated by optimizing their immunosuppression and adding methylprednisolone. About 50% of patients will have a solid response to methylprednisolone. If patients progress after 3 days or are not improved after 7 days, they will get salvage (second-line) immunosuppressive therapy for which there is currently no standard-of-care. Well-organized clinical trials are imperative to better define second-line therapies for this disease. Additional management issues are attention to wound infections in skin GVHD and fluid/nutrition management in gastrointestinal GVHD. About 50% of patients with acute GVHD will eventually have manifestations of chronic GVHD. PMID:17784964

Jacobsohn, David A; Vogelsang, Georgia B

2007-01-01

74

Pathogenesis of Lung Disease in Cystic Fibrosis  

Microsoft Academic Search

Lung disease in cystic fibrosis is primarily due to a defect in the cystic fibrosis transmembrane regulating protein (CFTR). This results in abnormal chloride transfer across epithelial membranes causing an excessively viscid mucus lining of the airways. Bacterial invasion particularly with Staphylococcus aureus, Haemophilus influenzae and Pseudomonas aeruginosa stimulates a vigorous and excessive primarily neutrophil-driven inflammatory response throughout the lungs.

R. Dinwiddie

2000-01-01

75

How Are Asbestos-Related Lung Diseases Treated?  

MedlinePLUS

... the NHLBI on Twitter. How Are Asbestos-Related Lung Diseases Treated? No treatments can reverse the effects of ... for lung infections. Rate This Content: Asbestos-Related Lung Diseases Clinical Trials Clinical trials are research studies that ...

76

NET balancing: a problem in inflammatory lung diseases  

PubMed Central

Neutrophil extracellular traps (NETs) are beneficial antimicrobial defense structures that can help fight against invading pathogens in the host. However, recent studies reveal that NETs exert adverse effects in a number of diseases including those of the lung. Many inflammatory lung diseases are characterized with a massive influx of neutrophils into the airways. Neutrophils contribute to the pathology of these diseases. To date, NETs have been identified in the lungs of cystic fibrosis (CF), acute lung injury (ALI), allergic asthma, and lungs infected with bacteria, virus, or fungi. These microbes and several host factors can stimulate NET formation, or NETosis. Different forms of NETosis have been identified and are dependent on varying types of stimuli. All of these pathways however appear to result in the formation of NETs that contain DNA, modified extracellular histones, proteases, and cytotoxic enzymes. Some of the NET components are immunogenic and damaging to host tissue. Innate immune collectins, such as pulmonary surfactant protein D (SP-D), bind NETs, and enhance the clearance of dying cells and DNA by alveolar macrophages. In many inflammatory lung diseases, bronchoalveolar SP-D levels are altered and its deficiency results in the accumulation of DNA in the lungs. Some of the other therapeutic molecules under consideration for treating NET-related diseases include DNases, antiproteases, myeloperoxidase (MPO) inhibitors, peptidylarginine deiminase-4 inhibitors, and anti-histone antibodies. NETs could provide important biological advantage for the host to fight against certain microbial infections. However, too much of a good thing can be a bad thing. Maintaining the right balance of NET formation and reducing the amount of NETs that accumulate in tissues are essential for harnessing the power of NETs with minimal damage to the hosts. PMID:23355837

Cheng, Olivia Z.; Palaniyar, Nades

2013-01-01

77

High incidence of acute lung injury in children with Down syndrome  

Microsoft Academic Search

Objective  Acute respiratory tract infection is a common reason for hospitalization in children with Down syndrome (CDS) and is characterized\\u000a by a high morbidity. The severe course of disease in CDS may be related to a higher incidence of acute lung injury (ALI).\\u000a This study evaluated the incidence of ALI and acute respiratory distress syndrome (ARDS) in mechanically ventilated CDS.\\u000a \\u000a \\u000a \\u000a Design and setting  Retrospective cohort

M. Bruijn; L. B. van der Aa; R. R. van Rijn; A. P. Bos; J. B. M. van Woensel

2007-01-01

78

Research Article Consumption of Hydrogen Water Reduces Paraquat-Induced Acute Lung Injury in Rats  

E-print Network

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Exposure to paraquat leads to acute lung injury and oxidative stress is widely accepted as a contributor to paraquat-induced acute lung injury. Recent studies have reported that consumption of water with dissolved molecular hydrogen to a saturated level (hydrogen water) prevents oxidative stress-induced diseases. Here, we investigated whether consumption of saturated hydrogen saline protects rats against paraquat-induced acute lung injury. Adult male Sprague-Dawley (SD) rats were randomly divided into four groups: Control group; hydrogen water-only group (HW group); paraquat-only group (PQ group); paraquat and hydrogen water group (PQ + HW group). The rats in control group and HW group drank pure water or hydrogen water; the rats in PQ group and PQ + HW group were intraperitonealy injected with paraquat (35 mg/kg) and then provided pure water or hydrogen water. Both biochemical and histological lung alterations were measured. The results showed that hydrogen water ameliorated these alterations, demonstrating that hydrogen water alleviated paraquat-induced acute lung injury possibly by inhibition of oxidative damage. 1.

Shulin Liu; Kan Liu; Qiang Sun; Wenwu Liu; Weigang Xu; Petar Denoble; Hengyi Tao; Xuejun Sun

2011-01-01

79

Transfusion-related acute lung injury after intravenous immunoglobulin treatment in a lung transplant recipient.  

PubMed

Three weeks after single-lung transplantation for pulmonary fibrosis, a patient with high serum levels of de novo donor-specific antibodies received high-dose intravenous immunoglobulin (IVIG) infusion (scheduled dose: 2?g/kg on 2?days) to prevent antibody-mediated rejection. Within the first hours after completion of infusions, he experienced acute lung injury involving the transplanted lung. Given the clinical evolution and the absence of an alternative diagnosis, transfusion-related acute lung injury (TRALI) was diagnosed. The IVIG administered on each day was from the same batch. At day 110, because of an increase in the serum titers of donor-specific antibodies, IVIG therapy was reintroduced but from a different batch, with excellent clinical tolerance. The lung injury was explored biologically, but no mechanism was revealed. Given the increasing use of IVIG in solid-organ recipients, clinicians should be aware of possible TRALI after IVIG infusion. PMID:22985417

Stoclin, A; Delbos, F; Dauriat, G; Brugière, O; Boeri, N; Métivier, A C; Thabut, G; Camus, P; Mal, H

2013-02-01

80

Aggressive and acute periodontal diseases.  

PubMed

Inflammatory periodontal diseases are highly prevalent, although most of these diseases develop and progress slowly, often unnoticed by the affected individual. However, a subgroup of these diseases include aggressive and acute forms that have a relatively low prevalence but show a rapid-course, high rate of progression leading to severe destruction of the periodontal tissues, or cause systemic symptoms that often require urgent attention from healthcare providers. Aggressive periodontitis is an early-onset, destructive disease that shows a high rate of periodontal progression and distinctive clinical features. A contemporary case definition of this disease is presented. Population studies show that the disease is more prevalent in certain geographic regions and ethnic groups. Aggressive periodontitis is an infectious disease, and recent data show that in affected subjects the subgingival microbiota is composed of a mixed microbial infection, with a wide heterogeneity in the types and proportions of microorganisms recovered. Furthermore, there are significant differences in the microbiota of the disease among different geographic regions and ethnicities. There is also evidence that the Aggregatibacter actinomycetemycomitans-JP2 clone may play an important role in the development of the disease in certain populations. The host response plays an important role in the susceptibility to aggressive periodontitis, where the immune response may be complex and involve multiple mechanisms. Also, genetic factors seem to play an important role in the pathogenesis of this disease, but the mechanisms of increased susceptibility are complex and not yet fully understood. The available data suggest that aggressive periodontitis is caused by mutations either in a few major genes or in multiple small-effect genes, and there is also evidence of gene-gene and gene-environment interaction effects. Diagnostic methods for this disease, based on a specific microbiologic, immunologic or genetic profile, currently do not exist. Genetic markers have the potential to be implemented as screening tools to identify subjects at risk. This approach may significantly enhance treatment outcome through the early detection and treatment of affected subjects, as well as using future approaches based on gene therapy. At present, the treatment of this disease is directed toward elimination of the subgingival bacterial load and other local risk factors. Adjunctive use of appropriate systemic antibiotics is recommended and may contribute to a longer suppression of the microbial infection. Other aggressive forms of periodontal diseases occur in patients who are affected with certain systemic diseases, including the leukocyte adhesion deficiency syndrome, Papillon-Lefèvre syndrome, Chediak-Higashi syndrome and Down syndrome. Management of the periodontal component of these diseases is very challenging. Acute gingival and periodontal lesions include a group of disorders that range from nondestructive to destructive forms, and these lesions are usually associated with pain and are a common reason for emergency dental consultations. Some of these lesions may cause a rapid and severe destruction of the periodontal tissues and loss of teeth. Oral infections, particularly acute infections, can spread to extra-oral sites and cause serious medical complications, and even death. Hence, prompt diagnosis and treatment are paramount. PMID:24738583

Albandar, Jasim M

2014-06-01

81

Original Contribution Acute Myocardial Infarction Mortality in Comparison with Lung and Bladder  

E-print Network

Original Contribution Acute Myocardial Infarction Mortality in Comparison with Lung and Bladder) in comparison with the unexposed region V. Increased risks were found for acute myocardial infarction (AMI; Chile; lung neoplasms; mortality; myocardial infarction; urinary bladder neoplasms; water Abbreviations

California at Berkeley, University of

82

Integrating microRNAs into a system biology approach to acute lung injury.  

PubMed

Acute lung injury (ALI), including the ventilator-induced lung injury (VILI) and the more severe acute respiratory distress syndrome (ARDS), are common and complex inflammatory lung diseases potentially affected by various genetic and nongenetic factors. Using the candidate gene approach, genetic variants associated with immune response and inflammatory pathways have been identified and implicated in ALI. Because gene expression is an intermediate phenotype that resides between the DNA sequence variation and the higher level cellular or whole-body phenotypes, the illustration of gene expression regulatory networks potentially could enhance understanding of disease susceptibility and the development of inflammatory lung syndromes. MicroRNAs (miRNAs) have emerged as a novel class of gene regulators that play critical roles in complex diseases including ALI. Comparisons of global miRNA profiles in animal models of ALI and VILI identified several miRNAs (eg, miR-146a and miR-155) previously implicated in immune response and inflammatory pathways. Therefore, via regulation of target genes in these biological processes and pathways, miRNAs potentially contribute to the development of ALI. Although this line of inquiry exists at a nascent stage, miRNAs have the potential to be critical components of a comprehensive model for inflammatory lung disease built by a systems biology approach that integrates genetic, genomic, proteomic, epigenetic as well as environmental stimuli information. Given their particularly recognized role in regulation of immune and inflammatory responses, miRNAs also serve as novel therapeutic targets and biomarkers for ALI/ARDS or VILI, thus facilitating the realization of personalized medicine for individuals with acute inflammatory lung disease. PMID:21420028

Zhou, Tong; Garcia, Joe G N; Zhang, Wei

2011-04-01

83

Interstitial lung disease in systemic sclerosis.  

PubMed

Based on international collaborative data, interstitial lung disease is now the most frequent cause of death in systemic sclerosis (SSc), having supplanted renal crisis in that regard. Despite detailed explorations of candidate mediators, no primary pathway in the pathogenesis of interstitial lung disease associated with SSc (SSc-ILD) has been definitively identified and, therefore, treatment with current agents is only partially successful. However, as immunomodulatory agents do, on average, retard progression of lung disease, early identification of SSc-ILD, using thoracic high resolution computed tomography (HRCT), is highly desirable. The decision whether to introduce therapy immediately is often difficult as the balance of risk and benefit favours a strategy of careful observation when lung disease is very limited, especially in long-standing SSc. The threshold for initiating treatment is substantially reduced when lung disease is severe, systemic disease is short in duration or ongoing progression is evident, based on pulmonary function tests and symptoms. This review summarises epidemiology, pathogenesis, difficult clinical problems and management issues in SSc-ILD. PMID:25217474

Wells, Athol U

2014-10-01

84

[Drug-induced interstitial lung diseases].  

PubMed

Drug-induced infiltrative lung disease may manifest as variable clinical radiological patterns, including subacute or chronic interstitial pneumonia, pulmonary fibrosis, eosinophilic pneumonia, organising pneumonia, pulmonary edema, or sarcoidosis. A large amount of drugs have been incriminated, including those used in cardiovascular diseases (amiodarone, statins and angiotensin converting enzyme inhibitors), antibiotics (minocycline, nitrofurantoin), most of anticancer drugs (and especially chemotherapy and chest radiation), treatment of rheumatoid arthritis, as well as more recent drugs. A high index of suspicion is therefore required in any patient with infiltrative lung disease and the web-based tool www.pneumotox.com will help to list possible causative drugs. The following steps are necessary: history and timing of drug exposure, clinical and imaging pattern, exclusion of other causes of infiltrative lung disease, improvement following drug discontinuation. Rechallenge, dangerous, is not recommended. PMID:25362778

Bonniaud, Philippe; Georges, Marjolaine; Favrolt, Nicolas; Camus, Philippe

2014-09-01

85

A case of interstitial lung disease associated with clinically amyopathic dermatomyositis: radiologic-pathologic correlation.  

PubMed

This case report describes a 64-year-old woman with interstitial lung disease associated with clinically amyopathic dermatomyositis. Chest computed tomography revealed consolidations along bronchovascular bundles in the periphery of the lower lungs. Interstitial lung disease developed acutely, and the patient died 3 months after the clinical diagnosis. An autopsy was performed, and a large section of the lung specimen was prepared. Various interstitial lesions including organizing pneumonia, cellular and fibrotic nonspecific interstitial pneumonia, and diffuse alveolar damage were seen in the large section. Correlating the large section and computed tomography images was useful for determining the distribution of diffuse alveolar damage. PMID:23047733

Okubo, Gosuke; Noma, Satoshi; Nishimoto, Yuko; Sada, Ryuichi; Kobashi, Yoichiro

2013-01-01

86

Berberine attenuates cigarette smoke-induced acute lung inflammation.  

PubMed

Berberine (Ber), the major constituent of Coptidis Rhizoma, possesses anti-inflammatory properties. In this study, we investigated the effects of Ber on cigarette smoke (CS)-mediated acute lung inflammation. C57BL/6 mice (6-8 weeks) were exposed to CS to induce acute lung injury. Ber was used to pretreat CS-exposed mice (50 mg/kg, intragastrically). Lung tissues were collected for histological examination, myeloperoxidase (MPO) activity assay, Western blot analysis, and electrophoretic mobility shift assay. Bronchoalveolar lavage fluid (BALF) was measured for cell counts and cytokine analysis. Histological examination showed that CS exposure caused infiltration of inflammatory cells into alveolar spaces and interstitial edema. Pretreatment with Ber significantly attenuated CS-induced lung inflammation. The numbers of total cells, macrophages, and neutrophils in BALF were decreased by 43, 40, and 53 %, respectively, by Ber pretreatment in CS-exposed mice, accompanied by decreased MPO activity, a marker of neutrophil accumulation. Ber pretreatment also profoundly diminished CS-induced secretions of macrophage inflammatory protein 2, tumor necrosis factor alpha, interleukin-6, and monocyte chemotactic protein-1 in BALF, along with less nuclear translocation of the pro-inflammatory transcription factor nuclear factor-kappa B (NF-?B) p65 subunit and lower NF-?B DNA-binding activity (P?acute lung injury through its anti-inflammatory activity. PMID:23605560

Lin, Kexiong; Liu, Shuanglin; Shen, Yibo; Li, Qi

2013-10-01

87

Baicalin attenuates air embolism-induced acute lung injury in rat isolated lungs  

PubMed Central

Background and purpose Baicalin has been reported to have anti-inflammatory effects and protect against various tissue injuries. However, the effect of baicalin on air embolism-induced acute lung injury has not been tested yet. Experimental approach Acute lung injury was induced by infusion of air at a rate of 0.25 mL·min?1 for 1 min into the pulmonary artery of rat isolated lungs. At the end of the experiment, samples were collected for assessment of lung injury, biochemical analysis and histology. Different doses of baicalin (1, 2 and 4 mg·kg?1) were given into the perfusate before air infusion. Key results Air embolism elicited a significant increase in microvascular permeability (Kf), lung weight gain, wet/dry weight ratio, pulmonary artery pressure and protein concentration in the bronchoalveolar lavage fluid. Levels of the cytokines, tumour necrosis factor ? and cytokine-induced neutrophil chemoattractant-1 in perfusate, and malondialdehyde levels and myeloperoxidase activities in lung tissue were also significantly increased. In addition, histological examination showed increased neutrophil infiltration in lung tissues. Furthermore, nuclear factor-?B activity and degradation of I?B-? were significantly increased in lungs. Pretreatment of the lungs with baicalin (4 mg·kg?1) showed a statistically significant difference in all of the assessed parameters, except for alteration in the pulmonary artery pressure. Conclusions and implications Our study suggests that baicalin attenuated air embolism-induced acute lung injury and may be considered a useful adjunct drug therapy in this clinical condition. PMID:19309358

Li, Min-Hui; Huang, Kun-Lun; Wu, Shu-Yu; Chen, Chien-Wen; Yan, Horng-Chin; Hsu, Kang; Hsu, Ching-Wang; Tsai, Shih-Hung; Chu, Shi-Jye

2009-01-01

88

Previous Lung Diseases and Lung Cancer Risk: A Pooled Analysis From the International Lung Cancer Consortium  

PubMed Central

To clarify the role of previous lung diseases (chronic bronchitis, emphysema, pneumonia, and tuberculosis) in the development of lung cancer, the authors conducted a pooled analysis of studies in the International Lung Cancer Consortium. Seventeen studies including 24,607 cases and 81,829 controls (noncases), mainly conducted in Europe and North America, were included (1984–2011). Using self-reported data on previous diagnoses of lung diseases, the authors derived study-specific effect estimates by means of logistic regression models or Cox proportional hazards models adjusted for age, sex, and cumulative tobacco smoking. Estimates were pooled using random-effects models. Analyses stratified by smoking status and histology were also conducted. A history of emphysema conferred a 2.44-fold increased risk of lung cancer (95% confidence interval (CI): 1.64, 3.62 (16 studies)). A history of chronic bronchitis conferred a relative risk of 1.47 (95% CI: 1.29, 1.68 (13 studies)). Tuberculosis (relative risk = 1.48, 95% CI: 1.17, 1.87 (16 studies)) and pneumonia (relative risk = 1.57, 95% CI: 1.22, 2.01 (12 studies)) were also associated with lung cancer risk. Among never smokers, elevated risks were observed for emphysema, pneumonia, and tuberculosis. These results suggest that previous lung diseases influence lung cancer risk independently of tobacco use and that these diseases are important for assessing individual risk. PMID:22986146

Brenner, Darren R.; Boffetta, Paolo; Duell, Eric J.; Bickeboller, Heike; Rosenberger, Albert; McCormack, Valerie; Muscat, Joshua E.; Yang, Ping; Wichmann, H.-Erich; Brueske-Hohlfeld, Irene; Schwartz, Ann G.; Cote, Michele L.; Tj?nneland, Anne; Friis, S?ren; Le Marchand, Loic; Zhang, Zuo-Feng; Morgenstern, Hal; Szeszenia-Dabrowska, Neonila; Lissowska, Jolanta; Zaridze, David; Rudnai, Peter; Fabianova, Eleonora; Foretova, Lenka; Janout, Vladimir; Bencko, Vladimir; Schejbalova, Miriam; Brennan, Paul; Mates, Ioan N.; Lazarus, Philip; Field, John K.; Raji, Olaide; McLaughlin, John R.; Liu, Geoffrey; Wiencke, John; Neri, Monica; Ugolini, Donatella; Andrew, Angeline S.; Lan, Qing; Hu, Wei; Orlow, Irene; Park, Bernard J.; Hung, Rayjean J.

2012-01-01

89

Assessment of Lung Inflammation With 18F-FDG PET During Acute Lung Injury  

PubMed Central

Objective The purpose of this review is to describe the current experimental and clinical data regarding the fundamentals and applications of 18F-FDG PET during acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Conclusion Lung inflammation is a key feature of ALI. During ALI, FDG PET can be used to monitor lung neutrophils, which are essential cells in the pathophysiologic mechanisms of ALI. Pulmonary FDG kinetics are altered during experimental and human ALI and are associated with regional lung dysfunction, histologic abnormalities, and prognosis. FDG PET may be a valuable noninvasive method for gaining comprehensive understanding of the mechanisms of ALI/ARDS and for evaluating therapeutic interventions. PMID:20651183

de Prost, Nicolas; Tucci, Mauro R.; Vidal Melo, Marcos F.

2011-01-01

90

Lung cancer following therapy for Hodgkin's disease  

PubMed Central

We describe a patient in whom lung cancer developed several years after he had received combined-modality therapy for Hodgkin's disease. The literature concerning second malignant diseases, particularly thoracic tumours, that occur following combined-modality therapy for cancer is reviewed. It is important to recognize these entities, because chest symptoms or findings on x-ray films may be misinterpreted as representing late recrudescence of the first neo-plastic disease. Imagesp533-a PMID:3971271

Oliphant, Lawrie; McFadden, Robin G.

1985-01-01

91

Hypoxia and chronic lung disease  

Microsoft Academic Search

The lung is both the conduit for oxygen uptake and is also affected by hypoxia and hypoxia signaling. Decreased ventilatory\\u000a drive, airway obstructive processes, intra-alveolar exudates, septal thickening by edema, inflammation, fibrosis, or damage\\u000a to alveolar capillaries will all interpose a significant and potentially life-threatening barrier to proper oxygenation, therefore\\u000a enhancing the alveolar\\/arterial pO2 gradient. These processes result in decreased

Rubin M. Tuder; Jeong H. Yun; Anil Bhunia; Iwona Fijalkowska

2007-01-01

92

Respiratory mechanics in patients ventilated for critical lung disease.  

PubMed

Respiratory mechanics, using flow interruption, was previously studied during the complete breath in healthy ventilated man, numerical techniques relieving constraints regarding flow pattern. The classical linear model of non-Newtonian behaviour was found to be valid. The present study was extended to subjects with critical lung disease. Subjects with acute lung injury (ALI; n = 2), acute respiratory distress syndrome (ARDS; n = 4), and chronic obstructive pulmonary disease (COPD; n = 3) were studied with and without positive end-expiratory pressure (PEEP). Functional residual capacity (FRC) was measured with sulphur hexafluoride (SF6) wash-out. The static pressure-volume (P-V) curve was linear at zero end-expiratory pressure (ZEEP), but nonlinear at PEEP. Its hysteresis was nonsignificant. In ALI/ARDS, PEEP increased lung volume by distension and recruitment, but only by distension in COPD. In ALI/ARDS, resistance was increased, at ZEEP. In COPD, resistance became extremely high during expiration at ZEEP. In ALI/ARDS at ZEEP, non-Newtonian behaviour, representing tissue stress relaxation and pendel-luft, complied with the classical linear model. At PEEP, the non-Newtonian compliance became volume-dependent to an extent correlated to the nonlinearity of the static P-V curve. In COPD, non-Newtonian behaviour was adequately explained only with a model with different inspiratory and expiratory behaviour. The classical model of the respiratory system is valid in ALI/ARDS at ZEEP. More advanced models are needed at PEEP and in COPD. PMID:8777962

Beydon, L; Svantesson, C; Brauer, K; Lemaire, F; Jonson, B

1996-02-01

93

Metallothionein-induced zinc partitioning exacerbates hyperoxic acute lung injury  

PubMed Central

Hypozincemia, with hepatic zinc accumulation at the expense of other organs, occurs in infection, inflammation, and aseptic lung injury. Mechanisms underlying zinc partitioning or its impact on extrahepatic organs are unclear. Here we show that the major zinc-binding protein, metallothionein (MT), is critical for zinc transmigration from lung to liver during hyperoxia and preservation of intrapulmonary zinc during hyperoxia is associated with an injury-resistant phenotype in MT-null mice. Particularly, lung-to-liver zinc ratios decreased in wild-type (WT) and increased significantly in MT-null mice breathing 95% oxygen for 72 h. Compared with female adult WT mice, MT-null mice were significantly protected against hyperoxic lung injury indicated by reduced inflammation and interstitial edema, fewer necrotic changes to distal airway epithelium, and sustained lung function at 72 h hyperoxia. Lungs of MT-null mice showed decreased levels of immunoreactive LC3, an autophagy marker, compared with WT mice. Analysis of superoxide dismutase (SOD) activity in the lungs revealed similar levels of manganese-SOD activity between strains under normoxia and hyperoxia. Lung extracellular SOD activity decreased significantly in both strains at 72 h of hyperoxia, although there was no difference between strains. Copper-zinc-SOD activity was ?4× higher under normoxic conditions in MT-null compared with WT mice but was not affected in either group by hyperoxia. Collectively the data suggest that genetic deletion of MT-I/II in mice is associated with compensatory increase in copper-zinc-SOD activity, prevention of hyperoxia-induced zinc transmigration from lung to liver, and hyperoxia-resistant phenotype strongly associated with differences in zinc homeostasis during hyperoxic acute lung injury. PMID:23275622

Lee, Sang-Min; McLaughlin, Joseph N.; Frederick, Daniel R.; Zhu, Lin; Thambiayya, Kalidasan; Wasserloos, Karla J.; Kaminski, Iris; Pearce, Linda L.; Peterson, Jim; Li, Jin; Latoche, Joseph D.; Peck Palmer, Octavia M.; Stolz, Donna Beer; Fattman, Cheryl L.; Alcorn, John F.; Oury, Tim D.; Angus, Derek C.; Pitt, Bruce R.

2013-01-01

94

Stem cell treatment for chronic lung diseases.  

PubMed

Chronic lung diseases such as idiopathic pulmonary fibrosis and cystic fibrosis or chronic obstructive pulmonary disease and asthma are leading causes of morbidity and mortality worldwide with a considerable human, societal and financial burden. In view of the current disappointing status of available pharmaceutical agents, there is an urgent need for alternative more effective therapeutic approaches that will not only help to relieve patient symptoms but will also affect the natural course of the respective disease. Regenerative medicine represents a promising option with several fruitful therapeutic applications in patients suffering from chronic lung diseases. Nevertheless, despite relative enthusiasm arising from experimental data, application of stem cell therapy in the clinical setting has been severely hampered by several safety concerns arising from the major lack of knowledge on the fate of exogenously administered stem cells within chronically injured lung as well as the mechanisms regulating the activation of resident progenitor cells. On the other hand, salient data arising from few 'brave' pilot investigations of the safety of stem cell treatment in chronic lung diseases seem promising. The main scope of this review article is to summarize the current state of knowledge regarding the application status of stem cell treatment in chronic lung diseases, address important safety and efficacy issues and present future challenges and perspectives. In this review, we argue in favor of large multicenter clinical trials setting realistic goals to assess treatment efficacy. We propose the use of biomarkers that reflect clinically inconspicuous alterations of the disease molecular phenotype before rigid conclusions can be safely drawn. PMID:23364286

Tzouvelekis, Argyris; Ntolios, Paschalis; Bouros, Demosthenes

2013-01-01

95

Computed tomography of diffuse interstitial lung disease in children.  

PubMed

Unlike diseases of the airways, interstitial lung diseases in childhood are exceedingly rare and are usually associated with significant morbidity and mortality. Interstitial lung disease in the paediatric age group is a particular diagnostic challenge because the clinical presentation and radiographic features are so non-specific. High resolution computed tomography (HRCT) has proved its worth in adults with interstitial lung disease and has a role, albeit more limited, in the non-invasive evaluation of paediatric interstitial lung disease. PMID:10988042

Koh, D M; Hansell, D M

2000-09-01

96

Xuan Bai Cheng Qi formula as an adjuvant treatment of acute exacerbation of chronic obstructive pulmonary disease of the syndrome type phlegm-heat obstructing the lungs: a multicenter, randomized, double-blind, placebo-controlled clinical trial  

PubMed Central

Background Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is a common cause of morbidity and mortality. Traditional Chinese medicine (TCM) is used to treat AECOPD as adjunctive therapy. This study aimed to evaluate the efficacy and safety of the TCM formula Xuan Bai Cheng Qi as an adjuvant therapy for AECOPD patients with the syndrome type of phlegm-heat obstructing the lungs. Methods A multicenter, randomized, double-blind, placebo-controlled clinical trial was conducted. A total of 244 patients were divided into the intervention group (n?=?122, treated with conventional medicine and Xuan Bai Cheng Qi) and the control group (n?=?122, treated with conventional medicine and placebo). Total symptom scores (cough, phlegm, wheezing, chest congestion) before treatment and at 3, 5, 7, 10 days post-treatment were recorded. Lung function, arterial blood gas, serum inflammatory cytokines, oxidation/anti-oxidation index were observed before treatment and at the end of the 10-day treatment. Results A total of 242 patients completed the study. The full analysis set (FAS) population was 244 and the per-protocol analysis set (PPS) population was 229. After the 10-day treatment, symptom scores of the Xuan Bai Cheng Qi group were significantly lower over time compared with the control group (FAS: mean difference -1.84, 95% CI -2.66 to -1.03, P?lungs syndrome type. PMID:25014996

2014-01-01

97

Acute lung injury after inhalation of nitric acid.  

PubMed

We report two cases of acute lung injury after the inhalation of nitric acid fumes in an industrial accident. The first patient, who was not using a respirator and standing in close proximity to the site of spillage of concentrated nitric acid, presented within 12 h with worsening dyspnea and required noninvasive ventilation for type 1 respiratory failure. The second case presented 1 day later with similar symptoms, but only required supportive treatment with high-flow oxygen. Both patients' chest radiographs showed widespread bilateral airspace shadows consistent with acute lung injury. Both received treatment with systemic steroids. They were discharged from hospital 5 days postexposure. Initial lung function test showed a restrictive pattern that normalized by 3 weeks postexposure. This case series describes the natural history after acute inhalation of nitric acid fumes, and demonstrates that the severity of lung injury is directly dependent on the exposure level. It also highlights the use of noninvasive ventilatory support in the management of such patients. PMID:19078840

Kao, Shih Ling; Yap, Eng Soo; Khoo, See Meng; Lim, Tow Keang; Mukhopadhyay, Amartya; Teo, Sylvia Tzu Li

2008-12-01

98

Stevioside protects LPS-induced acute lung injury in mice.  

PubMed

Stevioside, a diterpene glycoside component of Stevia rebaudiana, has been known to exhibit anti-inflammatory properties. To evaluate the effect and the possible mechanism of stevioside in lipopolysaccharide (LPS)-induced acute lung injury, male BALB/c mice were pretreated with stevioside or dexamethasone 1 h before intranasal instillation of LPS. Seven hours later, tumor necrosis factor-?, interleukin-1?, and interleukin-6 in bronchoalveolar lavage fluid (BALF) were measured by using enzyme-linked immunosorbent assay. The number of total cells, neutrophils, and macrophages in the BALF were also determined. The right lung was excised for histological examination and analysis of myeloperoxidase activity and nitrate/nitrite content. Cyclooxygenase 2 (COX-2), inducible NO synthase (iNOS), nuclear factor-kappa B (NF-?B), inhibitory kappa B protein were detected by western blot. The results showed that stevioside markedly attenuated the LPS-induced histological alterations in the lung. Stevioside inhibited the production of pro-inflammatory cytokines and the expression of COX-2 and iNOS induced by LPS. In addition, not only was the wet-to-dry weight ratio of lung tissue significantly decreased, the number of total cells, neutrophils, and macrophages in the BALF were also significantly reduced after treatment with stevioside. Moreover, western blotting showed that stevioside inhibited the phosphorylation of I?B-? and NF-?B caused by LPS. Taken together, our results suggest that anti-inflammatory effect of stevioside against the LPS-induced acute lung injury may be due to its ability of inhibition of the NF-?B signaling pathway. Stevioside may be a promising potential therapeutic reagent for acute lung injury treatment. PMID:22968433

Yingkun, Nie; Zhenyu, Wang; Jing, Lin; Xiuyun, Lu; Huimin, Yu

2013-02-01

99

Treatment of interstitial lung disease in children  

Microsoft Academic Search

The treatment of interstitial lung disease in children depends on the nature of the underlying pathology. In approximately 50% of cases a specific aetiology can be found such as: chronic viral infection, an auto-immune process, sarcoidosis or alveolar proteinosis. In the remainder, the process is idiopathic and the pathological findings are based on the descriptive morphological features seen in the

R Dinwiddie

2004-01-01

100

Update in Diffuse Parenchymal Lung Diseases 2005  

Microsoft Academic Search

CLINICAL ADVANCES A number of publications have shed light on important clinical concepts surrounding the clinical evaluation and management of diffuse parenchymal lung diseases (DPLDs). These include approaches to idiopathic interstitial pneumonias (IIPs), includ- ing nonspecific interstitial pneumonia (NSIP) and idiopathic pul- monary fibrosis (IPF; idiopathic usual interstitial pneumonia (UIP)), connective tissue-associated DPLD, hypersensitivity pneumonitis (HP), and lymphangioleiomyomatosis (LAM). IIPs

Fernando J. Martinez; Michael P. Keane

101

Electronic Nose for Identification of Lung Diseases  

Microsoft Academic Search

In the paper, the authors analyze the preliminary results of testing a classical gas sensing instrument - the electronic nose (a metal oxide transistor sensor of chemical substances) in a hospital where patients with different lung diseases are treated. To reveal the correlation between the amplitudes of the sensor's responses and the patients' diagnoses, different statistical analysis methods have been

V. Ogorodnik; J. Kleperis; I. Taivans; N. Jurka; M. Bukovskis

2008-01-01

102

Long-Term Control Medications for Lung Diseases  

MedlinePLUS

... Term Control Medications Long-Term Control Medications for Lung Diseases Long-term control medications are taken daily to control and prevent lung disease symptoms. These medicines should be taken every day ...

103

Cigar Smoking Causes Several Cancers and Lung and Heart Disease  

Cancer.gov

A report released by the NCI shows that daily cigar smoking causes cancers of the lip, tongue, mouth, throat, larynx, esophagus, and lung, as well as chronic obstructive pulmonary (lung) disease and coronary heart disease.

104

Extracellular matrix mechanics in lung parenchymal diseases  

PubMed Central

In this review, we examine how the extracellular matrix (ECM) of the lung contributes to the overall mechanical properties of the parenchyma, and how these properties change in disease. The connective tissues of the lung are composed of cells and ECM, which includes a variety of biological macromolecules and water. The macromolecules that are most important in determining the mechanical properties of the ECM are collagen, elastin, and proteoglycans. We first discuss the various components of the ECM and how their architectural organization gives rise to the mechanical properties of the parenchyma. Next, we examine how mechanical forces can affect the physiological functioning of the lung parenchyma. Collagen plays an especially important role in determining the homeostasis and cellular responses to injury because it is the most important load-bearing component of the parenchyma. We then demonstrate how the concept of percolation can be used to link microscopic pathologic alterations in the parenchyma to clinically measurable lung function during the progression of emphysema and fibrosis. Finally, we speculate about the possibility of using targeted tissue engineering to optimize treatment of these two major lung diseases. PMID:18485836

Suki, Bela; Bates, Jason H.T.

2008-01-01

105

Acute irreversible oxalate nephropathy in a lung transplant recipient treated successfully with a renal transplant.  

PubMed

We report a 29 year old male cystic fibrosis patient with end stage lung disease and normal renal function who underwent a sequential double lung transplant. Medical history included: an ileal resection and pancreatic exocrine dysfunction. The postoperative period was complicated with haemorrhage and repeat surgery, requiring multiple blood transfusions and extensive antibiotic cover. Pancreatic supplements were interrupted. Acute renal failure attributed to haemodynamically-mediated acute tubular necrosis was managed expectantly. He remained dialysis dependent 8 weeks post surgery and was maintained on triple immunosuppression with tacrolimus, mycophenolate and prednisolone. A DTPA study was consistent with ATN. Renal biopsy revealed features consistent with tubular injury due to acute oxalate nephropathy (AON). Further biochemical characterization excluded primary hyperoxaluria but confirmed increased 24 hour urinary oxalate. He was maintained on enhanced frequency HDF and subsequently received an uncomplicated live related renal transplant 10 months post lung transplant with only additional basiliximab. Calcium carbonate was continued to manage post transplant hyperoxaluria and an early renal biopsy excluded recurrent oxalate injury. Enteric hyperoxaluria due to malabsorption in patients with CF especially with ileal resection, in addition to loss of gut Oxalobacter formigenes due to prolonged antimicrobials, increases the risk of AON. Increased awareness of this condition and screening prior to lung transplant is recommended. PMID:22497648

Dheda, Shyam; Swaminathan, Ramyasuda; Musk, Michael; Sinniah, Rajalingam; Lawrence, Sharon; Irish, Ashley

2012-04-01

106

Presumptive acute lung injury following multiple surgeries in a cat  

PubMed Central

A 12-year-old, 3.5-kg spayed female domestic shorthair cat had a tracheal mass identified as malignant B-cell lymphoma. The cat had tracheal resection and subsequently developed laryngeal paralysis. Due to multiple episodes of respiratory distress the cat subsequently had tracheal surgeries. Finally, the cat had a sudden onset of severe respiratory distress and collapsed. Computed tomography imaging and arterial blood gas analysis supported a diagnosis of acute lung injury. PMID:24082167

Katayama, Masaaki; Okamura, Yasuhiko; Katayama, Rieko; Sasaki, Jun; Shimamura, Shunsuke; Uzuka, Yuji; Kamishina, Hiroaki; Nezu, Yoshinori

2013-01-01

107

New concepts of the pathogenesis of cystic fibrosis lung disease  

Microsoft Academic Search

New concepts of the pathogenesis of cystic fibrosis lung disease. R.C. Boucher. #ERS Journals Ltd 2004. ABSTRACT: Although there has been impressive progress in the elucidation of the genetic and molecular basis of cystic fibrosis (CF), the pathogenesis of CF lung disease remains obscure. The elucidation of the pathogenesis of CF lung disease requires both a full description of normal

R. C. Boucher

2004-01-01

108

Identification of Early Interstitial Lung Disease in Smokers from the  

E-print Network

: Early interstitial lung disease; CT scan; smoker. ªAUR, 2010 I diopathic pulmonary fibrosis (IPFIdentification of Early Interstitial Lung Disease in Smokers from the COPDGene Study George R interstitial lung disease (ILD) on chest computed tomographic (CT) scans. Materials and Methods: The CT scans

109

Zingerone attenuates lipopolysaccharide-induced acute lung injury in mice.  

PubMed

Zingerone, one of the active components of ginger, is a phenolic alkanone with antioxidant and anti-inflammatory properties. In the present study, we analyzed the role of zingerone against RAW 264.7 cells and acute lung injury induced by lipopolysaccharide (LPS) in mice. RAW cells or BALB/c mice were pretreated with zingerone one hour before stimulated with LPS. We found that zingerone significantly inhibited the production of LPS-induced proinflammatory cytokines in vitro and in vivo. When pretreated with zingerone, pulmonary histopathologic changes, as well as alveolar hemorrhage and neutrophil infiltration were substantially suppressed in lung tissues, with evidence of reduced myeloperoxidase (MPO) activity in murine acute lung injury model. The lung wet-to-dry weight (W/D) ratios, as the index of pulmonary edema, were markedly decreased by zingerone pretreatment. Furthermore, we demonstrated that zingerone attenuates the mitogen-activated protein kinases (MAPK) and nuclear factor-kappaB (NF-?B) signaling pathways through blocking the phosphorylation of ERK, p38/MAPK and I?B?, NF-?B/P65. These results suggest that zingerone may provide protective effects against LPS-induced ALI. PMID:24412620

Xie, Xianxing; Sun, Shicheng; Zhong, Weiting; Soromou, Lanan Wassy; Zhou, Xuan; Wei, Miaomiao; Ren, Yanling; Ding, Yu

2014-03-01

110

Does aluminum smelting cause lung disease  

SciTech Connect

The evidence concerning a relationship between work in the aluminum industry and lung disease has been reviewed using epidemiologic criteria. Adequate data on environmental exposure are rarely presented. Case series on aluminum potroom workers over the past 50 years have identified an asthmalike syndrome that appears to be due to an irritant rather than an allergic mechanism. These studies have been supported by evidence of within shift variability of measures of lung function. However, to date, there is inadequate evidence to resolve the question of whether potroom exposure initiates asthma or merely precipitates asthmalike symptoms in a predisposed individual. Cross-sectional studies have demonstrated evidence of reduced lung function, consistent with chronic airflow limitation. In exposed aluminum smelter workers compared to unexposed control subjects. Cigarette smoking, the major potential confounding variable, has been measured and accounted for in multivariate analyses. To date, evidence is lacking from longitudinal studies about the development of disabling chronic obstructive lung disease. Exposure to coal tar pitch volatiles in the production and consumption of anodes has biologic plausibility for an association of lung cancer with work in an aluminum smelter. Although retrospective mortality studies have failed to account for the probable high prevalence of smoking in blue collar workers, the relative risk of lung cancer is very low if present at all. Pulmonary fibrosis has not been shown to be a significant problem in aluminum smelter workers. Future research in the aluminum industry needs to concentrate on longitudinal studies, preferably with an inception cohort for the investigation of potroom asthma. 92 references.

Abramson, M.J.; Wlodarczyk, J.H.; Saunders, N.A.; Hensley, M.J.

1989-04-01

111

Lung diseases after bone marrow transplantation  

Microsoft Academic Search

Summary The case histories of 72 subsequently treated patients — 44 with acute leukemia, 10 with chronic myeloid leukemia, 16 with severe aplastic anemia and 2 with neuroblastoma — were analyzed after bone marrow transplantation (BMT) with respect to pulmonary diseases. Thirty-eight patients suffered from a total of 51 pulmonary complications, which led to death in 20. Of 13 patients,

H. Link; U. Reinhard; E. Walter; P. Wernet; E. M. Schneider; H. Fischbach; M. Blaurock; K. Wilms; D. Niethammer; P. Ostendorf

1986-01-01

112

OXIDANTS AND THE PATHOGENESIS OF LUNG DISEASES  

PubMed Central

The increasing number of population-based and epidemiological associations between oxidant pollutant exposures and cardiopulmonary disease exacerbation, decrements in pulmonary function, and mortality underscores the important detrimental effects of oxidants on public health. Because inhaled oxidants initiate a number of pathologic processes, including inflammation of the airways which may contribute to the pathogenesis and/or exacerbation of airways disease, it is critical to understand the mechanisms through which exogenous and endogenous oxidants interact with molecules in the cells, tissues, and epithelial lining fluid (ELF) of the lung. Furthermore, it is clear that inter-individual variation in response to a given exposure also exists across an individual lifetime. Because of the potential impact that oxidant exposures may have on reproductive outcomes and infant, child, and adult health, identification of the intrinsic and extrinsic factors that may influence susceptibility to oxidants remains an important issue. In this review, we discuss mechanisms of oxidant stress in the lung, the role of oxidants in lung disease pathogenesis and exacerbation (e.g. asthma, COPD, and ARDS), and the potential risk factors (e.g. age, genetics) for enhanced susceptibility to oxidant-induced disease. PMID:18774381

Ciencewicki, Jonathan; Trivedi, Shweta; Kleeberger, Steven R.

2009-01-01

113

Betulin protects mice from bacterial pneumonia and acute lung injury.  

PubMed

Betulin, a naturally occurring triterpene, has shown anti-HIV activity, but details on the anti-inflammatory activity are scanty. In this study, we sought to investigate the effect of Betulin on LPS-induced activation of cell lines with relevance for lung inflammation in vitro and on lung inflammation elicited by either LPS or viable Escherichia coli (E. coli) in vivo. In vitro, Betulin inhibited LPS-induced tumor necrosis factor ? (TNF-?) and (interleukin) IL-6 levels and up-regulated the level of IL-10. Also Betulin suppressed the phosphorylation of nuclear factor-?B (NF-?B) p65 protein in LPS-stimulated RAW 264.7 cells. In vivo, Betulin alleviated LPS-induced acute lung injury. Treatment with Betulin diminished pro-inflammatory cytokines, myeloperoxidase activity and bacterial loads in lung tissue during gram-negative pneumonia. Our findings demonstrated that Betulin inhibits pro-inflammatory responses induced by the gram-negative stimuli LPS and E. coli, suggesting that Betulin may represent a novel strategy for the treatment of lung inflammation. PMID:25173422

Wu, Qianchao; Li, Hongyu; Qiu, Jiaming; Feng, Haihua

2014-10-01

114

The role of toll-like receptors in acute and chronic lung inflammation  

PubMed Central

By virtue of its direct contact with the environment, the lung is constantly challenged by infectious and non-infectious stimuli that necessitate a robust yet highly controlled host response coordinated by the innate and adaptive arms of the immune system. Mammalian Toll-like receptors (TLRs) function as crucial sentinels of microbial and non-infectious antigens throughout the respiratory tract and mediate host innate immunity. Selective induction of inflammatory responses to harmful environmental exposures and tolerance to innocuous antigens are required to maintain tissue homeostasis and integrity. Conversely, dysregulated innate immune responses manifest as sustained and self-perpetuating tissue damage rather than controlled tissue repair. In this article we review aspects of Toll-like receptor function that are relevant to the development of acute lung injury and chronic obstructive lung diseases as well as resistance to frequently associated microbial infections. PMID:21108806

2010-01-01

115

Acute Respiratory Distress Syndrome Caused by Pulmonary and Extrapulmonary Disease Different Syndromes?  

Microsoft Academic Search

To assess the possible differences in respiratory mechanics between the acute respiratory distress syndrome (ARDS) originating from pulmonary disease (ARDS p ) and that originating from extrapul- monary disease (ARDS exp ) we measured the total respiratory system (Est,rs), chest wall (Est,w) and lung (Est,L) elastance, the intra-abdominal pressure (IAP), and the end-expiratory lung volume (EELV) at 0, 5, 10,

LUCIANO GATTINONI; PAOLO PELOSI; PETER M. SUTER; ALESSIA PEDOTO; PAOLA VERCESI; ALFREDO LISSONI

116

Cell proliferation in lung following acute fly ash exposure.  

PubMed

Cell proliferation was examined in the lung parenchyma, the ciliated airway epithelium and the lymph nodes of Fischer-344 rats following a 6-h exposure to fly ash obtained from the baghouse of an experimental fluidized bed combustor. The fly ash concentration was 142 mg/m3 with a mass median aerodynamic diameter (MMAD) of approximately 3.0 micron and a geometric standard deviation (sigma g) of approximately 2.6. Lung deposition of fly ash was measured in the right lung to be 90 +/- 20 and 80 +/- 30 mg for male and female rats, respectively, resulting in a calculated value for male rats of (140 +/- 30 micrograms/animal) and for female rats of 130 +/- 50 micrograms/animal). Autoradiographic methods were used to detect cells that incorporated [3H] thymidine. About a 10-fold increase in labeling of the lung epithelial type II cells was observed following the 6-h fly ash exposure. There was also an increase in [3H] thymidine incorporation into DNA of alveolar macrophages. Labeling activity of macrophages within the lung was increased for up to 4 days following fly ash exposure; however, the size of the macrophage population was not altered. Following exposure, a higher labeling index was also observed in the epithelial cells of the airways. Labeling in the trachea reached a peak at 4 days after exposure while in the bronchi and in small airways (inside diameter of less than 0.35 mm) the highest level of labeling was observed at 1 day after exposure. Labeling in airway epithelial cells was increased 2-4 times above that of sham-exposed animals. Lung-associated lymph nodes accumulated particulate material and had variable amounts of [3H]thymidine incorporation. These results demonstrate that acute inhalation exposure to fly ash initiated cell division or DNA synthesis in several cell populations of lung parenchyma and airways. PMID:6623476

Hackett, N A

1983-01-01

117

Trauma-associated lung injury differs clinically and biologically from acute lung injury due to other clinical disorders*  

PubMed Central

Objective Patients with trauma-associated acute lung injury have better outcomes than patients with other clinical risks for lung injury, but the mechanisms behind these improved outcomes are unclear. We sought to compare the clinical and biological features of patients with trauma-associated lung injury with those of patients with other risks for lung injury and to determine whether the improved outcomes of trauma patients reflect their baseline health status or less severe lung injury, or both. Design, Setting, and Patients Analysis of clinical and biological data from 1,451 patients enrolled in two large randomized, controlled trials of ventilator management in acute lung injury. Measurements and Main Results Compared with patients with other clinical risks for lung injury, trauma patients were younger and generally less acutely and chronically ill. Even after adjusting for these baseline differences, trauma patients had significantly lower plasma levels of intercellular adhesion molecule-1, von Willebrand factor antigen, surfactant protein-D, and soluble tumor necrosis factor receptor-1, which are biomarkers of lung epithelial and endothelial injury previously found to be prognostic in acute lung injury. In contrast, markers of acute inflammation, except for interleukin-6, and disordered coagulation were similar in trauma and nontrauma patients. Trauma-associated lung injury patients had a significantly lower odds of death at 90 days, even after adjusting for baseline clinical factors including age, gender, ethnicity, comorbidities, and severity of illness (odds ratio, 0.44; 95% confidence interval, 0.24 – 0.82; p = .01). Conclusions Patients with trauma-associated lung injury are less acutely and chronically ill than other lung injury patients; however, these baseline clinical differences do not adequately explain their improved outcomes. Instead, the better outcomes of the trauma population may be explained, in part, by less severe lung epithelial and endothelial injury. PMID:17944012

Calfee, Carolyn S.; Eisner, Mark D.; Ware, Lorraine B.; Thompson, B. Taylor; Parsons, Polly E.; Wheeler, Arthur P.; Korpak, Anna; Matthay, Michael A.

2009-01-01

118

Niacinamide mitigated the acute lung injury induced by phorbol myristate acetate in isolated rat's lungs  

PubMed Central

Background Phorbol myristate acetate (PMA) is a strong neutrophil activator and has been used to induce acute lung injury (ALI). Niacinamide (NAC) is a compound of B complex. It exerts protective effects on the ALI caused by various challenges. The purpose was to evaluate the protective effects of niacinamide (NAC) on the PMA-induced ALI and associated changes. Methods The rat's lungs were isolated in situ and perfused with constant flow. A total of 60 isolated lungs were randomized into 6 groups to received Vehicle (DMSO 100 ?g/g), PMA 4 ?g/g (lung weight), cotreated with NAC 0, 100, 200 and 400 mg/g (lung weight). There were 10 isolated lungs in each group. We measured the lung weight and parameters related to ALI. The pulmonary arterial pressure and capillary filtration coefficient (Kfc) were determined in isolated lungs. ATP (adenotriphosphate) and PARP [poly(adenosine diphophate-ribose) polymerase] contents in lung tissues were detected. Real-time PCR was employed to display the expression of inducible and endothelial NO synthases (iNOS and eNOS). The neutrophil-derived mediators in lung perfusate were determined. Results PMA caused increases in lung weight parameters. This agent produced pulmonary hypertension and increased microvascular permeability. It resulted in decrease in ATP and increase in PARP. The expression of iNOS and eNOS was upregulated following PMA. PMA increased the neutrophil-derived mediators. Pathological examination revealed lung edema and hemorrhage with inflammatory cell infiltration. Immunohistochemical stain disclosed the presence of iNOS-positive cells in macrophages and endothelial cells. These pathophysiological and biochemical changes were diminished by NAC treatment. The NAC effects were dose-dependent. Conclusions Our results suggest that neutrophil activation and release of neutrophil-derived mediators by PMA cause ALI and associated changes. NO production through the iNOS-producing cells plays a detrimental role in the PMA-induced lung injury. ATP is beneficial, while PARP plays a deteriorative effect on the PMA-induced ALI. NAC exerts protective effects on the inflammatory cascade leading to pulmonary injury. This B complex compound may be applied for clinical usage and therapeutic regimen. PMID:22375599

2012-01-01

119

Dust-induced interstitial lung disease in the tropics.  

PubMed

Inhalation of dusts is an important cause of interstitial lung disease in the tropical countries such as India. While dusts of organic origin, such as the cotton dust causing byssinosis, generally cause bronchial or bronchiolar involvement and hypersensitivity pneumonitis, inorganic metallic dusts cause progressive pulmonary fibrosis. Silicosis, coal workers' pneumoconiosis, and asbestosis are the three most commonly recognized forms of pneumoconiotic pulmonary fibrosis. Pulmonary tuberculosis is an important complication seen in up to 50% of patients of silicosis in some reports from India. The presentation is generally chronic, although acute and accelerated forms of silicosis are known when the exposures are heavy. Breathlessness, dry cough, and general constitutional symptoms are commonly seen. Patients with silicotuberculosis or other forms of infection may also have significant expectoration, hemoptysis, fever, and rapid progression. Respiratory failure and chronic cor pulmonale occur in the later stages. The diagnosis is easily established if the occupational history is available. Dense nodular opacities on chest roentgenograms, which may be large in patients with massive pulmonary fibrosis, are characteristic. Emphysematous changes generally appear in advanced stages or in patients who smoke. Bronchoalveolar lavage and/or lung biopsy may occasionally be required to establish or exclude other causes of interstitial lung disease. Treatment is largely palliative, although a variety of drugs including corticosteroids and procedures such as whole lung lavage have been tried. None of these methods has yet been found successful in the treatment. Preventive safety steps, including removal of the patient from the site of exposure, are the only effective strategies to control disease progression. PMID:11584175

Jindal, S K; Aggarwal, A N; Gupta, D

2001-09-01

120

Incidence and outcome of acute lung injury and acute respiratory distress syndrome in the surgical intensive care unit  

PubMed Central

Introduction: To determine the incidence and mortality of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) in a cohort of patients with risk factors admitted to the Surgical Intensive Care Unit (SICU). Materials and Methods: A prospective observational inception cohort study with no intervention was conducted over 12 months. All patients with at least one known risk factor for ALI/ARDS admitted to the SICU were included in the study. The APACHE II severity of disease classification system scoring was performed within 1 h of admission. The ventilatory parameters and chest radiographs were recorded every 24 h. The P/F ratio, PEEP and Lung Injury Score were calculated each day until the day of discharge from the Intensive Care Unit or for the first 7 days of admission, whichever was shorter. Results: The incidence of ARDS among those who were mechanically ventilated was 11.4%. Sepsis was the most common (34.6%) etiology. Among those with risk factors, the incidence of ARDS was 30% and that of ALI was 32.7%. The mortality in those with ARDS was 41.8%. Those who develop ARDS had higher APACHE II scores, lower pH and higher PaCO2 at admission compared with those who developed ALI or no lung injury. Conclusion: The incidence and mortality of ARDS was similar to other studies. Identifying those with risk factors for ARDS or mortality will enable appropriate interventional measures.

Singh, Georgene; Gladdy, George; Chandy, Tony Thomson; Sen, Nagamani

2014-01-01

121

Obstructive lung disease models: what is valid?  

PubMed

Use of disease simulation models has led to scrutiny of model methods and demand for evidence that models credibly simulate health outcomes. We sought to describe recent obstructive lung disease simulation models and their validation. Medline and EMBASE were used to identify obstructive lung disease simulation models published from January 2000 to June 2006. Publications were reviewed to assess model attributes and four types of validation: first-order (verification/debugging), second-order (comparison with studies used in model development), third-order (comparison with studies not used in model development), and predictive validity. Six asthma and seven chronic obstructive pulmonary disease models were identified. Seven (54%) models included second-order validation, typically by comparing observed outcomes to simulations of source study cohorts. Seven (54%) models included third-order validation, in which modeled outcomes were usually compared qualitatively for agreement with studies independent of the model. Validation endpoints included disease prevalence, exacerbation, and all-cause mortality. Validation was typically described as acceptable, despite near-universal absence of criteria for judging adequacy of validation. Although over half of recent obstructive lung disease simulation models report validation, inconsistencies in validation methods and lack of detailed reporting make assessing adequacy of validation difficult. For simulation modeling to be accepted as a tool for evaluating clinical and public health programs, models must be validated to credibly simulate health outcomes of interest. Defining the required level of validation and providing guidance for quantitative assessment and reporting of validation are important future steps in promoting simulation models as practical decision tools. PMID:19353353

Ferdinands, Jill M; Mannino, David M

2008-12-01

122

Adult Stem Cells for Acute Lung Injury: Remaining Questions & Concerns  

PubMed Central

Acute lung injury (ALI) or acute respiratory distress syndrome remains a major cause of morbidity and mortality in hospitalized patients. The pathophysiology of ALI involves complex interactions between the inciting event, such as pneumonia, sepsis or aspiration, and the host immune response resulting in lung protein permeability, impaired resolution of pulmonary edema, an intense inflammatory response in the injured alveolus and hypoxemia. In multiple pre-clinical studies, adult stem cells have been shown to be therapeutic due to both the ability to mitigate injury and inflammation through paracrine mechanisms and perhaps to regenerate tissue by virtue of their multi-potency. These characteristics have stimulated intensive research efforts to explore the possibility of using stem or progenitor cells for the treatment of lung injury. A variety of stem or progenitor cells have been isolated, characterized, and tested experimentally in pre-clinical animal models of ALI. However, questions remain concerning the optimal dose, route and the adult stem or progenitor cell to use. Here, we review current mechanisms underlying the therapeutic effect of stem cells in ALI as well as the questions that will arise as clinical trials for ALI are planned. PMID:23578018

Zhu, Ying-gang; Hao, Qi; Monsel, Antoine; Feng, Xiao-mei

2013-01-01

123

Instilled air promotes lipopolysaccharide-induced acute lung injury  

PubMed Central

Optimization of intratracheal instillation is necessary to establish an ideal animal model of acute lung injury (ALI) in order to further reveal the cellular and molecular pathogenesis of ALI. It is possible that instilling air from a prefilled syringe may promote the delivery of reagents into the alveolar spaces, resulting in different pulmonary responses. In the present study, the influence of instilling air by trans-tracheal intratracheal instillation in a lipopolysaccharide (LPS)-induced mouse model of ALI was investigated. The bronchoalveolar lavage (BAL) fluid biochemical index, BAL fluid differential cell counts, lung wet/dry weight ratio, lung histology and BAL fluid interleukin-8 (IL-8) levels were assessed 24 h subsequent to intratracheal instillation. Instilled air promoted LPS-induced ALI, as indicated by the severity of acute pulmonary inflammation and increased IL-8 release. In conclusion, this study indicates that instilled air may be used to improve the intratracheal instillation procedure and to establish a more reliable animal model of ALI. PMID:24660029

ZOU, YINGGANG; DONG, CHUNLING; YUAN, MINGZHEN; GAO, GUANGYUAN; WANG, SIYI; LIU, XIAODING; HAN, HUIQIAO; LI, BO

2014-01-01

124

Antioxidant vitamins and prevention of lung disease.  

PubMed

Although the evidence for oxidative stress for air pollution in the human lung is fragmentary, the hypothesis that oxidative stress is an important, if not the sole, mechanism of toxicity of oxidizing air pollutants and tobacco smoke is compelling and growing. First, biochemical mechanisms have been worked out for oxidation of lung lipids by the gas phase of cigarette smoke, NO2 and O3. The oxidation of lung lipids can be prevented by both vitamins C and E. Vitamin C is more effective in preventing oxidation by NO2, and vitamin E is more effective against O3. Second, multiple species of experimental animals develop lung disease similar to human bronchitis and emphysema from exposure to NO2 and O3, respectively. The development of these diseases occurs over a near lifetime exposure when the levels of NO2 or O3 are at near ambient air pollution values. Third, isolated human cells are protected against oxidative damage from NO2 and O3 by both vitamins C and E. Fourth, the vitamin C level in the lung either declines on exposure to NO2 for short-term exposures or increases on chronic cigarette smoke exposure. The effects of cigarette smoking on serum vitamin C is apparently complex and may be related to the daily intake of vitamin C as well as smoking. Serum vitamin C levels may be poor indicators of lung demands when daily vitamin C intakes are above 100 mg/day. Fifth, vitamin C supplementation protects against the effects of ambient levels of air pollution in adults as measured by histamine challenge. An augmented response to histamine challenge may represent increased lung permeability brought about by air pollution. In experimental animal and human experiments, the amount of vitamin C or E that afforded protection was in excess of the current recommended dietary allowance. Although animal studies do not provide evidence for complete protection against NO2 or O3, they do illustrate that current recommended daily allowances are inadequate for maximum protection against air pollution levels to which over 100 million Americans are exposed. The problem of air pollution and its effects on humans is truly of global concern. Air pollution is not restricted to North America or Japan where it was first recognized, but is a major public health problem in Europe as well. When data are available, air pollution probably will be shown to be a major public health problem in all urban areas of the world.(ABSTRACT TRUNCATED AT 400 WORDS) PMID:1444020

Menzel, D B

1992-09-30

125

Nilotinib-induced interstitial lung disease.  

PubMed

Nilotinib is a second-generation tyrosine kinase inhibitor active in patients with chronic myeloid leukemia (CML) resistant to imatinib, and has been recently approved for newly diagnosed patients. We present a case of nilotinib-induced interstitial lung disease (ILD). A 67-year-old female patient was initially treated with imatinib for chronic-phase Philadelphia chromosome-positive (Ph(+)) CML. Imatinib was replaced by nilotinib because of hematological toxicity. The patient had received nilotinib for about 3 years without significant adverse effects. She visited the clinic due to chronic cough; chest X-ray revealed consolidations in both lung fields. Nilotinib-induced ILD was diagnosed based on intensive workup, including lung biopsy. She responded dramatically to corticosteroid therapy. To our knowledge, this is the first reported case of nilotinib-induced ILD in a patient with Ph(+) CML. We emphasize that if unexplained lung abnormalities progress in patients receiving nilotinib, physicians should consider this potentially fatal complication in their differential diagnoses. PMID:23877149

Go, Se-Il; Lee, Won Sup; Lee, Gyeong-Won; Kang, Jung Hun; Kang, Myung Hee; Lee, Jeong-Hee; Kim, Hoon-Gu

2013-09-01

126

Angiotensin-converting enzyme 2 (ACE2) mediates influenza H7N9 virus-induced acute lung injury  

PubMed Central

Since March 2013, the emergence of an avian-origin influenza A (H7N9) virus has raised concern in China. Although most infections resulted in respiratory illness, some severe cases resulted in acute respiratory distress syndrome (ARDS), which is a severe form of acute lung injury (ALI) that further contributes to morbidity. To date, no effective drugs that improve the clinical outcome of influenza A (H7N9) virus-infected patients have been identified. Angiotensin-converting enzyme (ACE) and ACE2 are involved in several pathologies such as cardiovascular functions, renal disease, and acute lung injury. In the current study, we report that ACE2 could mediate the severe acute lung injury induced by influenza A (H7N9) virus infection in an experimental mouse model. Moreover, ACE2 deficiency worsened the disease pathogenesis markedly, mainly by targeting the angiotensin II type 1 receptor (AT1). The current findings demonstrate that ACE2 plays a critical role in influenza A (H7N9) virus-induced acute lung injury, and suggest that might be a useful potential therapeutic target for future influenza A (H7N9) outbreaks. PMID:25391767

Yang, Penghui; Gu, Hongjing; Zhao, Zhongpeng; Wang, Wei; Cao, Bin; Lai, Chengcai; Yang, Xiaolan; Zhang, LiangYan; Duan, Yueqiang; Zhang, Shaogeng; Chen, Weiwen; Zhen, Wenbo; Cai, Maosheng; Penninger, Josef M.; Jiang, Chengyu; Wang, Xiliang

2014-01-01

127

Angiotensin-converting enzyme 2 (ACE2) mediates influenza H7N9 virus-induced acute lung injury.  

PubMed

Since March 2013, the emergence of an avian-origin influenza A (H7N9) virus has raised concern in China. Although most infections resulted in respiratory illness, some severe cases resulted in acute respiratory distress syndrome (ARDS), which is a severe form of acute lung injury (ALI) that further contributes to morbidity. To date, no effective drugs that improve the clinical outcome of influenza A (H7N9) virus-infected patients have been identified. Angiotensin-converting enzyme (ACE) and ACE2 are involved in several pathologies such as cardiovascular functions, renal disease, and acute lung injury. In the current study, we report that ACE2 could mediate the severe acute lung injury induced by influenza A (H7N9) virus infection in an experimental mouse model. Moreover, ACE2 deficiency worsened the disease pathogenesis markedly, mainly by targeting the angiotensin II type 1 receptor (AT1). The current findings demonstrate that ACE2 plays a critical role in influenza A (H7N9) virus-induced acute lung injury, and suggest that might be a useful potential therapeutic target for future influenza A (H7N9) outbreaks. PMID:25391767

Yang, Penghui; Gu, Hongjing; Zhao, Zhongpeng; Wang, Wei; Cao, Bin; Lai, Chengcai; Yang, Xiaolan; Zhang, LiangYan; Duan, Yueqiang; Zhang, Shaogeng; Chen, Weiwen; Zhen, Wenbo; Cai, Maosheng; Penninger, Josef M; Jiang, Chengyu; Wang, Xiliang

2014-01-01

128

Electroacupuncture Ameliorates Acute Lung Injury through Promoting Gastrointestinal Motility in Rats with Acute Pancreatitis.  

PubMed

Objective. Gastrointestinal disfunction and acute lung injury (ALI) were common in acute pancreatitis (AP). The effect of electro-acupuncture (EA) on gastrointestinal motility and ALI in rats with AP was investigated to verify the theory of "lung and large intestine are interior exteriorly related" in traditional Chinese medicine. Methods. Male Sprague-Dawley rats were randomly divided into the normal group, model group, and EA group. AP model was established by three injections of 20% L-arginine at 1?h intervals. EA were applied to bilateral ST-25 and ST-36 for 30 minutes twice a day after modeling for 3 days. Arterial blood, pancreas, lung, and intestinal tissues were collected for detecting the inflammatory factors and histopathology. Intestinal propulsion rate (IPR) was also measured at 72?h. Results. EA treatment improved IPR and increased CCK-8 level compared with model group (P < 0.05). It lowered the serum levels of TNF- ? and IL-6 and increased the level of IL-4 with no effect on IL-10. EA treatment reduced serum vasoactive intestinal peptide (VIP) and myeloperoxidase (MPO) level in the lung and the pathologic scores of pancreas, lung and intestine were decreased (P < 0.05). Conclusion. EA treatment could promote gastrointestinal motility through inhibiting VIP, and promoting CCK expression and regulate pro- and anti-inflammatory mediators to ameliorate ALI in AP. PMID:24876883

Guo, Hui; Zhu, Shi-Feng; Zhang, Rong-Rong; Zhao, Xian-Lin; Wan, Mei-Hua; Tang, Wen-Fu

2014-01-01

129

Electroacupuncture Ameliorates Acute Lung Injury through Promoting Gastrointestinal Motility in Rats with Acute Pancreatitis  

PubMed Central

Objective. Gastrointestinal disfunction and acute lung injury (ALI) were common in acute pancreatitis (AP). The effect of electro-acupuncture (EA) on gastrointestinal motility and ALI in rats with AP was investigated to verify the theory of “lung and large intestine are interior exteriorly related” in traditional Chinese medicine. Methods. Male Sprague-Dawley rats were randomly divided into the normal group, model group, and EA group. AP model was established by three injections of 20% L-arginine at 1?h intervals. EA were applied to bilateral ST-25 and ST-36 for 30 minutes twice a day after modeling for 3 days. Arterial blood, pancreas, lung, and intestinal tissues were collected for detecting the inflammatory factors and histopathology. Intestinal propulsion rate (IPR) was also measured at 72?h. Results. EA treatment improved IPR and increased CCK-8 level compared with model group (P < 0.05). It lowered the serum levels of TNF-? and IL-6 and increased the level of IL-4 with no effect on IL-10. EA treatment reduced serum vasoactive intestinal peptide (VIP) and myeloperoxidase (MPO) level in the lung and the pathologic scores of pancreas, lung and intestine were decreased (P < 0.05). Conclusion. EA treatment could promote gastrointestinal motility through inhibiting VIP, and promoting CCK expression and regulate pro- and anti-inflammatory mediators to ameliorate ALI in AP. PMID:24876883

Guo, Hui; Zhu, Shi-Feng; Zhang, Rong-Rong; Zhao, Xian-Lin; Wan, Mei-Hua; Tang, Wen-Fu

2014-01-01

130

Cystathionine-gamma-lyase inhibitor attenuates acute lung injury induced by acute pancreatitis in rats  

PubMed Central

Introduction Acute pancreatitis (AP) is known to induce injuries to extrapancreatic organs. Because respiratory dysfunction is the main cause of death in patients with severe AP, acute pancreatitis-associated lung injury (APALI) is a great challenge for clinicians. This study aimed to investigate the potential role of hydrogen sulfide (H2S) in the pathogenesis of APALI. Material and methods Fifty-four SD rats were randomly divided into three groups: the AP group of rats that received injection of sodium deoxycholate into the common bile duct, the control group that underwent a sham operation, and the treatment group made by intraperitoneal injection of propargylglycine (PAG), an inhibitor of cystathionine-?-lyase (CSE), into rats with AP. Histopathology of the lung was examined and the expression of CSE and TNF-? mRNA in lung tissue was detected by real-time polymerase chain reaction. The H2S level in the serum was detected spectrophotometrically. Results The serum concentration of H2S and CSE and TNF-? expression in the lung were increased in AP rats modeled after 3 h and 6 h than in control rats (p < 0.05). Intraperitoneal injection of PAG could reduce the serum concentration of H2S, reduce CSE and TNF-? expression, and alleviate the lung pathology (p < 0.05). Conclusions Taken together, our findings suggest that the H2S/CSE system is crucially involved in the pathological process of APALI and represents a novel target for the therapy of APALI.

Qu, Zhen; Wu, Bao-Qiang; Duan, Yun-Fei; Sun, Zhen-Di; Luo, Guang-Hua

2014-01-01

131

Epithelial Cell Apoptosis Causes Acute Lung Injury Masquerading as Emphysema  

PubMed Central

Theories of emphysema traditionally revolved around proteolytic destruction of extracellular matrix. Models have recently been developed that show airspace enlargement with the induction of pulmonary cell apoptosis. The purpose of this study was to determine the mechanism by which a model of epithelial cell apoptosis caused airspace enlargement. Mice were treated with either intratracheal microcystin (MC) to induce apoptosis, intratracheal porcine pancreatic elastase (PPE), or their respective vehicles. Mice from all groups were inflated and morphometry was measured at various time points. Physiology measurements were performed for airway resistance, tissue elastance, and lung volumes. The groups were further analyzed by air–saline quasistatic measurements, surfactant staining, and surfactant functional studies. Mice treated with MC showed evidence of reversible airspace enlargement. In contrast, PPE-treated mice showed irreversible airspace enlargement. The airspace enlargement in MC-treated mice was associated with an increase in elastic recoil due to an increase in alveolar surface tension. PPE-treated mice showed a loss of lung elastic recoil and normal alveolar surface tension, a pattern more consistent with human emphysema. Airspace enlargement that occurs with the MC model of pulmonary epithelial cell apoptosis displays physiology distinct from human emphysema. Reversibility, restrictive physiology due to changes in surface tension, and alveolar enlargement associated with heterogeneous alveolar collapse are most consistent with a mild acute lung injury. Inflation near total lung capacity gives the appearance of enlarged alveoli as neighboring collapsed alveoli exert tethering forces. PMID:19188661

Mouded, Majd; Egea, Eduardo E.; Brown, Matthew J.; Hanlon, Shane M.; Houghton, A. McGarry; Tsai, Larry W.; Ingenito, Edward P.; Shapiro, Steven D.

2009-01-01

132

[Erroneous diagnosis of acute appendicitis in acute gynecological diseases].  

PubMed

On the basis of an analysis of 84 observations the authors describe special features of the clinical course and diagnosis of gynecological diseases simulating acute appendicitis (rupture of the ovary, extrauterine pregnancy, torsion or rupture of the ovarian cyst, adnexitis). PMID:4013010

Genyk, S N; Sokol, B G

1985-04-01

133

Bilateral versus single lung transplantation for chronic obstructive pulmonary disease  

Microsoft Academic Search

Objective: Traditionally, despite ventilation\\/perfusion mismatch, single lung transplantation has been the mainstay for end-stage chronic obstructive pulmonary disease. We tested the hypothesis that bilateral sequential lung transplantation has better short- and intermediate-term results than single lung transplantation for chronic obstructive pulmonary disease.Methods: One hundred twenty-six consecutive lung transplants have been performed from November 1991 to March 1996. Seventy-six have been

Joseph E. Bavaria; Robert Kotloff; Harold Palevsky; Bruce Rosengard; John R. Roberts; Peter M. Wahl; Nancy Blumenthal; Christine Archer; Larry R. Kaiser

1997-01-01

134

Blockade of PDE4B limits lung vascular permeability and lung inflammation in LPS-induced acute lung injury.  

PubMed

Acute lung injury (ALI), acute respiratory distress syndrome (ARDS), is actually involved in an ongoing and uncontrolled inflammatory response in lung tissues. Although extensive studies suggested that phospodiesterase type 4B (PDE4B) may be related to inflammation, the underlying cell biological mechanism of ALI remains unclear. To further investigate the mechanism how PDE4B take part in inflammatory response and the maintenance of vascular integrity, we established the experimental model of ALI in vitro and in vivo. In vitro, we found that Cilomilast, Diazepam and PDE4B knockout could potently inhibit the LPS-induced NF-?B activation and inflammatory response in multiple cell types, including lung epithelial cells (A549), pulmonary microvascular endothelial cells (PMVECs) and vascular smooth muscle cells (VSMCs). Besides, PDE4B deletion attenuated the LPS-induced ROS generation. In vivo, PDE4B deletion could attenuate the lung water content, histological signs of pulmonary injury and elevate the ratio of partial pressure of arterial O2 to fraction of inspired O2 (PaO2/FIO2 ratio). Additionally, PDE4B deletion reduced LPS-induced vascular permeability. Collectively, our results strongly indicates that PDE4B is a valid target for anti-ALI. PMID:25019986

Ma, Hongyan; Shi, Jinghui; Wang, Changsong; Guo, Lei; Gong, Yulei; Li, Jie; Gong, Yongtai; Yun, Fengxiang; Zhao, Hongwei; Li, Enyou

2014-08-01

135

Mannose prevents lipopolysaccharide-induced acute lung injury in rats  

Microsoft Academic Search

.\\u000a Objective:  To investigate the effect of mannose on lipopolysaccharide (LPS) induced acute lung injury (ALI) in rats.\\u000a \\u000a \\u000a \\u000a Methods:  Ten groups of Sprague–Dawley rats were used: 1) the control group received an intratracheal instillation of saline, 2) the LPS group received an intratracheal instillation of LPS (3 mg\\/kg), 3–6) the mannose groups were injected i.v. with 15, 45, 135, and 405 mg\\/kg mannose, 7–9)

X. L. Xu; Q. M. Xie; Y. H. Shen; J. J. Jiang; Y. Y. Chen; H. Y. Yao; J. Y. Zhou

2008-01-01

136

Agmatine Protects against Zymosan-Induced Acute Lung Injury in Mice by Inhibiting NF-?B-Mediated Inflammatory Response  

PubMed Central

Acute lung injury (ALI) is characterized by overwhelming lung inflammation and anti-inflammation treatment is proposed to be a therapeutic strategy for ALI. Agmatine, a cationic polyamine formed by decarboxylation of L-arginine, is an endogenous neuromodulator that plays protective roles in diverse central nervous system (CNS) disorders. Consistent with its neuromodulatory and neuroprotective properties, agmatine has been reported to have beneficial effects on depression, anxiety, hypoxic ischemia, Parkinson's disease, and gastric disorder. In this study, we tested the effect of agmatine on the lung inflammation induced by Zymosan (ZYM) challenge in mice. We found that agmatine treatment relieved ZYM-induced acute lung injury, as evidenced by the reduced histological scores, wet/dry weight ratio, and myeloperoxidase activity in the lung tissue. This was accompanied by reduced levels of TNF-?, IL-1?, and IL-6 in lung and bronchoalveolar lavage fluid and decreased iNOS expression in lung. Furthermore, agmatine inhibited the phosphorylation and degradation of I?B and subsequently blocked the activation of nuclear factor (NF)-?B induced by Zymosan. Taken together, our results showed that agmatine treatment inhibited NF-?B signaling in lungs and protected mice against ALI induced by Zymosan, suggesting agmatine may be a potential safe and effective approach for the treatment of ALI. PMID:25243152

Liu, Zheng; Jin, He; Fan, Xia; Yang, Xue; Tang, Wanqi; Liang, Huaping

2014-01-01

137

Neuraminidase reprograms lung tissue and potentiates LPS-induced acute lung injury in mice  

PubMed Central

We previously reported that removal of sialyl residues primed PBMCs to respond to bacterial LPS stimulation in vitro. Therefore, we speculated that prior desialylation can sensitize the host to generate an enhanced inflammatory response upon exposure to a TLR ligand, such as LPS, in a murine model of acute lung injury. Intratracheal instillation of neuraminidase (NA) 30 min prior to intratracheal administration of LPS increased PMNs in the bronchoalveolar lavage fluid (BALF) and the wet-to-dry lung weight ratio, a measure of pulmonary edema, compared to mice that received LPS alone. Administration of NA alone resulted in desialylation of bronchiolar and alveolar surfaces and induction of TNF-?, IL-1?, and chemokines in lung homogenates and BALF; however, PMN recruitment in mice treated with NA alone did not differ from those of PBS-administered controls. NA pretreatment alone induced apoptosis and markedly enhanced LPS-induced endothelial apoptosis. Administration of recombinant Bcl-2, an anti-apoptotic molecule, abolished the effect of NA treatment on LPS-induced PMN recruitment and pulmonary edema formation. We conclude that NA pretreatment potentiates LPS-induced lung injury through enhanced PMN recruitment, pulmonary edema formation, and endothelial and myeloid cell apoptosis. A similar “reprogramming” of immune responses with desialylation may occur during respiratory infection with NA-expressing microbes and contribute to severe lung injury. PMID:24068662

Feng, Chiguang; Zhang, Lei; Nguyen, Chinh; Vogel, Stefanie N.; Goldblum, Simeon E.; Blackwelder, William C.; Cross, Alan S.

2013-01-01

138

Multiple lung adenocarcinomas associated with von hippel-lindau disease.  

PubMed

Lung adenocarcinoma has never before been reported to be associated with von Hippel-Lindau (VHL) disease. Here, we report a case of VHL disease in a patient who had metachronous multiple lung adenocarcinomas. The patient is a 64-year-old-woman with VHL disease. She underwent surgical resection of one adenocarcinoma and one atypical adenomatous hyperplasia. A second lung adenocarcinoma developed metachronously. A point mutation in the VHL gene was confirmed in DNA from a blood sample, and loss of heterozygosity at the VHL locus was detected in the lung adenocarcinoma. The VHL dysfunction may have a role in the development of multiple lung adenocarcinomas. PMID:25282218

Ikeda, Koei; Osumi, Hironobu; Matsuishi, Kentaro; Matsubara, Eri; Fujino, Kousuke; Shibata, Hidekatsu; Yoshimoto, Kentaro; Shiraishi, Kenji; Mori, Takeshi; Suzuki, Makoto

2014-10-01

139

Carbon-nanoparticle-triggered acute lung inflammation and its resolution are not altered in PPARgamma-defective (P465L) mice  

E-print Network

inflammatory disorders. This is particularly relevant since AM play a critical role in pathogenesis of asthma, chronic obstructive pulmonary disease (COPD), lung fibrosis (IPF) and lung sarcoidosis (for review see [9]). Moreover PPARg binding to the respective... -induced epithelial mucin production [30]. Improved pathophysiological states in models for asthma, COPD, IPF, and acute lung injury have also been found [29,31-33]. In contrast, PPARg deficiency or lack of receptor activation in macrophages resulted in increased...

Gotz, Alexander A; Vidal-Puig, Antonio; Rodel, Heiko G; Hrabe de Angelis, Martin; Stoeger, Tobias

2011-09-20

140

Common Respiratory Diseases Tied to Lung Cancer Risk  

MedlinePLUS

... sharing features on this page, please enable JavaScript. Common Respiratory Diseases Tied to Lung Cancer Risk Chronic ... Diseases FRIDAY, Aug. 15, 2014 (HealthDay News) -- Three common respiratory diseases seem to be associated with an ...

141

Cardiovascular biomarkers in acute Kawasaki disease  

PubMed Central

Background Endomycocardial biopsies have demonstrated that subclinical myocarditis is a universal feature of acute Kawasaki disease (KD). Methods We investigated biochemical evidence of myocardial strain, oxidative stress, and cardiomyocyte injury in 55 acute KD subjects (30 with paired convalescent samples), 54 febrile control (FC), and 50 healthy control (HC) children by measuring concentrations of cardiovascular biomarkers. Results Levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and soluble ST2 (sST2) were elevated in acute vs. convalescent KD, FC, and HC (p?0.0002), while ?-glutamyl transferase and alanine amino transferase as measures of oxidative stress were increased in acute vs. FC (p?0.0008). Cardiac troponin I (cTnI) levels, using a highly sensitive assay, were elevated in 30% and 40% of paired acute and convalescent KD subjects, respectively, and normalized within two years of disease onset. NT-proBNP and sST2 negatively correlated with measures of diastolic function (MV E:A ratio and deceleration time), but only NT-proBNP positively correlated with the coronary artery Z score. Conclusions NT-proBNP and sST2 were elevated in acute KD subjects and correlated with impaired myocardial relaxation. These findings, combined with elevated levels of cTnI, suggest that both cardiomyocyte stress and cell death are associated with myocardial inflammation in acute KD. PMID:21777987

Sato, Yuichiro Z.; Molkara, Delaram P.; Daniels, Lori B.; Tremoulet, Adriana H.; Shimizu, Chisato; Kanegaye, John T.; Best, Brookie M.; Snider, James V.; Frazer, Jeffrey R.; Maisel, Alan; Burns, Jane C.

2011-01-01

142

Treatment of interstitial lung disease in children.  

PubMed

The treatment of interstitial lung disease in children depends on the nature of the underlying pathology. In approximately 50% of cases a specific aetiology can be found such as: chronic viral infection, an auto-immune process, sarcoidosis or alveolar proteinosis. In the remainder, the process is idiopathic and the pathological findings are based on the descriptive morphological features seen in the diagnostic lung biopsy. If a specific cause is found then targeted treatment with antivirals, steroids or other immunosuppressive agents is available. Alveolar proteinosis can be treated by bronchial lavage and GM-CSF. Idiopathic cases are treated primarily with intravenous pulsed methylprednisolone or oral prednisolone backed up hydroxychloroquine. Other immunosuppressive agents such as azathioprine, methotrexate or ciclosporin have been used successfully in individual patients. The prognosis is very variable and includes no response to any therapy, partial response with chronic long term morbidity, to virtually complete recovery. The overall mortality rate is 15%. There are no controlled therapeutic trials available because of the rarity of these conditions in childhood. Unlike in adult practice, no correlation has as yet been demonstrated between the initial pattern of chest x-ray change or the degree of pathological change on the lung biopsy and the clinical outcome. The recurrence rate within families is 1 in 8. PMID:15135120

Dinwiddie, R

2004-06-01

143

Ventilator-associated lung injury in patients without acute lung injury at the onset of mechanical ventilation  

Microsoft Academic Search

of mechanical ventilation. When expressed per predicted body weight, women were ventilated with larger tidal volume than men (mean 11.4 vs. 10.4 mL\\/kg predicted body weight, p < .001) and tended to develop acute lung injury more often (29% vs. 20%, p .068). In a multivariate analysis, the main risk factors associated with the development of acute lung injury were

Ognjen Gajic; Saqib I. Dara; Jose L. Mendez; Adebola O. Adesanya; Emir Festic; Sean M. Caples; Rimki Rana; Jennifer L. St. Sauver; James F. Lymp; Bekele Afessa; Rolf D. Hubmayr

2004-01-01

144

Prognostic Factors for Myositis-Associated Interstitial Lung Disease  

PubMed Central

Background Interstitial lung disease (ILD) is a common manifestation of polymyositis (PM), dermatomyositis (DM), and clinically amyopathic dermatomyositis (CADM); however, little is known about the factors influencing the prognosis for PM/DM/CADM-associated ILD. (PM/DM/CADM-ILD). The aim of the present study is to assess prognostic factors for PM/DM/CADM-ILD. Methods The clinical features and survival of 114 consecutive patients diagnosed with PM/DM/CADM-ILD (39 men and 75 women; median age, 56 years) were analyzed retrospectively. Results The study group included 30 PM-associated ILD, 41 DM-associated ILD, and 43 CADM-associated ILD cases. The clinical presentation of ILD was acute/subacute form in 59 patients (51.8%) and chronic form in 55 patients (48.2%). The major pulmonary symptoms were dyspnea, cough, and fever. High-resolution computed tomography frequently revealed ground-glass opacities, traction bronchiectasis, and consolidation. Most of the patients were treated with corticosteroids or corticosteroids in combination with immunosuppressive agents. The all-cause mortality was 27.2%. Acute/subacute form, % forced vital capacity (FVC), age, % of neutrophils in bronchoalveolar lavage (BAL) fluid, and a diagnosis of CADM (vs. PM) were significantly associated with poor outcome in univariate Cox proportional hazards models. Multivariate Cox proportional hazards analysis validated acute/subacute ILD, %FVC, age, and diagnosis of CADM (vs. PM) as significant predictors of overall mortality. Patients with acute/subacute ILD had a much lower survival rate than those with the chronic form (p<0.001). Patients with CADM-ILD had a lower survival rate than those with PM-ILD (p?=?0.034). Conclusions Acute/subacute form, older age, lower level of FVC and diagnosis of CADM predict poor outcome in PM/DM/CADM-ILD. PMID:24905449

Fujisawa, Tomoyuki; Hozumi, Hironao; Kono, Masato; Enomoto, Noriyuki; Hashimoto, Dai; Nakamura, Yutaro; Inui, Naoki; Yokomura, Koshi; Koshimizu, Naoki; Toyoshima, Mikio; Shirai, Toshihiro; Yasuda, Kazumasa; Hayakawa, Hiroshi; Suda, Takafumi

2014-01-01

145

Task force on chronic interstitial lung disease in immunocompetent children  

Microsoft Academic Search

Task force on chronic interstitial lung disease in immunocompetent children. A. Clement, and committee members. #ERS Journals Ltd 2004. ABSTRACT: Chronic interstitial lung diseases in children represent a heterogeneous group of disorders of both known and unknown causes that share common histological features. Despite many efforts these diseases continue to present clinical management dilemmas, principally because of their rare frequency

A. Clement; J. Allen; B. Corrin; R. Dinwiddie; H. Ducou; E. Eber; G. Laurent; R. Marshall; F. Midulla; A. G. Nicholson

146

Inhibition of Neutrophil Exocytosis Ameliorates Acute Lung Injury in Rats  

PubMed Central

Exocytosis of neutrophil granules contributes to acute lung injury (ALI) induced by infection or inflammation, suggesting that inhibition of neutrophil exocytosis in vivo could be a viable therapeutic strategy. This study was conducted to determine the effect of a cell-permeable fusion protein that inhibits neutrophil exocytosis (TAT-SNAP-23) on ALI using an immune complex deposition model in rats. The effect of inhibition of neutrophil exocytosis by intravenous administration of TAT-SNAP-23 on ALI was assessed by albumin leakage, neutrophil infiltration, lung histology, and proteomic analysis of bronchoalveolar lavage fluid (BALf). Administration of TAT-SNAP-23, but not TAT-Control, significantly reduced albumin leakage, total protein levels in the BALf, and intra-alveolar edema and hemorrhage. Evidence that TAT-SNAP-23 inhibits neutrophil exocytosis included a reduction in plasma membrane CD18 expression by BALf neutrophils and a decrease in neutrophil granule proteins in BALf. Similar degree of neutrophil accumulation in the lungs and/or BALf suggests that TAT-SNAP-23 did not alter vascular endothelial cell function. Proteomic analysis of BALf revealed that components of the complement and coagulation pathways were significantly reduced in BALf from TAT-SNAP-23-treated animals. Our results indicate that administration of a TAT-fusion protein that inhibits neutrophil exocytosis reduces in vivo ALI. Targeting neutrophil exocytosis is a potential therapeutic strategy to ameliorate ALI. PMID:23364427

Uriarte, Silvia M.; Rane, Madhavi J.; Merchant, Michael L.; Jin, Shunying; Lentsch, Alex B.; Ward, Richard A.; McLeish, Kenneth R.

2013-01-01

147

Inhibition of neutrophil exocytosis ameliorates acute lung injury in rats.  

PubMed

Exocytosis of neutrophil granules contributes to acute lung injury (ALI) induced by infection or inflammation, suggesting that inhibition of neutrophil exocytosis in vivo could be a viable therapeutic strategy. This study was conducted to determine the effect of a cell-permeable fusion protein that inhibits neutrophil exocytosis (TAT-SNAP-23) on ALI using an immune complex deposition model in rats. The effect of inhibition of neutrophil exocytosis by intravenous administration of TAT-SNAP-23 on ALI was assessed by albumin leakage, neutrophil infiltration, lung histology, and proteomic analysis of bronchoalveolar lavage fluid (BALF). Administration of TAT-SNAP-23, but not TAT-control, significantly reduced albumin leakage, total protein levels in the BALF, and intra-alveolar edema and hemorrhage. Evidence that TAT-SNAP-23 inhibits neutrophil exocytosis included a reduction in plasma membrane CD18 expression by BALF neutrophils and a decrease in neutrophil granule proteins in BALF. Similar degree of neutrophil accumulation in the lungs and/or BALF suggests that TAT-SNAP-23 did not alter vascular endothelial cell function. Proteomic analysis of BALF revealed that components of the complement and coagulation pathways were significantly reduced in BALF from TAT-SNAP-23-treated animals. Our results indicate that administration of a TAT-fusion protein that inhibits neutrophil exocytosis reduces in vivo ALI. Targeting neutrophil exocytosis is a potential therapeutic strategy to ameliorate ALI. PMID:23364427

Uriarte, Silvia M; Rane, Madhavi J; Merchant, Michael L; Jin, Shunying; Lentsch, Alex B; Ward, Richard A; McLeish, Kenneth R

2013-03-01

148

Image based diagnostic aid system for interstitial lung diseases  

Microsoft Academic Search

Automatic classification of lung tissue patterns in high-resolution computed tomography (HRCT) images of patients affected with interstitial lung diseases (ILD) is an important stage in the construction of a computer-aided diagnosis system. In this study, we propose a new image based system for classification of lung tissue patterns. The proposed system comprises three stages. In the first stage, the parenchyma

Azar Tolouee; Hamid Abrishami Moghaddam; Mohamad Forouzanfar; Masoumeh Gity; Rahil Garnavi

2011-01-01

149

Advanced Malignant Lung Disease: What the Specialist Can Offer  

Microsoft Academic Search

Lung cancer is not only the most commonly diagnosed cancer worldwide, but it is still the leading cause for cancer-related death. The 5-year survival for lung cancer in Europe and in the USA is totally 16%. Therefore, a palliative therapy regimen is required to control the disease and reduce symptoms with the objective of enhancing quality of life of lung

D. Gompelmann; R. Eberhardt; F. J. F. Herth

2011-01-01

150

Interpretation of autoantibody positivity in interstitial lung disease and lung-dominant connective tissue disease.  

PubMed

The initial evaluation of patients with interstitial lung disease (ILD) primarily involves a comprehensive, active search for the cause. Autoantibody assays, which can suggest the presence of a rheumatic disease, are routinely performed at various referral centers. When interstitial lung involvement is the condition that allows the definitive diagnosis of connective tissue disease and the classical criteria are met, there is little debate. However, there is still debate regarding the significance, relevance, specificity, and pathophysiological role of autoimmunity in patients with predominant pulmonary involvement and only mild symptoms or formes frustes of connective tissue disease. The purpose of this article was to review the current knowledge of autoantibody positivity and to discuss its possible interpretations in patients with ILD and without clear etiologic associations, as well as to enhance the understanding of the natural history of an allegedly new disease and to describe the possible prognostic implications. We also discuss the proposition of a new term to be used in the classification of ILDs: lung-dominant connective tissue disease. PMID:24473767

Pereira, Daniel Antunes Silva; Kawassaki, Alexandre de Melo; Baldi, Bruno Guedes

2013-01-01

151

Reflux esophagitis in war-related sulfur mustard lung disease  

PubMed Central

Background Sulfur mustard (SM) has acute and chronic effects on skin and mucosal surfaces. The aim of the study was to evaluate the frequency of esophagitis in a historical cohort of veterans who had been exposed to SM in Iran-Iraq war nearly 25 years ago. Methods: One hundred two veterans with dyspepsia and/or heartburn underwent esophago-gastroduodenoscopy. Of them, 52 cases had been exposed to SM and had chronic mustard lung disease. Controls included 50 veterans without SM exposure. Esophagitis was defined according to standard criteria. Results: 81.6% of cases and 70.6% of controls had heart burn and/or regurgitation (p= 0.224). Esophagitis was seen in 40% of cases and 26.5% of controls (p= 0.155). Conclusion: Based on our findings, SM exposure seems not to be associated with increased esophagitis.

Roushan, Nader; Zali, Fateme; Abtahi, Hamidreza; Asadi, Mehrnaz; Taslimi, Reza; Aletaha, Najme

2014-01-01

152

Stem Cells and Regenerative Medicine in Lung Biology and Diseases  

PubMed Central

A number of novel approaches for repair and regeneration of injured lung have developed over the past several years. These include a better understanding of endogenous stem and progenitor cells in the lung that can function in reparative capacity as well as extensive exploration of the potential efficacy of administering exogenous stem or progenitor cells to function in lung repair. Recent advances in ex vivo lung engineering have also been increasingly applied to the lung. The current status of these approaches as well as initial clinical trials of cell therapies for lung diseases are reviewed below. PMID:22395528

Lau, Allison N; Goodwin, Meagan; Kim, Carla F; Weiss, Daniel J

2012-01-01

153

Lung Reperfusion Injury after Chronic or Acute Unilateral Pulmonary Artery Occlusion  

Microsoft Academic Search

Because the lungs receive their blood supply from both the pulmonary and bronchial systems, chronic pulmonary artery obstruction does not necessarily result in severe ischemia. Ischemia-reper- fusion (IR) lung injury may therefore be attenuated after long-term pulmonary artery obstruction. To test this hypothesis, isolated left lungs of pigs were reperfused two days (acute IR group) or 5 wk (chronic IR

ELIE FADEL; GUY-MICHEL MAZMANIAN; ALAIN CHAPELIER; BRUNO BAUDET; HÉLÈNE DETRUIT; JEAN-MARIE LIBERT; MYRIAM WARTSKI; PHILIPPE HERVE; PHILIPPE DARTEVELLE

154

Suppression of Acute Lung Inflammation by Intracellular Peptide Delivery of a Nuclear Import Inhibitor  

Microsoft Academic Search

Acute lung inflammation is a potentially life-threatening complication of infections due to community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA), a worldwide emerging pathogen, which causes necrotizing pneumonia and acute respiratory distress syndrome (ARDS). MRSA virulence factors encompass immunotoxins termed superantigens that contribute to lung inflammation. In this study, we demonstrate that staphylococcal enterotoxin B (SEB)-induced lung inflammation is attenuated by a cell-penetrating

Danya Liu; Jozef Zienkiewicz; Antonio DiGiandomenico; Jacek Hawiger

2009-01-01

155

Necrotic, ulcerative bronchitis, the presenting feature of lymphoproliferative disease following heart-lung transplantation.  

PubMed Central

Following heart-lung transplantation two of 21 patients who survived more than 100 days developed post-transplant lymphoproliferative disease. Both presented with localised ulcerative bronchitis documented at flexible bronchoscopy four months after transplantation. Histological examination showed necrosis with acute inflammation and ulceration. Case 2 demonstrated lymphoproliferative disease from biopsies subsequently taken at rigid bronchoscopy. Case 1 later developed lung nodules and a monoclonal high grade B cell non-Hodgkin's lymphoma was confirmed by an open lung biopsy. The bronchoscopic features described should alert clinicians to post-transplant lymphoproliferative disease as an underlying diagnosis and suggest that bronchus associated lymphoid tissue is the initial site for clonal proliferation in the disease. Images PMID:7701465

Egan, J. J.; Hasleton, P. S.; Yonan, N.; Rahman, A. N.; Deiraniya, A. K.; Carroll, K. B.; Woodcock, A. A.

1995-01-01

156

Altered mucosal immune response after acute lung injury in a murine model of Ataxia Telangiectasia  

PubMed Central

Background Ataxia telangiectasia (A-T) is a rare but devastating and progressive disorder characterized by cerebellar dysfunction, lymphoreticular malignancies and recurrent sinopulmonary infections. In A-T, disease of the respiratory system causes significant morbidity and is a frequent cause of death. Methods We used a self-limited murine model of hydrochloric acid-induced acute lung injury (ALI) to determine the inflammatory answer due to mucosal injury in Atm (A-T mutated)- deficient mice (Atm-/-). Results ATM deficiency increased peak lung inflammation as demonstrated by bronchoalveolar lavage fluid (BALF) neutrophils and lymphocytes and increased levels of BALF pro-inflammatory cytokines (e.g. IL-6, TNF). Furthermore, bronchial epithelial damage after ALI was increased in Atm-/- mice. ATM deficiency increased airway resistance and tissue compliance before ALI was performed. Conclusions Together, these findings indicate that ATM plays a key role in inflammatory response after airway mucosal injury. PMID:24884546

2014-01-01

157

Rikkunshito ameliorates bleomycin-induced acute lung injury in a ghrelin-independent manner.  

PubMed

Acute lung injury (ALI) is a critical syndrome consisting of acute respiratory failure associated with extensive pulmonary infiltrates. The pathological characterization of ALI includes injuries of alveolar epithelial cells (AECs), alveolar neutrophilic infiltration, and increases in proinflammatory cytokines, which cause destruction of the alveolar capillary barrier and subsequent devastating lung fibrosis. Rikkunshito (RKT), a traditional Japanese herbal medicine, is widely used for the treatment of patients with gastrointestinal symptoms and is known to stimulate ghrelin secretion. The therapeutic effects of RKT on organ inflammation and fibrosis remain unknown. We investigated the pharmacological potential of RKT in the treatment of ALI by using a bleomycin-induced ALI model in mice. RKT or distilled water (DW) was given to mice daily starting 12 h after bleomycin administration. The RKT-treated mice showed a definitively higher survival rate than the DW-treated mice after injury. They also had smaller reductions in body weight and food intake. The amelioration of neutrophil alveolar infiltration, pulmonary vascular permeability, induction of proinflammatory cytokines, activation of the NF-?B pathway, apoptosis of AECs, and subsequent lung fibrosis were notable in the RKT-treated mice. RKT administration increased the plasma ghrelin levels in wild-type mice, and it also mitigated the ALI response in both ghrelin-deficient mice and growth hormone secretagogue receptor-deficient mice after lung injury. Our results indicate that RKT administration exerts protective effects against ALI by protecting the AECs and regulating lung inflammation independently of the ghrelin system, and they highlight RKT as a promising therapeutic agent for the management of this intractable disease. PMID:24285267

Tsubouchi, Hironobu; Yanagi, Shigehisa; Miura, Ayako; Iizuka, Seiichi; Mogami, Sachiko; Yamada, Chihiro; Hattori, Tomohisa; Nakazato, Masamitsu

2014-02-01

158

Analysis of reports on orphan lung diseases in Korean children  

PubMed Central

Purpose Orphan lung diseases are defined as lung diseases with a prevalence of 1 or less in 2,000 individuals. Despite an increase in the numbers of patients with such diseases, few studies on Korean children have appeared. To obtain epidemiologic and demographic data on these diseases, we systematically reviewed reports on pediatric orphan lung diseases in Korea over the last 50 years. Methods We reviewed 223 articles that have appeared since 1958 on orphan lung diseases in Korean children. These articles described a total of 519 patients aged between 0 and 18 years. We classified patients by year of publication, diagnosis, geographic region, and journal. Results Of 519 patients, 401 had congenital cystic lung diseases and 66 had bronchiolitis obliterans. About 80% of patients were described in reports published in three journals, Pediatric Allergy and Respiratory Disease (Korea), the Korean Journal of Pediatrics, and the Korean Journal of Thoracic and Cardiovascular Surgery, in which papers on 157 (30.2%), 138 (26.6%), and 111 (21.4%) patients appeared, respectively. The frequency of publication of case reports has increased since 1990. Of the 519 patients, 401 (77.3%) were from Seoul/Gyeonggi-do and 72 (13.9%) from Busan/Gyeongsangnam-do. Conclusion The prevalence of pediatric orphan lung disease has increased since 1990, and some provinces of Korea have a higher incidence of these diseases than do others. Studies exploring the incidence of pediatric orphan lung diseases in Korea are needed for effective disease management. PMID:21189943

Jang, Sun Jung; Seo, Hyun Kyung; Yi, Sung Jae; Kim, Kyong Min; Jee, Hye Mi

2010-01-01

159

Pathogenetic and prognostic significance of altered coagulation and fibrinolysis in acute lung injury/acute respiratory distress syndrome*  

PubMed Central

Objective The coagulation and inflammatory cascades may be linked in the pathogenesis of acute lung injury and acute respiratory distress syndrome. However, direct evidence for the contribution of abnormalities in coagulation and fibrinolysis proteins to outcomes in patients with acute lung injury/acute respiratory distress syndrome is lacking. Design Retrospective measurement of plasma levels of protein C and plasminogen activator inhibitor-1 in plasma samples that were collected prospectively as part of a large multicenter clinical trial. The primary outcome was hospital mortality. To evaluate the potential additive value of abnormalities of these biomarkers, the excess relative risk of death was calculated for each combination of quartiles of protein-C and plasminogen activator inhibitor-1 levels. Setting Ten university medical centers. Patients The study included 779 patients from a multicenter clinical trial of a protective ventilatory strategy in acute lung injury/acute respiratory distress syndrome and 99 patients with acute cardiogenic pulmonary edema, as well as ten normal controls. Measurements and Main Results Compared with plasma from controls and patients with acute cardiogenic pulmonary edema, baseline protein-C levels were low and baseline plasminogen activator inhibitor-1 levels were elevated in acute lung injury/acute respiratory distress syndrome. By multivariate analysis, lower protein C and higher plasminogen activator inhibitor-1 were strong independent predictors of mortality, and ventilator-free and organ-failure-free days. Plasminogen activator inhibitor-1 and protein C had a synergistic interaction for the risk of death. Conclusions Early acute lung injury/acute respiratory distress syndrome is characterized by decreased plasma levels of protein C and increased plasma levels of plasminogen activator inhibitor-1 that are independent risk factors for mortality and adverse clinical outcomes. Measurement of plasminogen activator inhibitor-1 and protein-C levels may be useful to identify those at highest risk of adverse clinical outcomes for the development of new therapies. PMID:17667242

Ware, Lorraine B.; Matthay, Michael A.; Parsons, Polly E.; Thompson, B. Taylor; Januzzi, James L.; Eisner, Mark D.

2009-01-01

160

Extravascular lung water as an indicator of pulmonary dysfunction in acute hemorrhagic pancreatitis.  

PubMed Central

This study quantifies lung water in acute hemorrhagic pancreatitis to determine the degree to which pulmonary dysfunction occurs subclinically, before alterations in the arterial blood gases can be measured. Pancreatitis was induced in ten dogs by injecting 0.5 ml/kg of bile into the pancreatic ducts, which had been surgically cannulated. Pulmonary and systemic blood gases and blood pressures, heart rate, extravascular lung water, and lung blood flows were studied over 5 hours while cardiac output and mean arterial pressure were maintained at control values by Ringer's lactate infusion. The percentage of water in lung tissue was determined at the time of sacrifice using gravimetric measurements. Mean arterial pressure, cardiac output, and pulmonary capillary wedge pressure, reflecting intravascular volume status, did not change through at the experiment. By contrast, major disturbances were measured in the pulmonary bed with pulmonary artery pressures rising from 15.6 +/- 1.8/8.1 +/- 1.3 mmHg to 22.0 +/- 1.2/15.6 +/- 1.7 mmHg over 5 hours (p less than 0.01). Peripheral vascular resistance rose from 3.6 +/- 0.6 units to 6.6 +/- 0.4 units (p less than 0.05), whereas bronchial blood flow to the lung fell significantly. These changes in pulmonary hemodynamics were not reflected by changes in the arterial blood gases. Arterial oxygenation was maintained during 5 hours of pancreatitis. The partial pressure of carbon dioxide and the serum pH did not change significantly. There was, however, a progressive rise in extravascular lung water measured by the double-dilution technique from 10.2 +/- 0.8 ml/kg at control to 18.1 +/- 2.8 ml/kg (p less than 0.01) at 5 hours. This was confirmed by direct gravimetric measurements, which revealed an increase in the water content of the lung from 78.1 +/- 0.3% to 86.4 +/- 2.4% over the course of the experiment. Arterial blood gases, therefore, do not necessarily reflect the pulmonary deterioration in acute pancreatitis. These data supported a mechanism of lung dysfunction independent of the circulatory compromise, which often accompanies the disease in the clinical setting. PMID:2447844

Burnweit, C A; Horton, J W

1988-01-01

161

Higher urine desmosine levels are associated with mortality in patients with acute lung injury  

PubMed Central

Desmosine is a stable breakdown product of elastin that can be reliably measured in urine samples. We tested the hypothesis that higher baseline urine desmosine would be associated with higher mortality in 579 of 861 patients included in the recent Acute Respiratory Distress Syndrome Network trial of lower tidal volume ventilation (1). We also correlated urine desmosine levels with indexes of disease severity. Finally, we assessed whether urine desmosine was lower in patients who received lower tidal volumes. Desmosine was measured by radioimmunoassay in urine samples from days 0, 1, and 3 of the study. The data were expressed as a ratio of urine desmosine to urine creatinine to control for renal dilution. The results show that higher baseline (day 0) urine desmosine-to-creatinine concentration was associated with a higher risk of death on adjusted analysis (odds ratio 1.36, 95% confidence interval 1.02-1.82, P = 0.03). Urine desmosine increased in both ventilator groups from day 0 to day 3, but the average rise was higher in the 12-ml/kg predicted body weight group compared with the 6-ml/kg predicted body weight group (P = 0.053, repeated-measures model). In conclusion, patients with acute lung injury ventilated with lower tidal volumes have lower urine desmosine levels, a finding that may reflect reduced extracellular matrix breakdown. These results illustrate the value of evaluating urinary biological markers that may have prognostic and pathogenetic significance in acute lung injury. PMID:16698854

McClintock, Dana E.; Starcher, Barry; Eisner, Mark D.; Thompson, B. Taylor; Hayden, Doug L.; Church, Gwynne D.; Matthay, Michael A.

2009-01-01

162

Traditional Chinese medicine, Qing Ying Tang, ameliorates the severity of acute lung injury induced by severe acute pancreatitis in rats via the upregulation of aquaporin-1  

PubMed Central

Aquaporin-1 (AQP-1) is expressed in lung endothelial cells and regulates water transport; thus, AQP-1 plays an important role in a number of edema-associated lung diseases. Qing Yin Tang (QYT), a traditional Chinese medicine, has been shown to effectively reduce the mortality rate of acute lung injury (ALI) induced by severe acute pancreatitis (SAP). The current study aimed to investigate the detailed mechanisms underlying the effects of QYT on ALI induced by SAP, particularly the effects on the expression levels of AQP-1 in the lung tissue. ALI was established in Wister rats who were subsequently divided into four groups: SHAM, ALI, dexamethasone (DEX) and QYT groups (n=8 per group). In the QYT group, 20 ml/kg QYT was administered by gavage immediately following the induction of SAP. Blood and lung tissues were collected 8 h following the induction of pancreatitis. The lung wet/dry ratio, as well as the levels of blood gases, serum amylase and tumor necrosis factor-? (TNF-?), were measured at 4, 8 and 12 h following SAP-associated ALI induction surgery. The expression levels of AQP-1 in the lung tissue were detected by quantitative polymerase chain reaction, immunohistochemistry and western blot analysis. No statistically significant differences were observed with regard to the levels of serum amylase, wet/dry ratio, partial pressure of oxygen, serum TNF-? and pathological changes in the pulmonary tissue between the QYT and DEX groups; however, a statistically significant difference was observed when compared with the ALI group. The expression levels of AQP-1 significantly increased (P<0.05) and lung edema was alleviated in the QYT and DEX groups, when compared with ALI group. Therefore, the expression level of AQP-1 is associated with pulmonary edema. QYT protects the lungs from injury induced by SAP via the upregulation of AQP-1, which suppresses TNF-? expression. PMID:25371738

GAO, ZHENMING; XU, JUNFENG; SUN, DEGUANG; ZHANG, RIXIN; LIANG, RUI; WANG, LIMING; FAN, RONG

2014-01-01

163

Pulmonary hypertension complicating interstitial lung disease and COPD.  

PubMed

Pulmonary hypertension (PH) may complicate parenchymal lung disease, specifically interstitial lung diseases and chronic obstructive pulmonary disease, and uniformly increases the mortality risk. The epidemiology and degree of PH is variable and unique to the underlying lung disease. The clinician should exercise a high index of suspicion for PH complicating parenchymal lung disease especially given the nonspecific symptomatology and the limitations of echocardiography in this patient population. In general, PH-specific therapies in this setting have been poorly studied, with concern for increased shunting and/or ventilation/perfusion (V/Q) mismatch and resultant hypoxemia. A better understanding of the mechanisms underlying PH related to parenchymal lung disease may lead to novel pharmacological targets to prevent or treat this serious complication. PMID:24037628

Shino, Michael Y; Lynch, Joseph P; Saggar, Rajeev; Abtin, Fereidoun; Belperio, John A; Saggar, Rajan

2013-10-01

164

Pneumovirus in dogs with acute respiratory disease.  

PubMed

To determine which respiratory viruses circulate among confined dogs, we analyzed nasal and pharyngeal swab specimens from shelter dogs with acute respiratory disease. An unknown virus was isolated. Monoclonal antibody testing indicated that it was probably a pneumovirus. PCR and sequence analysis indicated that it was closely related to murine pneumovirus. PMID:20507755

Renshaw, Randall W; Zylich, Nancy C; Laverack, Melissa A; Glaser, Amy L; Dubovi, Edward J

2010-06-01

165

Anti-Inflammatory Effects of Ellagic Acid on Acute Lung Injury Induced by Acid in Mice  

PubMed Central

Acute lung injury (ALI) is characterized by alveolar edema and uncontrolled neutrophil migration to the lung, and no specific therapy is still available. Ellagic acid, a compound present in several fruits and medicinal plants, has shown anti-inflammatory activity in several experimental disease models. We used the nonlethal acid aspiration model of ALI in mice to determine whether preventive or therapeutic administration of ellagic acid (10?mg/kg; oral route) could interfere with the development or establishment of ALI inflammation. Dexamethasone (1?mg/kg; subcutaneous route) was used as a positive control. In both preventive and therapeutic treatments, ellagic acid reduced the vascular permeability changes and neutrophil recruitment to the bronchoalveolar lavage fluid (BALF) and to lung compared to the vehicle. In addition, the ellagic acid accelerated the resolution for lung neutrophilia. Moreover, ellagic acid reduced the COX-2-induced exacerbation of inflammation. These results were similar to the dexamethasone. However, while the anti-inflammatory effects of dexamethasone treatment were due to the reduced activation of NF-?B and AP-1, the ellagic acid treatment led to reduced BALF levels of IL-6 and increased levels of IL-10. In addition, dexamethasone treatment reduced IL-1?. Together, these findings identify ellagic acid as a potential therapeutic agent for ALI-associated inflammation. PMID:23533300

Cornelio Favarin, Daniely; Martins Teixeira, Maxelle; Lemos de Andrade, Edneia; de Freitas Alves, Claudiney; Lazo Chica, Javier Emilio; Arterio Sorgi, Carlos; Paula Rogerio, Alexandre

2013-01-01

166

Endothelial Semaphorin 7A Promotes Inflammation in Seawater Aspiration-Induced Acute Lung Injury.  

PubMed

Inflammation is involved in the pathogenesis of seawater aspiration-induced acute lung injury (ALI). Although several studies have shown that Semaphorin 7A (SEMA7A) promotes inflammation, there are limited reports regarding immunological function of SEMA7A in seawater aspiration-induced ALI. Therefore, we investigated the role of SEMA7A during seawater aspiration-induced ALI. Male Sprague-Dawley rats were underwent seawater instillation. Then, lung samples were collected at an indicated time for analysis. In addition, rat pulmonary microvascular endothelial cells (RPMVECs) were cultured and then stimulated with 25% seawater for indicated time point. After these treatments, cells samples were collected for analysis. In vivo, seawater instillation induced lung histopathologic changes, pro-inflammation cytokines release and increased expression of SEMA7A. In vitro, seawater stimulation led to pro-inflammation cytokine release, cytoskeleton remodeling and increased monolayer permeability in pulmonary microvascular endothelial cells. In addition, knockdown of hypoxia-inducible factor (HIF)-1? inhibited the seawater induced increase expression of SEMA7A. Meanwhile, knockdown of SEMA7A by specific siRNA inhibited the seawater induced aberrant inflammation, endothelial cytoskeleton remodeling and endothelial permeability. These results suggest that SEMA7A is critical in the development of lung inflammation and pulmonary edema in seawater aspiration-induced ALI, and may be a therapeutic target for this disease. PMID:25353180

Zhang, Minlong; Wang, Li; Dong, Mingqing; Li, Zhichao; Jin, Faguang

2014-01-01

167

Work-Related Lung Disease: All Pneumoconioses and Related Exposures  

MedlinePLUS

... visit this page: About CDC.gov . Work-Related Lung Disease Surveillance System (eWoRLD) NIOSH > Workplace Safety and Health ... Share Compartir Welcome to eWoRLD The Work-Related Lung Disease Surveillance System (eWoRLD) presents data on selected work- ...

168

Clinical review: Lung imaging in acute respiratory distress syndrome patients - an update  

PubMed Central

Over the past 30 years lung imaging has greatly contributed to the current understanding of the pathophysiology and the management of acute respiratory distress syndrome (ARDS). In the past few years, in addition to chest X-ray and lung computed tomography, newer functional lung imaging techniques, such as lung ultrasound, positron emission tomography, electrical impedance tomography and magnetic resonance, have been gaining a role as diagnostic tools to optimize lung assessment and ventilator management in ARDS patients. Here we provide an updated clinical review of lung imaging in ARDS over the past few years to offer an overview of the literature on the available imaging techniques from a clinical perspective. PMID:24238477

2013-01-01

169

Connective Tissue Disease-associated Interstitial Lung Disease: A review  

PubMed Central

Interstitial lung disease (ILD) is commonly encountered in patients with connective tissue diseases (CTD). Besides the lung parenchyma, the airways, pulmonary vasculature and structures of the chest wall may all be involved, depending on the type of CTD. As a result of this so-called multi-compartment involvement, airflow limitation, pulmonary hypertension, vasculitis and extrapulmonary restriction can occur alongside fibro-inflammatory parenchymal abnormalities in CTD. Rheumatoid arthritis (RA), systemic sclerosis (SSc), poly-/dermatomyositis (PM/DM), Sjögren’s syndrome (SjS), systemic lupus erythematosus (SLE), and undifferentiated (UCTD) as well as mixed connective tissue disease (MCTD) can all be associated with the development of ILD. Non-specific interstitial pneumonia (NSIP) is the most commonly observed histopathological pattern in CTD-ILD, but other patterns including usual interstitial pneumonia (UIP), organizing pneumonia (OP), diffuse alveolar damage (DAD) and lymphocytic interstitial pneumonia (LIP) may occur. Although the majority of patients with CTD-ILD experience stable or slowly advancing ILD, a small yet significant group exhibits a more severe and progressive course. Randomized placebo-controlled trials evaluating the efficacy of immunomodulatory treatments have been conducted only in SSc-associated ILD. However, clinical experience suggests that a handful of immunosuppressive medications are potentially effective in a sizeable portion of patients with ILD caused by other CTDs. In this manuscript, we review the clinical characteristics and management of the most common CTD-ILDs. PMID:23125954

Gutsche, Markus; Rosen, Glenn D.; Swigris, Jeffrey J.

2012-01-01

170

Effects of contrast material on computed tomographic measurements of lung volumes in patients with acute lung injury  

PubMed Central

Background Intravenous injection of contrast material is routinely performed in order to differentiate nonaerated lung parenchyma from pleural effusion in critically ill patients undergoing thoracic computed tomography (CT). The aim of the present study was to evaluate the effects of contrast material on CT measurement of lung volumes in 14 patients with acute lung injury. Method A spiral thoracic CT scan, consisting of contiguous axial sections of 10 mm thickness, was performed from the apex to the diaphragm at end-expiration both before and 30 s (group 1; n = 7) or 15 min (group 2; n = 7) after injection of 80 ml contrast material. Volumes of gas and tissue, and volumic distribution of CT attenuations were measured before and after injection using specially designed software (Lungview®; Institut National des Télécommunications, Evry, France). The maximal artifactual increase in lung tissue resulting from a hypothetical leakage within the lung of the 80 ml contrast material was calculated. Results Injection of contrast material significantly increased the apparent volume of lung tissue by 83 ± 57 ml in group 1 and 102 ± 80 ml in group 2, whereas the corresponding maximal artifactual increases in lung tissue were 42 ± 52 ml and 31 ± 18 ml. Conclusion Because systematic injection of contrast material increases the amount of extravascular lung water in patients with acute lung injury, it seems prudent to avoid this procedure in critically ill patients undergoing a thoracic CT scan and to reserve its use for specific indications. PMID:12617742

Bouhemad, Belaid; Richecoeur, Jack; Lu, Qin; Malbouisson, Luiz M; Cluzel, Philippe; Rouby, Jean-Jacques

2003-01-01

171

Stem Cells and Cell Therapy Approaches in Lung Biology and Diseases  

PubMed Central

Cell-based therapies with embryonic or adult stem cells, including induced pluripotent stem cells, have emerged as potential novel approaches for several devastating and otherwise incurable lung diseases including emphysema, pulmonary fibrosis, pulmonary hypertension, and the acute respiratory distress syndrome. Although initial studies suggested engraftment of exogenously administered stem cells in lung, this is now generally felt to be a rare occurrence of uncertain physiologic significance. However, more recent studies have demonstrated paracrine effects of administered cells, including stimulation of angiogenesis and modulation of local inflammatory and immune responses in mouse lung disease models. Based on these studies and on safety and initial efficacy data from trials of adult stem cells in other diseases, groundbreaking clinical trials of cell-based therapy have been initiated for pulmonary hypertension and for chronic obstructive pulmonary disease. In parallel, the identity and role of endogenous lung progenitor cells in development and in repair from injury and potential contribution as lung cancer stem cells continue to be elucidated. Most recently, novel bioengineering approaches have been applied to develop functional lung tissue ex vivo. Advances in each of these areas will be described in this review with particular reference to animal models. PMID:20801416

Sueblinvong, Viranuj; Weiss, Daniel J.

2013-01-01

172

Future Directions in Early Cystic Fibrosis Lung Disease Research  

PubMed Central

Since the 1989 discovery that mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene cause cystic fibrosis (CF), there has been substantial progress toward understanding the molecular basis for CF lung disease, leading to the discovery and development of new therapeutic approaches. However, the earliest impact of the loss of CFTR function on airway physiology and structure and its relationship to initial infection and inflammation are poorly understood. Universal newborn screening for CF in the United States represents an unprecedented opportunity for investigating CF clinical manifestations very early in life. Recently developed animal models with pulmonary phenotypic manifestations also provide a window into the early consequences of this genetic disorder. For these reasons, the National Heart, Lung, and Blood Institute (NHLBI) convened a working group of extramural experts, entitled “Future Research Directions in Early CF Lung Disease” on September 21–22, 2010, to identify future research directions of great promise in CF. The priority areas identified included (1) exploring pathogenic mechanisms of early CF lung disease; (2) leveraging newborn screening to elucidate the natural history of early lung disease; (3) developing a spectrum of biomarkers of early lung disease that reflects CF pathophysiology, clinical outcome, and response to treatment; (4) exploring the role of genetics/genomics (e.g., modifier genes, gene–environmental interactions, and epigenetics) in early CF pathogenesis; (5) defining early microbiological events in CF lung disease; and (6) elucidating the initial airway inflammatory, remodeling, and repair mechanisms in CF lung disease. PMID:22312017

Banks-Schlegel, Susan; Accurso, Frank J.; Boucher, Richard C.; Cutting, Garry R.; Engelhardt, John F.; Guggino, William B.; Karp, Christopher L.; Knowles, Michael R.; Kolls, Jay K.; LiPuma, John J.; Lynch, Susan; McCray, Paul B.; Rubenstein, Ronald C.; Singh, Pradeep K.; Sorscher, Eric; Welsh, Michael

2012-01-01

173

Successful crizotinib rechallenge after crizotinib-induced interstitial lung disease.  

PubMed

We report the case of a 70-year-old Japanese male diagnosed with advanced lung adenocarcinoma harboring the echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase fusion gene. As soon as crizotinib was administered, tumor shrank immediately. On Day 25, he developed interstitial lung disease. Bronchoalveolar lavage fluid analysis demonstrated elevated lymphocytes fractionation. A drug lymphocyte stimulating test for crizotinib with the bronchoalveolar lavage lymphocytes was negative. Crizotinib administration was discontinued, but a life-threatening flare of tumor growth occurred. Since there was no alternative treatment for the lung cancer, we restarted crizotinib in combination with prednisolone. The patient experienced neither disease progression nor recurrence of interstitial lung disease at 6 months. In cases in which no alternate treatment is known, crizotinib retreatment combined with steroid therapy after crizotinib-induced interstitial lung disease could be considered after a careful consideration of the potential risks and benefits. PMID:24872405

Tachihara, Motoko; Kobayashi, Kazuyuki; Ishikawa, Yumiko; Hori, Suya; Tamura, Daisuke; Otera, Hiroshi; Funada, Yasuhiro; Nishimura, Yoshihiro

2014-08-01

174

Inflammatory Lung Disease in Rett Syndrome  

PubMed Central

Rett syndrome (RTT) is a pervasive neurodevelopmental disorder mainly linked to mutations in the gene encoding the methyl-CpG-binding protein 2 (MeCP2). Respiratory dysfunction, historically credited to brainstem immaturity, represents a major challenge in RTT. Our aim was to characterize the relationships between pulmonary gas exchange abnormality (GEA), upper airway obstruction, and redox status in patients with typical RTT (n = 228) and to examine lung histology in a Mecp2-null mouse model of the disease. GEA was detectable in ~80% (184/228) of patients versus ~18% of healthy controls, with “high” (39.8%) and “low” (34.8%) patterns dominating over “mixed” (19.6%) and “simple mismatch” (5.9%) types. Increased plasma levels of non-protein-bound iron (NPBI), F2-isoprostanes (F2-IsoPs), intraerythrocyte NPBI (IE-NPBI), and reduced and oxidized glutathione (i.e., GSH and GSSG) were evidenced in RTT with consequently decreased GSH/GSSG ratios. Apnea frequency/severity was positively correlated with IE-NPBI, F2-IsoPs, and GSSG and negatively with GSH/GSSG ratio. A diffuse inflammatory infiltrate of the terminal bronchioles and alveoli was evidenced in half of the examined Mecp2-mutant mice, well fitting with the radiological findings previously observed in RTT patients. Our findings indicate that GEA is a key feature of RTT and that terminal bronchioles are a likely major target of the disease. PMID:24757286

De Felice, Claudio; Rossi, Marcello; Chisci, Glauco; Lonetti, Giuseppina; Vannuccini, Laura; Spina, Donatella; Iacona, Ingrid; Cortelazzo, Alessio; Ciccoli, Lucia; Pizzorusso, Tommaso; Hayek, Joussef

2014-01-01

175

Respiratory bronchiolitis-interstitial lung disease  

PubMed Central

Respiratory bronchiolitis-associated interstitial lung disease (RB-ILD) is a rare, mild inflammatory pulmonary disorder that occurs almost exclusively in current or former heavy smokers, usually between the third and sixth decades, most likely with no gender predilection. The onset is usually insidious with exertional dyspnea and persistent cough, which may be non-productive, developing over a course of weeks or months. RB-ILD may also be diagnosed in asymptomatic patients with functional impairment and chest radiograph or high-resolution computed tomography (HRCT) abnormalities. Histologically, RB-ILD is characterized by the accumulation of yellow-brown pigmented macrophages within the lumens of respiratory bronchioles and alveolar ducts, associated with a patchy submucosal and peribronchiolar chronic inflammation. Common findings also include mild bronchiolar and peribronchiolar alveolar fibrosis that expands contiguous alveolar septa and leads to architectural distortion as well as centrilobular emphysema. Chest radiographs in patients with RB-ILD typically show fine reticulonodular interstitial opacities, while on HRCT central and peripheral bronchial wall thickening, centrilobular nodules, and ground-glass opacities associated with upper lobe centrilobular emphysema are most frequently reported. Pulmonary function testing may be normal but usually demonstrates mixed, predominantly obstructive abnormalities, often combined with hyperinflation and usually associated with a mild to moderate reduction in carbon monoxide diffusion capacity (DLco). The course of RB-ILD is heterogeneous. Some patients respond favorably to corticosteroids and/or smoking cessation, but often there is no functional improvement and the disease progresses despite smoking cessation and treatment. PMID:25011486

2014-01-01

176

Treatment of Acute Pelvic Inflammatory Disease  

PubMed Central

Pelvic inflammatory disease (PID), one of the most common infections in nonpregnant women of reproductive age, remains an important public health problem. It is associated with major long-term sequelae, including tubal factor infertility, ectopic pregnancy, and chronic pelvic pain. In addition, treatment of acute PID and its complications incurs substantial health care costs. Prevention of these long-term sequelae is dependent upon development of treatment strategies based on knowledge of the microbiologic etiology of acute PID. It is well accepted that acute PID is a polymicrobic infection. The sexually transmitted organisms, Neisseria gonorrhoeae and Chlamydia trachomatis, are present in many cases, and microorganisms comprising the endogenous vaginal and cervical flora are frequently associated with PID. This includes anaerobic and facultative bacteria, similar to those associated with bacterial vaginosis. Genital tract mycoplasmas, most importantly Mycoplasma genitalium, have recently also been implicated as a cause of acute PID. As a consequence, treatment regimens for acute PID should provide broad spectrum coverage that is effective against these microorganisms. PMID:22228985

Sweet, Richard L.

2011-01-01

177

Development of a Multicomponent Prediction Model for Acute Esophagitis in Lung Cancer Patients Receiving Chemoradiotherapy  

SciTech Connect

Purpose: To construct a model for the prediction of acute esophagitis in lung cancer patients receiving chemoradiotherapy by combining clinical data, treatment parameters, and genotyping profile. Patients and Methods: Data were available for 273 lung cancer patients treated with curative chemoradiotherapy. Clinical data included gender, age, World Health Organization performance score, nicotine use, diabetes, chronic disease, tumor type, tumor stage, lymph node stage, tumor location, and medical center. Treatment parameters included chemotherapy, surgery, radiotherapy technique, tumor dose, mean fractionation size, mean and maximal esophageal dose, and overall treatment time. A total of 332 genetic polymorphisms were considered in 112 candidate genes. The predicting model was achieved by lasso logistic regression for predictor selection, followed by classic logistic regression for unbiased estimation of the coefficients. Performance of the model was expressed as the area under the curve of the receiver operating characteristic and as the false-negative rate in the optimal point on the receiver operating characteristic curve. Results: A total of 110 patients (40%) developed acute esophagitis Grade {>=}2 (Common Terminology Criteria for Adverse Events v3.0). The final model contained chemotherapy treatment, lymph node stage, mean esophageal dose, gender, overall treatment time, radiotherapy technique, rs2302535 (EGFR), rs16930129 (ENG), rs1131877 (TRAF3), and rs2230528 (ITGB2). The area under the curve was 0.87, and the false-negative rate was 16%. Conclusion: Prediction of acute esophagitis can be improved by combining clinical, treatment, and genetic factors. A multicomponent prediction model for acute esophagitis with a sensitivity of 84% was constructed with two clinical parameters, four treatment parameters, and four genetic polymorphisms.

De Ruyck, Kim, E-mail: kim.deruyck@UGent.be [Department of Basic Medical Sciences, Ghent University, Ghent (Belgium); Sabbe, Nick [Department of Applied Mathematics, Biometrics and Process Control, Ghent University, Ghent (Belgium); Oberije, Cary [Department of Radiation Oncology (MAASTRO Clinic), Research Institute of Growth and Development, Maastricht University Medical Center, Maastricht (Netherlands); Vandecasteele, Katrien [Department of Radiation Oncology, Ghent University Hospital, Ghent (Belgium); Thas, Olivier [Department of Applied Mathematics, Biometrics and Process Control, Ghent University, Ghent (Belgium); De Ruysscher, Dirk; Lambin, Phillipe [Department of Radiation Oncology (MAASTRO Clinic), Research Institute of Growth and Development, Maastricht University Medical Center, Maastricht (Netherlands); Van Meerbeeck, Jan [Department of Respiratory Medicine, Ghent University Hospital, Ghent (Belgium); De Neve, Wilfried [Department of Radiation Oncology, Ghent University Hospital, Ghent (Belgium); Thierens, Hubert [Department of Basic Medical Sciences, Ghent University, Ghent (Belgium)

2011-10-01

178

The role of female hormones on lung function in chronic lung diseases  

Microsoft Academic Search

Background  The prevalence, morbidity, and mortality of inflammatory lung diseases such as asthma, chronic obstructive pulmonary disease\\u000a (COPD) and cystic fibrosis (CF) are increasing in women. There is a dearth of data on the biological mechanisms to explain\\u000a such observations. However, some large epidemiologic studies suggest that lung function fluctuates during the menstrual cycle\\u000a in female patients with airways disease but

Anthony Tam; Don Morrish; Samuel Wadsworth; Delbert Dorscheid; SF Paul Man; Don D Sin

2011-01-01

179

Early high volume lung lavage for acute severe smoke inhalation injury in dogs.  

PubMed

The aim of the present study was to investigate the safety and short?term results of early high volume lung lavage in the treatment of acute severe smoke inhalation injuries in dogs. A high?volume normal saline complex solution lavage in the left lung was performed 1 h subsequent to bilateral pulmonary acute severe sawdust smoke inhalation injury in dogs. Lavage of the right lung was conducted following an interval of 30 min or 4 h. The perfluorodecalin lavage was performed in dogs with unilateral pulmonary acute severe sawdust smoke inhalation injury. The present study identified that lavage with an interval of 4 h between two lungs was safer compared with a 30?min interval. Following lavage, the increase in the levels of free radical metabolites and inflammatory mediators in the lung homogenate was reduced. Acute severe smoke inhalation injury in one lung evidently caused a secondary injury to the other lung in the dogs. Perfluorodecalin lavage did not achieve the same effect in cleansing the lungs as the normal saline, but a greater comprehensive short?term outcome was obtained. These observations demonstrated that early high?volume lung lavage following severe smoke inhalation injury could relieve primary injuries and secondary local and general inflammatory reactions in dogs. An improved comprehensive short?term outcome was obtained in the perfluorodecalin?lavaged dogs. PMID:24366331

Nie, Fachuan; Su, Dong; Shi, Ying; Chen, Jinmei; Wang, Haihui; Qin, Wanxiang; Wang, Suxia; Chen, Yaohua

2014-03-01

180

Significance of the microbiome in obstructive lung disease.  

PubMed

The composition of the lung microbiome contributes to both health and disease, including obstructive lung disease. Because it has been estimated that over 70% of the bacterial species on body surfaces cannot be cultured by currently available techniques, traditional culture techniques are no longer the gold standard for microbial investigation. Advanced techniques that identify bacterial sequences, including the 16S ribosomal RNA gene, have provided new insights into the depth and breadth of microbiota present both in the diseased and normal lung. In asthma, the composition of the microbiome of the lung and gut during early childhood development may play a key role in the development of asthma, while specific airway microbiota are associated with chronic asthma in adults. Early bacterial stimulation appears to reduce asthma susceptibility by helping the immune system develop lifelong tolerance to innocuous antigens. By contrast, perturbations in the microbiome from antibiotic use may increase the risk for asthma development. In chronic obstructive pulmonary disease, bacterial colonisation has been associated with a chronic bronchitic phenotype, increased risk of exacerbations, and accelerated loss of lung function. In cystic fibrosis, studies utilising culture-independent methods have identified associations between decreased bacterial community diversity and reduced lung function; colonisation with Pseudomonas aeruginosa has been associated with the presence of certain CFTR mutations. Genomic analysis of the lung microbiome is a young field, but has the potential to define the relationship between lung microbiome composition and disease course. Whether we can manipulate bacterial communities to improve clinical outcomes remains to be seen. PMID:22318161

Han, Meilan K; Huang, Yvonne J; Lipuma, John J; Boushey, Homer A; Boucher, Richard C; Cookson, William O; Curtis, Jeffrey L; Erb-Downward, John; Lynch, Susan V; Sethi, Sanjay; Toews, Galen B; Young, Vincent B; Wolfgang, Matthew C; Huffnagle, Gary B; Martinez, Fernando J

2012-05-01

181

PAMAM nanoparticles promote acute lung injury by inducing autophagic cell death through the Akt-TSC2-mTOR signaling pathway.  

PubMed

Nanotechnology is an important and emerging industry with a projected annual market of around one trillion US dollars by 2011-2015. Concerns about the toxicity of nanomaterials in humans, however, have recently been raised. Although studies of nanoparticle toxicity have focused on lung disease the molecular link between nanoparticle exposure and lung injury remained unclear. In this report, we show that cationic Starburst polyamidoamine dendrimer (PAMAM), a class of nanomaterials that are being widely developed for clinical applications can induce acute lung injury in vivo. PAMAM triggers autophagic cell death by deregulating the Akt-TSC2-mTOR signaling pathway. The autophagy inhibitor 3-methyladenine rescued PAMAM dendrimer-induced cell death and ameliorated acute lung injury caused by PAMAM in mice. Our data provide a molecular explanation for nanoparticle-induced lung injury, and suggest potential remedies to address the growing concerns of nanotechnology safety. PMID:19516051

Li, Chenggang; Liu, Haolin; Sun, Yang; Wang, Hongliang; Guo, Feng; Rao, Shuan; Deng, Jiejie; Zhang, Yanli; Miao, Yufa; Guo, Chenying; Meng, Jie; Chen, Xiping; Li, Limin; Li, Dangsheng; Xu, Haiyan; Wang, Heng; Li, Bo; Jiang, Chengyu

2009-10-01

182

Animal models of beryllium-induced lung disease  

Microsoft Academic Search

The Inhalation Toxicology Research Institute (ITRI) is conducting research to improve the understanding of chronic beryllium disease (CBD) and beryllium-induced lung cancer. Initial animal studies examined beagle dogs that inhaled BeO calcined at either 500 or 1000°C. At similar lung burdens, the 500°C BeO induced more severe and extensive granulomatous pneumonia, lymphocytic infiltration into the lung, and positive Be-specific lymphocyte

G. L. Finch; M. D. Hoover; F. F. Hahn

1996-01-01

183

Monoacylglycerol Lipase (MAGL) Inhibition Attenuates Acute Lung Injury in Mice  

PubMed Central

Endocannabinoid signaling is terminated by enzymatic hydrolysis, a process that, for 2-Arachidonoylglycerol (2-AG), is mediated by monoacylglycerol lipase (MAGL). The piperidine carbamate, 4-?nitrophenyl- ?4-?(dibenzo[d] [1,3]dioxol-?5-?yl (hydroxy) methyl) piperidine- 1-?carboxylate (JZL184), is a drug that inhibits MAGL and presents high potency and selectivity. Thus, JZL184 increases the levels of 2-AG, an endocannabinoid that acts on the CB1 and CB2 cannabinoid receptors. Here, we investigated the effects of MAGL inhibition, with a single dose (16 mg/kg, intraperitoneally (i.p.)) of JZL184, in a murine model of lipopolysaccharide (LPS) -induced acute lung injury (ALI) 6, 24 and 48 hours after the inflammatory insult. Treatment with JZL184 decreased the leukocyte migration into the lungs as well as the vascular permeability measured through the bronchoalveolar lavage fluid (BAL) and histological analysis. JZL184 also reduced the cytokine and chemokine levels in the BAL and adhesion molecule expression in the blood and BAL. The CB1 and CB2 receptors were considered involved in the anti-inflammatory effects of JZL184 because the AM281 selective CB1 receptor antagonist (1-(2,4-dichlorophenyl)-5-(4-iodophenyl)-4-methyl-N-4-morpholinyl-1H-pyrazole-3-carboxamide) and the AM630 selective CB2 receptor antagonist ([6-?iodo-?2-?methyl-?1-?[2-?(4-?morpholinyl)ethyl]-?1H-?indol-?3-?yl](4-?methoxyphenyl)-?methanone) blocked the anti-inflammatory effects previously described for JZL184. It was concluded that MAGL inhibition, and consequently the increase in 2-AG levels, produced anti-inflammatory effects in a murine model of LPS-induced ALI, a finding that was considered a consequence of the activation of the CB1 and CB2 receptors. PMID:24204926

Costola-de-Souza, Carolina; Ribeiro, Alison; Ferraz-de-Paula, Viviane; Calefi, Atilio Sersun; Aloia, Thiago Pinheiro Arrais; Gimenes-Junior, Joao Antonio; de Almeida, Vinicius Izidio; Pinheiro, Milena Lobao; Palermo-Neto, Joao

2013-01-01

184

Kinetics of the angiogenic response in lung endothelium following acute inflammatory injury with bleomycin  

PubMed Central

Purpose/Aim Angiogenesis is a central component of normal wound healing but it has not been fully characterized in lung repair following acute inflammatory injury. The current literature lacks vital information pertaining to the extent, timing, and location of this process. This information is necessary for examining mechanisms that drive normal lung repair in resolving acute inflammatory injury. The goal of our study was to formally characterize lung angiogenesis over a time course of bleomycin induced lung injury. Materials and Methods Female C57BL/6 mice age 8-12 weeks were treated with a single dose of intratracheal bleomycin. Total lung endothelial cells were quantified with flow cytometry 0, 7, 14, 21, and 28 days following bleomycin administration, and endothelial cell replication was assessed using bromodeoxyuridine (BrdU) incorporation. Results Endothelial cell replication was maximal 14 days after bleomycin administration, while total lung endothelial cells peaked at day 21. Tissue analysis with stereology was performed to measure total lung vascular surface area in bleomycin at day 21 relative to controls and demonstrated a trend toward increased vasculature in the bleomycin group. Conclusions Angiogenesis begins shortly after injury in the bleomycin model and leads to an expansion in the lung endothelial cell population that peaks at day 21. This study offers the first longitudinal examination of angiogenesis following acute inflammatory lung injury induced by bleomycin. Information provided in this study will be vital for further investigating mechanisms of angiogenesis in both normal and abnormal lung repair. PMID:25153689

Yunt, Zulma X; Mohning, Michael P; Barthel, Lea; Kearns, Mark T; Tuder, Rubin M; Hyde, Dallas M; Henson, Peter M; Janssen, William J

2014-01-01

185

Report of the workshop on environmentally related nononcogenic lung disease  

SciTech Connect

During the week of March 13-18, 1983, 37 government and university health scientists participated in the Workshop on environmentally related nononcogenic lung disease. The workshop represented a major effort by the interagency Task Force on Environmental Cancer and Heart and Lung Disease to address in fiscal year 1983 its mandate to assess current evidence and recommend integrated federal research programs toward relating human illness with environmental pollution. The subject of nononcogenic lung disease was approached through three concurrent discussion sessions: epidemiology, statistics, and risk assessment; clinical research; and basic and animal research. Each session produced an immediate set of recommendations on research needs, complete with background information and literature references.

Whittenberger, J.L.

1985-12-01

186

Increased elastin production in experimental granulomatous lung disease.  

PubMed Central

In the normal, healthy lung, elastin production is restricted to periods of development and growth. However, elastin expression in the adult lung has been observed in some forms of pulmonary injury, including pulmonary fibrosis. Here, we report that elastin production is significantly increased within precise interstitial compartments of the lung in an experimental model of granulomatous lung disease. An increase in the number and volume of elastic fibers within the alveolar walls was apparent on histological examination of Verhoeff-van Gieson-stained sections of silicotic rat lungs. Quantitation of mature elastin cross-links indicated that silicosis was accompanied by a 17-fold increase in lung elastin content when compared with values from saline-treated controls. In situ hybridization for tropoelastin mRNA revealed that elastin production was absent from granulomatous lesions yet was prominent at nonfibrotic alveolar septal tips, where a high density of elastic fibers is seen in the normal lung. Immunohistochemistry indicated tropoelastin was being expressed by alpha-smooth muscle actin-containing cells. Transforming growth factor-beta was immunolocalized to granulomatous regions of the silicotic lung but was absent from regions showing increased tropoelastin expression. These data indicate that the reinitiation of tropoelastin gene expression is associated with granulomatous lung disease, and this expression leads to the aberrant accumulation of mature elastin in the lung. Images Figure 1 Figure 2 Figure 4 Figure 5 Figure 6 PMID:7573374

Mariani, T. J.; Crouch, E.; Roby, J. D.; Starcher, B.; Pierce, R. A.

1995-01-01

187

Neurofibromatosis-associated diffuse lung disease: case report.  

PubMed

Since the initial report in 1963 several small case series described an association between neurofibromatosis (NF) and interstitial lung disease. To date, more than 60 cases of interstitial lung disease associated with NF have been reported, but relatively few reports included high-resolution computed tomographic (HRCT) scans. Typical findings on HRCT include upper lobe predominant cystic and bullous disease, ground-glass opacification, and basilar reticular abnormalities. We present the case of a 34-year-old male smoker with NF and HRCT findings of diffuse lung disease including bullous emphysema, thin-walled cysts, and diffuse ground glass. Although NF-associated diffuse lung disease (NF-DLD) is disputed as a clinical entity by some, the case presented here adds to the accumulating evidence that NF-DLD is a distinct manifestation of neurofibromatosis. PMID:23001809

Shino, Michael Y; Rabbani, Shehrzad; Belperio, John A; Lynch, Joseph P; Weigt, S Samuel

2012-10-01

188

Sphingosine-1-Phosphate Receptor-3 Is a Novel Biomarker in Acute Lung Injury  

PubMed Central

The inflamed lung exhibits oxidative and nitrative modifications of multiple target proteins, potentially reflecting disease severity and progression. We identified sphingosine-1–phosphate receptor–3 (S1PR3), a critical signaling molecule mediating cell proliferation and vascular permeability, as a nitrated plasma protein in mice with acute lung injury (ALI). We explored S1PR3 as a potential biomarker in murine and human ALI. In vivo nitrated and total S1PR3 concentrations were determined by immunoprecipitation and microarray studies in mice, and by ELISA in human plasma. In vitro nitrated S1PR3 concentrations were evaluated in human lung vascular endothelial cells (ECs) or within microparticles shed from ECs after exposure to barrier-disrupting agonists (LPS, low-molecular-weight hyaluronan, and thrombin). The effects of S1PR3-containing microparticles on EC barrier function were assessed by transendothelial electrical resistance (TER). Nitrated S1PR3 was identified in the plasma of murine ALI and in humans with severe sepsis-induced ALI. Elevated total S1PR3 plasma concentrations (> 251 pg/ml) were linked to sepsis and ALI mortality. In vitro EC exposure to barrier-disrupting agents induced S1PR3 nitration and the shedding of S1PR3-containing microparticles, which significantly reduced TER, consistent with increased permeability. These changes were attenuated by reduced S1PR3 expression (small interfering RNAs). These results suggest that microparticles containing nitrated S1PR3 shed into the circulation during inflammatory lung states, and represent a novel ALI biomarker linked to disease severity and outcome. PMID:22771388

Sun, Xiaoguang; Singleton, Patrick A.; Letsiou, Eleftheria; Zhao, Jing; Belvitch, Patrick; Sammani, Saad; Chiang, Eddie T.; Moreno-Vinasco, Liliana; Wade, Michael S.; Zhou, Tong; Liu, Bin; Parastatidis, Ioannis; Thomson, Leonor; Ischiropoulos, Harry; Natarajan, Viswanathan; Jacobson, Jeffrey R.; Machado, Roberto F.; Dudek, Steven M.

2012-01-01

189

Clinical potentials of human pluripotent stem cells in lung diseases  

PubMed Central

Lung possesses very limited regenerative capacity. Failure to maintain homeostasis of lung epithelial cell populations has been implicated in the development of many life-threatening pulmonary diseases leading to substantial morbidity and mortality worldwide, and currently there is no known cure for these end-stage pulmonary diseases. Embryonic stem cells (ESCs) and somatic cell-derived induced pluripotent stem cells (iPSCs) possess unlimited self-renewal capacity and great potential to differentiate to various cell types of three embryonic germ layers (ectodermal, mesodermal, and endodermal). Therapeutic use of human ESC/iPSC-derived lung progenitor cells for regeneration of injured or diseased lungs will have an enormous clinical impact. This article provides an overview of recent advances in research on pluripotent stem cells in lung tissue regeneration and discusses technical challenges that must be overcome for their clinical applications in the future. PMID:24995122

2014-01-01

190

Erythropoetin as a novel agent with pleiotropic effects against acute lung injury  

Microsoft Academic Search

Current pharmacotherapy for acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) is not optimal, and the\\u000a biological and physiological complexity of these severe lung injury syndromes requires consideration of combined-agent treatments\\u000a or agents with pleiotropic action. In this regard, exogenous erythropoietin (EPO) represents a possible candidate since a\\u000a number of preclinical studies have revealed beneficial effects of EPO

Sotirios Kakavas; Theano Demestiha; Panagiotis Vasileiou; Theodoros Xanthos

2011-01-01

191

Bench-to-bedside review: Adenosine receptors – promising targets in acute lung injury?  

Microsoft Academic Search

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are life-threatening disorders that have substantial\\u000a adverse effects on outcomes in critically ill patients. ALI\\/ARDS develops in response to pulmonary or extrapulmonary injury\\u000a and is characterized by increased leakage from the pulmonary microvasculature and excessive infiltration of polymorphonuclear\\u000a cells into the lung. Currently, no therapeutic strategies are available to control

Carsten P Schepp; Jörg Reutershan

2008-01-01

192

Proteomic Analysis of Lung Tissue in a Rat Acute Lung Injury Model: Identification of PRDX1 as a Promoter of Inflammation  

PubMed Central

Acute respiratory distress syndrome (ARDS) remains a high morbidity and mortality disease entity in critically ill patients, despite decades of numerous investigations into its pathogenesis. To obtain global protein expression changes in acute lung injury (ALI) lung tissues, we employed a high-throughput proteomics method to identify key components which may be involved in the pathogenesis of ALI. In the present study, we analyzed lung tissue proteomes of Pseudomonas aeruginosa-induced ALI rats and identified eighteen proteins whose expression levels changed more than twofold as compared to normal controls. In particular, we found that PRDX1 expression in culture medium was elevated by a lipopolysaccharide (LPS) challenge in airway epithelial cells in vitro. Furthermore, overexpression of PRDX1 increased the expression of proinflammatory cytokines interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-? (TNF-?), whereas knockdown of PRDX1 led to downregulated expression of cytokines induced by LPS. In conclusion, our findings provide a global alteration in the proteome of lung tissues in the ALI rat model and indicate that PRDX1 may play a critical role in the pathogenesis of ARDS by promoting inflammation and represent a novel strategy for the development of new therapies against ALI. PMID:25024510

Liu, Dongdong; Mao, Pu; Huang, Yongbo; Liu, Yiting; Liu, Xiaoqing; Pang, Xiaoqing; Li, Yimin

2014-01-01

193

Interstitial lung disease associated with vindesine and radiation therapy for carcinoma of the lung  

SciTech Connect

Diffuse interstitial lung disease and pulmonary fibrosis occurred after the use of vindesine and radiation therapy in a patient with squamous cell carcinoma of the lung. Clinical improvement occurred after the drug was discontinued and corticosteroid therapy was initiated. Review of the literature reveals no previously reported cases of pulmonary toxicity due to vindesine when used alone or in combination with other therapeutic modalities.

Bott, S.J.; Stewart, F.M.; Prince-Fiocco, M.A.

1986-07-01

194

Chronic Obstructive Pulmonary Disease and Lung Cancer: New Molecular Insights  

Microsoft Academic Search

Both chronic obstructive pulmonary disease (COPD) and lung cancer are major causes of death worldwide. In most cases this reflects cigarette smoke exposure which is able to induce an inflammatory response in the airways of smokers. Indeed, COPD is characterized by lower airway inflammation, and importantly, the presence of COPD is by far the greatest risk factor for lung cancer

Ian M. Adcock; Gaetano Caramori; Peter J. Barnes

2011-01-01

195

Oxygen therapy in acute exacerbations of chronic obstructive pulmonary disease  

PubMed Central

Acute exacerbations of chronic obstructive pulmonary disease (COPD) are important events in the history of this debilitating lung condition. Associated health care utilization and morbidity are high, and many patients require supplemental oxygen or ventilatory support. The last 2 decades have seen a substantial increase in our understanding of the best way to manage the respiratory failure suffered by many patients during this high-risk period. This review article examines the evidence underlying supplemental oxygen therapy during exacerbations of COPD. We first discuss the epidemiology and pathophysiology of respiratory failure in COPD during exacerbations. The rationale and evidence underlying oxygen therapy, including the risks when administered inappropriately, are then discussed, along with further strategies for ventilatory support. We also review current recommendations for best practice, including methods for improving oxygen provision in the future.

Brill, Simon E; Wedzicha, Jadwiga A

2014-01-01

196

New insights into mechanisms controlling the NLRP3 inflammasome and its role in lung disease.  

PubMed

Inflammasomes are large macromolecular signaling complexes that control the proteolytic activation of two highly proinflammatory IL-1 family cytokines, IL-1? and IL-18. The NLRP3 inflammasome is of special interest because it can assemble in response to a diverse array of stimuli and because the inflammation it triggers has been implicated in a wide variety of disease pathologies. To avoid aberrant activation, the NLRP3 inflammasome is modulated on multiple levels, ranging from transcriptional control to post-translational protein modifications. Emerging genetic and pharmacological evidence suggests that NLRP3 inflammasome activation may also be involved in acute lung inflammation after viral infection and during progression of several chronic pulmonary diseases, including idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, and asthma. Here, we review the most recent contributions to our understanding of the regulatory mechanisms controlling activation of the NLRP3 inflammasome and discuss the contribution of the NLRP3 inflammasome to the pathology of lung diseases. PMID:24183846

De Nardo, Dominic; De Nardo, Christine M; Latz, Eicke

2014-01-01

197

Partial Liquid Ventilation for Acute Allograft Dysfunction After Canine Lung Transplantation  

Microsoft Academic Search

Background. This study was designed to investigate the efficacy of partial liquid ventilation (PLV) on acute allo- graft dysfunction after lung transplantation. Methods. The canine left lung allotransplantation model was used, with the graft preserved in 4°C low- potassium dextran glucose solution for 18 hours. The control group (n 5 6) had conventional mechanical ven- tilation, and the PLV group

Hideki Itano; Motoi Aoe; Shingo Ichiba; Motohiro Yamashita; Hiroshi Date; Akio Andou; Nobuyoshi Shimizu

198

CT in the diagnosis of interstitial lung disease  

SciTech Connect

The computed tomographic (CT) appearance of interstitial lung disease was assessed in 23 patients with known interstitial disease. These included seven patients with fibrosing alveolitis, six with silicosis, two with hypersensitivity pneumonitis, three with lymphangitic spread of tumor, two with sarcoidosis, one with rheumatoid lung disease, and two with neurofibromatosis. The CT appearance of the interstitial changes in the different disease entities was assessed. Nodules were a prominent CT feature in silicosis, sarcoidosis, and lymphangitic spread of malignancy. Distribution of nodules and associated interlobular septal thickening provided further distinguishing features in these diseases. Reticular densities were the predominant CT change in fibrosing alveolitis, rheumatoid lung disease, and extrinsic allergic alveolitis. CT can be useful in the investigation of selected instances of interstitial pulmonary disease.

Bergin, C.J.; Mueller, N.L.

1985-09-01

199

Prone position reduces lung stress and strain in severe acute respiratory distress syndrome  

Microsoft Academic Search

The present authors hypothesised that in severe acute respiratory distress syndrome (ARDS), pronation may reduce ventilator-induced overall stress (i.e. transpulmonary pressure (PL)) and strain of lung parenchyma (i.e. tidal volume (VT)\\/end-expiratory lung volume (EELV) ratio), which constitute major ventilator-induced lung injury determinants. The authors sought to determine whether potential pronation benefits are maintained in post-prone semirecumbent (SRPP) posture under pressure-volume

S. D. Mentzelopoulos; C. Roussos; S. G. Zakynthinos

2005-01-01

200

Epigenetics and the Developmental Origins of Lung Disease  

PubMed Central

The developmental origins of disease hypothesis has recently been expanded to include the early origins of lung disease, particularly early events that alter lung development. Intrauterine growth restriction (IUGR), preterm birth with the need for prolonged mechanical ventilation, and maternal tobacco smoke (MTS) or nicotine exposure produce neonatal and adult lung disease. These perinatal insults are characterized by alterations in alveolar formation and changes in the expression of genes that regulate alveolarization, including IGF1 and PPAR?. A potential mechanism for such changes in gene expression is epigenetics. IGF1 and PPAR? have altered epigenetic states in response to these perinatal insults. Identification of the specific epigenetic mechanisms involved in the developmental origins of lung disease may facilitate identification of molecular biomarkers with the potential to personalize respiratory disease risk assessment and treatment. The purpose of this review is to summarize what is known about the developmental origins of lung disease, the epigenetic contributions to lung disease, and areas that need further investigation. PMID:21835665

Joss-Moore, Lisa A; Albertine, Kurt H; Lane, Robert H

2011-01-01

201

Diagnostic Pathology of Diffuse Lung Disease in Children.  

PubMed

The pathologic classification of diffuse lung disease in children and adolescents has undergone revision in recent years in response to rapid developments and new discoveries in the field. A number of important advancements have been made in the last 10 years including the description of new genetic mutations causing severe lung disease in infants and children, as well as the description of new pathologic entities in infants. These recently described entities, including ABCA3 surfactant disorders, pulmonary interstitial glycogenosis, and neuroendocrine cell hyperplasia of infancy, are being recognized with increasing frequency. This review will include brief discussion of the etiology and pathogenesis of the major groups of diffuse lung disease in children. Histopathologic features are discussed for each of the major categories of diffuse lung disease in children, beginning with the genetic, developmental, and alveolar growth disorders common in infancy, followed by brief discussion of airway diseases, immunologic diseases, and pulmonary vascular diseases seen more commonly in older children. A protocol for handling pediatric wedge lung biopsies is also discussed, which optimizes the diagnostic yield of lung biopsies in this population. PMID:22332032

Dishop, Megan K

2010-03-01

202

Spirometry: Simulations of Obstructive and Restrictive Lung Diseases  

NSDL National Science Digital Library

Description of spirometry exercises that enhance studentsÃÂ understanding of pulmonary physiology and pathophysiology, as well as allowing them to experience the difficulty, discomfort, and apprehension associated with lung disease

Mr. David W. Rodenbaugh (Wayne State University Department of Physiology); PhD Heidi L. Collins (Wayne State Univ. School of Medicine Dept. of Physiology); PhD Stephen M. DiCarlo (Wayne State Univ Sch Med Dept of Physiology)

2002-09-01

203

Amniotic Fluid Stem Cells from EGFP Transgenic Mice Attenuate Hyperoxia-Induced Acute Lung Injury  

PubMed Central

High concentrations of oxygen aggravate the severity of lung injury in patients requiring mechanical ventilation. Although mesenchymal stem cells have been shown to effectively attenuate various injured tissues, there is limited information regarding a role for amniotic fluid stem cells (AFSCs) in treating acute lung injury. We hypothesized that intravenous delivery of AFSCs would attenuate lung injury in an experimental model of hyperoxia-induced lung injury. AFSCs were isolated from EGFP transgenic mice. The in vitro differentiation, surface markers, and migration of the AFSCs were assessed by specific staining, flow cytometry, and a co-culture system, respectively. The in vivo therapeutic potential of AFSCs was evaluated in a model of acute hyperoxia-induced lung injury in mice. The administration of AFSCs significantly reduced the hyperoxia-induced pulmonary inflammation, as reflected by significant reductions in lung wet/dry ratio, neutrophil counts, and the level of apoptosis, as well as reducing the levels of inflammatory cytokine (IL-1?, IL-6, and TNF-?) and early-stage fibrosis in lung tissues. Moreover, EGFP-expressing AFSCs were detected and engrafted into a peripheral lung epithelial cell lineage by fluorescence microscopy and DAPI stain. Intravenous administration of AFSCs may offer a new therapeutic strategy for acute lung injury (ALI), for which efficient treatments are currently unavailable. PMID:24040409

Lai, Cheng-Wei; Yen, Chih-Ching; Lee, Kun-Hsiung; Wu, Shinn-Chih; Chen, Chuan-Mu

2013-01-01

204

Asbestos lung burden and disease patterns in man  

SciTech Connect

This article discusses the relationship between disease and asbestos burden in the human lung. The differences in this relationship for various types of asbestos are also discussed. Finally the outstanding issues in the field of asbestos research and disease are presented including the following: discrepancies between data derived from animal experiments, predictions based on mathematical models, and data derived from actual analysis of autopsied human lungs. 75 refs., 3 figs., 3 tab.

Churg, A. [Univ. of British Columbia, Vancouver (Canada)

1993-12-31

205

Perioperative Management of Interscalene Block in Patients with Lung Disease  

PubMed Central

Interscalene nerve block impairs ipsilateral lung function and is relatively contraindicated for patients with lung impairment. We present a case of an 89-year-old female smoker with prior left lung lower lobectomy and mild to moderate lung disease who presented for right shoulder arthroplasty and insisted on regional anesthesia. The patient received a multimodal perioperative regimen that consisted of a continuous interscalene block, acetaminophen, ketorolac, and opioids. Surgery proceeded uneventfully and postoperative analgesia was excellent. Pulmonary physiology and management of these patients will be discussed. A risk/benefit discussion should occur with patients having impaired lung function before performance of interscalene blocks. In this particular patient with mild to moderate disease, analgesia was well managed through a multimodal approach including a continuous interscalene block, and close monitoring of respiratory status took place throughout the perioperative period, leading to a successful outcome. PMID:24369510

Schwenk, Eric S.; Gandhi, Kishor; Viscusi, Eugene R.

2013-01-01

206

Wading into the Genomic Pool to Unravel Acute Lung Injury Genetics  

Microsoft Academic Search

Acute lung injury (ALI) is a common and often devastating illness characterized by acute hypoxemia, alveolar flooding, and an unac- ceptably high morbidity and mortality. Because only a fraction of the patients exposed to ALI-inciting events progress to develop- ment of the syndrome, there is significant interest in the identifica- tion of genetic factors potentially contributing to ALI susceptibility or

Nuala J. Meyer; Joe G. N. Garcia

2007-01-01

207

[The use of Timalin in the treatment of the acute lung abscess].  

PubMed

The study was aimed to research levels of main acute inflammation phase peptides, coagulative and fibrinolitic plasma activity on the background of traditional treatment and with addition of Timalin in patients with acute lung abscess. The study demonstrated that induction of bioregulative therapy leads to faster normalization of main indicators of SIRS and plasma fibrinolitic activity and eliminates hypercoagulation. PMID:23258355

Tsybikov, M N; Likhanov, I D; Borshchevski?, V S; Kuznik, B I; Tsepelev, V L; Maslo, E Iu; Tsybikov, N N

2012-01-01

208

Coal mine dust lung disease. New lessons from old exposure.  

PubMed

Coal mining remains a sizable industry, with millions of working and retired coal miners worldwide. This article provides an update on recent advances in the understanding of respiratory health issues in coal miners and focuses on the spectrum of disease caused by inhalation of coal mine dust, termed coal mine dust lung disease. In addition to the historical interstitial lung diseases (coal worker's pneumoconiosis, silicosis, and mixed dust pneumoconiosis), coal miners are at risk for dust-related diffuse fibrosis and chronic airway diseases, including emphysema and chronic bronchitis. Recent recognition of rapidly progressive pneumoconiosis in younger miners, mainly in the eastern United States, has increased the sense of urgency and the need for vigilance in medical research, clinical diagnosis, and exposure prevention. Given the risk for disease progression even after exposure removal, along with few medical treatment options, there is an important role for chest physicians in the recognition and management of lung disease associated with work in coal mining. PMID:23590267

Petsonk, Edward L; Rose, Cecile; Cohen, Robert

2013-06-01

209

Lung and brainstem cytokine levels are associated with breathing pattern changes in a rodent model of acute lung injury  

Microsoft Academic Search

Acute lung injury evokes a pulmonary inflammatory response and changes in the breathing pattern. The inflammatory response has a centrally mediated component which depends on the vagi. We hypothesize that the central inflammatory response, complimentary to the pulmonary inflammatory response, is expressed in the nuclei tractus solitarii (nTS) and that the expression of cytokines in the nTS is associated with

Frank J. Jacono; Catherine A. Mayer; Yee-Hsee Hsieh; Christopher G. Wilson; Thomas E. Dick

2011-01-01

210

Integrin ?3 mutations with kidney, lung, and skin disease.  

PubMed

Integrin ?(3) is a transmembrane integrin receptor subunit that mediates signals between the cells and their microenvironment. We identified three patients with homozygous mutations in the integrin ?(3) gene that were associated with disrupted basement-membrane structures and compromised barrier functions in kidney, lung, and skin. The patients had a multiorgan disorder that included congenital nephrotic syndrome, interstitial lung disease, and epidermolysis bullosa. The renal and respiratory features predominated, and the lung involvement accounted for the lethal course of the disease. Although skin fragility was mild, it provided clues to the diagnosis. PMID:22512483

Has, Cristina; Spartà, Giuseppina; Kiritsi, Dimitra; Weibel, Lisa; Moeller, Alexander; Vega-Warner, Virginia; Waters, Aoife; He, Yinghong; Anikster, Yair; Esser, Philipp; Straub, Beate K; Hausser, Ingrid; Bockenhauer, Detlef; Dekel, Benjamin; Hildebrandt, Friedhelm; Bruckner-Tuderman, Leena; Laube, Guido F

2012-04-19

211

Dosimetric correlations of acute esophagitis in lung cancer patients treated with radiotherapy  

SciTech Connect

Purpose: To evaluate the factors associated with acute esophagitis in lung cancer patients treated with thoracic radiotherapy. Methods and Materials: We examined 35 patients with non-small-cell lung cancer (n = 27, 77%) and small-cell lung cancer (n = 8, 23%) treated with thoracic radiotherapy between February 2003 and November 2004. The median patient age was 70 years (range, 50-83 years). The disease stage was Stage I in 2 patients (6%), Stage II in 1 (3%), Stage IIIa in 10 (28%), Stage IIIb in 9 (26%), and Stage IV in 9 (26%); 4 patients (11%) had recurrent disease after surgery. A median dose of 60 Gy (range, 50-67 Gy) was given to the isocenter and delivered in single daily fractions of 1.8 or 2 Gy. With heterogeneity corrections, the median given dose to the isocenter was 60.3 Gy (range, 49.9-67.2 Gy). Of the 35 patients, 30 (86%) received concurrent chemotherapy consisting of a platinum agent, cisplatin or carboplatin, combined with paclitaxel in 18 patients (52%), irinotecan hydrochloride in 7 (20%), vincristine sulfate and etoposide in 2 (5%), vinorelbine ditartrate in 1 (3%), etoposide in 1 (3%), and docetaxel in 1 patient (3%). Three of these patients underwent induction therapy with cisplatin and irinotecan hydrochloride, administered before thoracic radiotherapy, and concurrent chemotherapy. Esophageal toxicity was graded according to the Radiation Therapy Oncology Group criteria. The following factors were analyzed with respect to their association with Grade 1 or worse esophagitis by univariate and multivariate analyses: age, gender, concurrent chemotherapy, chemotherapeutic agents, maximal esophageal dose, mean esophageal dose, and percentage of esophageal volume receiving >10 to >65 Gy in 5-Gy increments. Results: Of the 35 patients, 25 (71%) developed acute esophagitis, with Grade 1 in 20 (57%) and Grade 2 in 5 (14%). None of the patients had Grade 3 or worse toxicity. The most significant correlation was between esophagitis and percentage of esophageal volume receiving >35 Gy on univariate (p = 0.002) and multivariate (p = 0.018) analyses. Conclusion: The percentage of esophageal volume receiving >35 Gy was the most statistically significant factor associated with mild acute esophagitis.

Takeda, Ken [Department of Radiology, National Hospital Organization Sendai Medical Center, Sendai (Japan)]. E-mail: takedak41@yahoo.co.jp; Nemoto, Kenji [Department of Radiation Oncology, Tohoku University School of Medicine, Sendai (Japan); Saito, Haruo [Department of Radiology, National Hospital Organization Sendai Medical Center, Sendai (Japan); Ogawa, Yoshihiro [Department of Radiation Oncology, Tohoku University School of Medicine, Sendai (Japan); Takai, Yoshihiro [Department of Radiation Oncology, Tohoku University School of Medicine, Sendai (Japan); Yamada, Shogo [Department of Radiation Oncology, Tohoku University School of Medicine, Sendai (Japan)

2005-07-01

212

Increased T cell glucose uptake reflects acute rejection in lung grafts  

PubMed Central

Although T cells are required for acute lung rejection, other graft-infiltrating cells such as neutrophils accumulate in allografts and are also high glucose utilizers. Positron emission tomography (PET) with the glucose probe [18F]fluorodeoxyglucose ([18F]FDG) has been employed to image solid organ acute rejection, but the sources of glucose utilization remain undefined. Using a mouse model of orthotopic lung transplantation, we analyzed glucose probe uptake in the grafts of syngeneic and allogeneic recipients with or without immunosuppression treatment. Pulmonary microPET scans demonstrated significantly higher [18F]FDG uptake in rejecting allografts when compared to transplanted lungs of either immunosuppressed or syngeneic recipients. [18F]FDG uptake was also markedly attenuated following T cell depletion therapy in lung recipients with ongoing acute rejection. Flow-cytometric analysis using the fluorescent deoxyglucose analog 2-NBDG revealed that T cells, and in particular CD8+ T cells, were the largest glucose utilizers in acutely rejecting lung grafts followed by neutrophils and antigen presenting cells. These data indicate that imaging modalities tailored toward assessing T cell metabolism may be useful in identifying acute rejection in lung recipients PMID:23927673

Chen, Delphine L.; Wang, Xingan; Yamamoto, Sumiharu; Carpenter, Danielle; Engle, Jacquelyn T.; Li, Wenjun; Lin, Xue; Kreisel, Daniel; Krupnick, Alexander S.; Huang, Howard J.; Gelman, Andrew E.

2013-01-01

213

Clinical and prognostic significance of lung thallium uptake on rest imaging in acute myocardial infarction  

SciTech Connect

Exercise-induced pulmonary uptake of thallium-201 in patients with ischemic heart disease is probably due to transient pulmonary edema and left ventricular failure induced by exercise. The significance of increased lung uptake of thallium-201 at rest after acute myocardial infarction (AMI) has not been described. Ninety-six patients admitted with chest pain for suspected AMI or unstable angina underwent thallium-201 imaging at rest. Using conventional diagnostic criteria, 62 had AMI, 12 had unstable angina and 22 had neither. Increased lung uptake of thallium-201 was present in 24 of the total 96 (25%) patients, 20 of the 62 (32%) patients with AMI and 4 of 34 (13%) patients with no evidence of infarction. In the AMI group, those with increased lung thallium-201 uptake had a higher mean +/- standard deviation segmental thallium-201 defect score (22 +/- 7 vs 12 +/- 8, p less than 0.0001), lower ejection fraction (35 +/- 14 vs 49 +/- 14%, p less than 0.002), higher peak creatine kinase levels (2,410 +/- 1,247 vs 1,496 +/- 1,228 IU/liter, p less than 0.01), higher wall motion abnormality score (25 +/- 13 vs 13 +/- 12, p less than 0.0001), increased incidence of clinical in-hospital heart failure (15 of 20 vs 7 of 42, p less than 0.0001) and higher short-term mortality (4 of 20 vs 1 of 42, p less than 0.02) compared to those without increased lung thallium-201 uptake.

Jain, D.; Lahiri, A.; Raftery, E.B. (Northwick Park Hospital, Harrow, Middlesex (England))

1990-01-15

214

Changes in the Bacterial Microbiota in Gut, Blood, and Lungs following Acute LPS Instillation into Mice Lungs  

PubMed Central

Introduction Previous reports have shown that the gastrointestinal (GI) bacterial microbiota can have profound effects on the lungs, which has been described as the “gut-lung axis”. However, whether a “lung-gut” axis exists wherein acute lung inflammation perturbs the gut and blood microbiota is unknown. Methods Adult C57/Bl6 mice were exposed to one dose of LPS or PBS instillation (n?=?3 for each group) directly into lungs. Bacterial microbiota of the bronchoalveolar lavage fluid, blood, and cecum were determined using 454 pyrotag sequencing and quantitative polymerase chain reaction (qPCR) at 4 through 168 hours post-instillation. We then investigated the effects of oral neomycin and streptomycin (n?=?8) on the microbiota at 4 and 24 hours post LPS instillation versus control treatment (n?=?5 at baseline and 4 hours, n?=?7 at 24 hours). Results At 24 hours post LPS instillation, the total bacterial count was significantly increased in the cecum (P<0.05); whereas the total bacterial count in blood was increased at 4, 48, and 72 hours (P<0.05). Antibiotic treatment reduced the total bacteria in blood but not in the cecum. The increase in total bacteria in the blood correlated with Phyllobacteriaceae OTU 40 and was significantly reduced in the blood for both antibiotic groups (P<0.05). Conclusion LPS instillation in lungs leads to acute changes in the bacterial microbiota in the blood and cecum, which can be modulated with antibiotics. PMID:25333938

Sze, Marc A.; Tsuruta, Masashi; Yang, Shun-Wei Julia; Oh, Yeni; Man, S. F. Paul; Hogg, James C.; Sin, Don D.

2014-01-01

215

Effects of acute and chronic administration of methylprednisolone on oxidative stress in rat lungs* **  

PubMed Central

Objective: To determine the effects of acute and chronic administration of methylprednisolone on oxidative stress, as quantified by measuring lipid peroxidation (LPO) and total reactive antioxidant potential (TRAP), in rat lungs. Methods: Forty Wistar rats were divided into four groups: acute treatment, comprising rats receiving a single injection of methylprednisolone (50 mg/kg i.p.); acute control, comprising rats i.p. injected with saline; chronic treatment, comprising rats receiving methylprednisolone in drinking water (6 mg/kg per day for 30 days); and chronic control, comprising rats receiving normal drinking water. Results: The levels of TRAP were significantly higher in the acute treatment group rats than in the acute control rats, suggesting an improvement in the pulmonary defenses of the former. The levels of lung LPO were significantly higher in the chronic treatment group rats than in the chronic control rats, indicating oxidative damage in the lung tissue of the former. Conclusions: Our results suggest that the acute use of corticosteroids is beneficial to lung tissue, whereas their chronic use is not. The chronic use of methylprednisolone appears to increase lung LPO levels. PMID:25029646

Torres, Ronaldo Lopes; Torres, Iraci Lucena da Silva; Laste, Gabriela; Ferreira, Maria Beatriz Cardoso; Cardoso, Paulo Francisco Guerreiro; Bello-Klein, Adriane

2014-01-01

216

Mycobacterium abscessus Lung Disease in a Patient with Kartagener Syndrome  

PubMed Central

Primary ciliary dyskinesia (PCD) is characterized by the congenital impairment of mucociliary clearance. When accompanied by situs inversus, chronic sinusitis and bronchiectasis, PCD is known as Kartagener syndrome. The main consequence of impaired ciliary function is a reduced mucus clearance from the lungs, and susceptibility to chronic respiratory infections due to opportunistic pathogens, including nontuberculous mycobacteria (NTM). There has been no report of NTM lung disease combined with Kartagener syndrome in Korea. Here, we report an adult patient with Kartagener syndrome complicated with Mycobacterium abscessus lung disease. A 37-year-old female presented to our hospital with chronic cough and sputum. She was ultimately diagnosed with M. abscessus lung disease and Kartagener syndrome. M. abscessus was repeatedly isolated from sputum specimens collected from the patient, despite prolonged antibiotic treatment. The patient's condition improved and negative sputum culture conversion was achieved after sequential bilateral pulmonary resection. PMID:25309609

Kim, Jung Hoon; Jun, Ji Eun; Ryu, Duck Hyun; Lee, Ji Eun; Jeong, Ho Jung; Jeong, Suk Hyeon; Kang, Hyung Koo; Kim, Jung Soo; Lee, Hyun; Chon, Hae Ri; Jeon, Kyeongman; Kim, Dohun; Kim, Jhingook; Koh, Won-Jung

2014-01-01

217

The Rabbit as a Model for Studying Lung Disease and Stem Cell Therapy  

PubMed Central

No single animal model can reproduce all of the human features of both acute and chronic lung diseases. However, the rabbit is a reliable model and clinically relevant facsimile of human disease. The similarities between rabbits and humans in terms of airway anatomy and responses to inflammatory mediators highlight the value of this species in the investigation of lung disease pathophysiology and in the development of therapeutic agents. The inflammatory responses shown by the rabbit model, especially in the case of asthma, are comparable with those that occur in humans. The allergic rabbit model has been used extensively in drug screening tests, and this model and humans appear to be sensitive to similar drugs. In addition, recent studies have shown that the rabbit serves as a good platform for cell delivery for the purpose of stem-cell-based therapy. PMID:23653896

Kamaruzaman, Nurfatin Asyikhin; Kamaldin, Nurulain 'Atikah; Latahir, Ahmad Zaeri; Yahaya, Badrul Hisham

2013-01-01

218

Heritability of Lung Disease Severity in Cystic Fibrosis  

PubMed Central

Rationale: Obstructive lung disease, the major cause of mortality in cystic fibrosis (CF), is poorly correlated with mutations in the disease-causing gene, indicating that other factors determine severity of lung disease. Objectives: To quantify the contribution of modifier genes to variation in CF lung disease severity. Methods: Pulmonary function data from patients with CF living with their affected twin or sibling were converted into reference values based on both healthy and CF populations. The best measure of FEV1 within the last year was used for cross-sectional analysis. FEV1 measures collected over at least 4 years were used for longitudinal analysis. Genetic contribution to disease variation (i.e., heritability) was estimated in two ways: by comparing similarity of lung function in monozygous (MZ) twins (? 100% gene sharing) with that of dizygous (DZ) twins/siblings (? 50% gene sharing), and by comparing similarity of lung function measures for related siblings to similarity for all study subjects. Measurements and Main Results: Forty-seven MZ twin pairs, 10 DZ twin pairs, and 231 sibling pairs (of a total of 526 patients) with CF were studied. Correlations for all measures of lung function for MZ twins (0.82–0.91, p < 0.0001) were higher than for DZ twins and siblings (0.50–0.64, p < 0.001). Heritability estimates from both methods were consistent for each measure of lung function and ranged from 0.54 to 1.0. Heritability estimates generally increased after adjustment for differences in nutritional status (measured as body mass index z-score). Conclusions: Our heritability estimates indicate substantial genetic control of variation in CF lung disease severity, independent of CFTR genotype. PMID:17332481

Vanscoy, Lori L.; Blackman, Scott M.; Collaco, Joseph M.; Bowers, Amanda; Lai, Teresa; Naughton, Kathleen; Algire, Marilyn; McWilliams, Rita; Beck, Suzanne; Hoover-Fong, Julie; Hamosh, Ada; Cutler, Dave; Cutting, Garry R.

2007-01-01

219

General anxiety symptoms after acute lung injury: Predictors and correlates  

PubMed Central

Objective Acute lung injury (ALI) is common in the intensive care unit (ICU), typically requiring life support ventilation. Survivors often experience anxiety after hospital discharge. We evaluated general anxiety symptoms 3 months after ALI for: (1) associations with patient characteristics and ICU variables, and (2) cross-sectional associations with physical function and quality of life (QOL). Methods General anxiety was assessed as part of a prospective cohort study recruiting patients from 13 ICUs at four hospitals in Baltimore, MD using the Hospital Anxiety and Depression Scale — Anxiety Subscale (HAD-A), with associations evaluated using multivariable linear and logistic regression models. Results Of 152 patients, 38% had a positive screening test for general anxiety (HAD-A ? 8). Pre-ICU body mass index and psychiatric comorbidity were associated with general anxiety (OR, 95% confidence interval (CI): 1.06 (1.00, 1.13) and 3.59 (1.25, 10.30), respectively). No ICU-related variables were associated with general anxiety. General anxiety was associated with the number of instrumental ADL dependencies (Spearman's rho = 0.22; p = 0.004) and worse overall QOL as measured by EQ-5D visual analog scale (VAS) (rho = ?0.34; p < 0.001) and utility score (rho = ?0.30; p < 0.001), and by the SF-36 mental health domain (rho = ?0.70; p < 0.001) and Mental Component Summary score (rho = ?0.73; p < 0.001). Conclusion Many patients have substantial general anxiety symptoms 3 months after ALI. General anxiety was associated with patient characteristics and impaired physical function and quality of life. Early identification and treatment of general anxiety may enhance physical and emotional function in patients surviving critical illnesses. PMID:23972420

Stevenson, Jennifer E.; Colantuoni, Elizabeth; Bienvenu, O. Joseph; Sricharoenchai, Thiti; Wozniak, Amy; Shanholtz, Carl; Mendez-Tellez, Pedro A.; Needham, Dale M.

2014-01-01

220

Depressive Symptoms and Impaired Physical Function after Acute Lung Injury  

PubMed Central

Rationale: Survivors of acute lung injury (ALI) frequently have substantial depressive symptoms and physical impairment, but the longitudinal epidemiology of these conditions remains unclear. Objectives: To evaluate the 2-year incidence and duration of depressive symptoms and physical impairment after ALI, as well as risk factors for these conditions. Methods: This prospective, longitudinal cohort study recruited patients from 13 intensive care units (ICUs) in four hospitals, with follow-up 3, 6, 12, and 24 months after ALI. The outcomes were Hospital Anxiety and Depression Scale depression score greater than or equal to 8 (“depressive symptoms”) in patients without a history of depression before ALI, and two or more dependencies in instrumental activities of daily living (“impaired physical function”) in patients without baseline impairment. Measurements and Main Results: During 2-year follow-up of 186 ALI survivors, the cumulative incidences of depressive symptoms and impaired physical function were 40 and 66%, respectively, with greatest incidence by 3-month follow-up; modal durations were greater than 21 months for each outcome. Risk factors for incident depressive symptoms were education 12 years or less, baseline disability or unemployment, higher baseline medical comorbidity, and lower blood glucose in the ICU. Risk factors for incident impaired physical function were longer ICU stay and prior depressive symptoms. Conclusions: Incident depressive symptoms and impaired physical function are common and long-lasting during the first 2 years after ALI. Interventions targeting potentially modifiable risk factors (e.g., substantial depressive symptoms in early recovery) should be evaluated to improve ALI survivors’ long-term outcomes. PMID:22161158

Colantuoni, Elizabeth; Mendez-Tellez, Pedro A.; Dinglas, Victor D.; Shanholtz, Carl; Husain, Nadia; Dennison, Cheryl R.; Herridge, Margaret S.; Pronovost, Peter J.; Needham, Dale M.

2012-01-01

221

Animal models of beryllium-induced lung disease.  

PubMed Central

The inhalation Toxicology Research Institute (ITRI) is conducting research to improve the understanding of chronic beryllium disease (CBD) and beryllium-induced lung cancer. Initial animal studies examined beagle dogs that inhaled BeO calcined at either 500 or 1000 degrees C. At similar lung burdens, the 500 degrees C BeO induced more severe and extensive granulomatous pneumonia, lymphocytic infiltration into the lung, and positive Be-specific lymphocyte proliferative responses in vitro than the 1000 degrees C BeO. However, the progressive nature of human CBD was not duplicated. More recently, Strains A/J and C3H/Hej mice were exposed to Be metal by inhalation. This produced a marked granulomatous pneumonia, diffuse infiltrates, and multifocal aggregates of interstitial lymphocytes with a pronounced T helper component and pulmonary in situ lymphocyte proliferation. With respect to lung cancer, at a mean lung burden as low as 17 micrograms Be/g lung, inhaled Be metal induced benign and/or malignant lung tumors in over 50% of male and female F344 rats surviving > or = 1 year on study. Substantial tumor multiplicity was found, but K-ras and p53 gene mutations were virtually absent. In mice, however, a lung burden of approximately 60 micrograms (-300 micrograms Be/g lung) caused only a slight increase in crude lung tumor incidence and multiplicity over controls in strain A/J mice and no elevated incidence in strain C3H mice. Taken together, this research program constitutes a coordinated effort to understand beryllium-induced lung disease in experimental animal models. PMID:8933044

Finch, G L; Hoover, M D; Hahn, F F; Nikula, K J; Belinsky, S A; Haley, P J; Griffith, W C

1996-01-01

222

Animal models of beryllium-induced lung disease  

SciTech Connect

The Inhalation Toxicology Research Institute (ITRI) is conducting research to improve the understanding of chronic beryllium disease (CBD) and beryllium-induced lung cancer. Initial animal studies examined beagle dogs that inhaled BeO calcined at either 500 or 1000{degrees}C. At similar lung burdens, the 500{degrees}C BeO induced more severe and extensive granulomatous pneumonia, lymphocytic infiltration into the lung, and positive Be-specific lymphocyte proliferative responses in vitro than the 1000{degrees}C BeO. However, the progressive nature of human CBD was not duplicated. More recently, Strains A/J and C3H/HeJ mice were exposed to Be metal by inhalation. This produced a marked granulomatous pneumonia, diffuse infiltrates, and multifocal aggregates of interstitial lymphocytes with a pronounced T helper component and pulmonary in situ lymphocyte proliferation. With respect to lung cancer, at a mean lung burden as low as 17 pg Be/g lung, inhaled Be metal induced benign and/or malignant lung tumors in over 50% of male and female F344 rats surviving {ge}1 year on study. Substantial tumor multiplicity was found, but K-ras and p53 gene mutations were virtually absent. In mice, however, a lung burden of approximately 60 {mu}g ({approximately}300 {mu}g Be/g lung) caused only a slight increase in crude lung tumor incidence and multiplicity over controls in strain A/J mice and no elevated incidence in strain C3H mice. Taken together, this research program constitutes a coordinated effort to understand beryllium-induced lung disease in experimental animal models. 47 refs., 1 fig., 3 tabs.

Finch, G.L.; Hoover, M.D.; Hahn, F.F. [Inhalation Toxicology Research Institute, Albuquerque, NM (United States)] [and others

1996-10-01

223

Acute renal dysfunction in liver diseases  

PubMed Central

Renal dysfunction is common in liver diseases, either as part of multiorgan involvement in acute illness or secondary to advanced liver disease. The presence of renal impairment in both groups is a poor prognostic indicator. Renal failure is often multifactorial and can present as pre-renal or intrinsic renal dysfunction. Obstructive or post renal dysfunction only rarely complicates liver disease. Hepatorenal syndrome (HRS) is a unique form of renal failure associated with advanced liver disease or cirrhosis, and is characterized by functional renal impairment without significant changes in renal histology. Irrespective of the type of renal failure, renal hypoperfusion is the central pathogenetic mechanism, due either to reduced perfusion pressure or increased renal vascular resistance. Volume expansion, avoidance of precipitating factors and treatment of underlying liver disease constitute the mainstay of therapy to prevent and reverse renal impairment. Splanchnic vasoconstrictor agents, such as terlipressin, along with volume expansion, and early placement of transjugular intrahepatic portosystemic shunt (TIPS) may be effective in improving renal function in HRS. Continuous renal replacement therapy (CRRT) and molecular absorbent recirculating system (MARS) in selected patients may be life saving while awaiting liver transplantation. PMID:17948928

Betrosian, Alex P; Agarwal, Banwari; Douzinas, Emmanuel E

2007-01-01

224

Use of risk reclassification with multiple biomarkers improves mortality prediction in acute lung injury  

PubMed Central

Objective Multiple single biomarkers have been associated with poor outcomes in acute lung injury; however, no single biomarker has sufficient discriminating power to clearly indicate prognosis. Using both derivation and replication cohorts, we tested novel risk reclassification methods to determine whether measurement of multiple plasma biomarkers at the time of acute lung injury diagnosis would improve mortality prediction in acute lung injury. Design Analysis of plasma biomarker levels and prospectively collected clinical data from patients enrolled in two randomized controlled trials of ventilator therapy for acute lung injury. Setting Intensive care units of university hospitals participating in the National Institutes of Health Acute Respiratory Distress Syndrome Network. Patients Subjects enrolled in a trial of lower tidal volume ventilation (derivation cohort) and subjects enrolled in a trial of higher vs. lower positive end-expiratory pressure (replication cohort). Interventions None. Measurements and Main Results The plasma biomarkers were intercellular adhesion molecule-1, von Willebrand factor, interleukin-8, soluble tumor necrosis factor receptor-1, and surfactant protein-D. In the derivation cohort (n = 547), adding data on these biomarkers to clinical predictors (Acute Physiology and Chronic Health Evaluation III score) at the time of study enrollment improved the accuracy of risk prediction, as reflected by a net reclassification improvement of 22% (95% confidence interval 13% to 32%; p < .001). In the replication cohort (n = 500), the net reclassification improvement was 17% (95% confidence interval 7% to 26%; p < .001). A reduced set of three biomarkers (interleukin-8, soluble tumor necrosis factor receptor-1, and surfactant protein-D) had nearly equivalent prognostic value in both cohorts. Conclusions When combined with clinical data, plasma biomarkers measured at the onset of acute lung injury can improve the accuracy of risk prediction. Combining three or more biomarkers may be useful for selecting a high-risk acute lung injury population for enrollment in clinical trials of novel therapies. PMID:21283009

Calfee, Carolyn S.; Ware, Lorraine B.; Glidden, David V.; Eisner, Mark D.; Parsons, Polly E.; Thompson, B. Taylor; Matthay, Michael A.

2012-01-01

225

The role of leukocytes in the pathogenesis of fibrin deposition in bovine acute lung injury.  

PubMed Central

The peculiarly fibrinous nature of bovine acute lung injury due to infection with Pasteurella haemolytica A1 suggests an imbalance between leukocyte-directed procoagulant and profibrinolytic influences in the inflamed bovine lung. Calves with experimental pneumonia produced by intratracheal inoculation with P. haemolytica A1 developed acute locally extensive cranioventral fibrinopurulent bronchopneumonia. Pulmonary alveolar macrophages (PAM) recovered by segmental lavage from affected lung lobes were 30 times more procoagulant than PAM obtained from unaffected lung lobes and 37-fold more procoagulant than PAM from control calf lungs. Unlike the enhancement of procoagulant activity, profibrinolytic activity (plasminogen activator amidolysis) of total lung leukocytes (PAM and plasminogen activator neutrophils [PMN]) was decreased 23 times in cells obtained from affected lung lobes and also was decreased four times in cells obtained from unaffected lobes of infected animals. This marked imbalance in cellular procoagulant and fibrinolytic activity probably contributes significantly to enhanced fibrin deposition and retarded fibrin removal. In addition, PAM from inflamed lungs were strongly positive for bovine tissue factor antigen as demonstrated by immunocytochemistry. Intensely tissue factor-positive PAM enmeshed in fibrinocellular exudates and positive alveolar walls were situated such that they were likely to have, in concert, initiated extrinsic activation of coagulation in the acutely inflamed lung. These data collectively suggest that enhanced PAM-directed procoagulant activity and diminished PAM- and PMN-directed profibrinolytic activity represent important modifications of local leukocyte function in bovine acute lung injury that are central to the pathogenesis of lesion development with extensive fibrin deposition and retarded fibrin removal. Images Figure 2 Figure 3 PMID:2024707

Car, B. D.; Suyemoto, M. M.; Neilsen, N. R.; Slauson, D. O.

1991-01-01

226

Exercise limitation in interstitial lung disease - mechanisms, significance and therapeutic options.  

PubMed

Exercise limitation is a cardinal feature of the interstitial lung diseases and is frequently associated with marked dyspnoea on exertion. People with interstitial lung disease exhibit a rapid, shallow breathing pattern during exercise that worsens as disease progresses. Despite this, ventilatory mechanics are not the major limitation to exercise in most patients, with impaired gas exchange and circulatory limitation playing a more important role. Peripheral and respiratory muscle dysfunction may also contribute to impaired exercise tolerance, either due to systemic manifestations of the underlying disease, treatment side-effects or deconditioning. Measures of exercise capacity or desaturation obtained from maximal and submaximal exercise tests are good predictors of survival in patients with idiopathic pulmonary fibrosis. However, to date few pharmaceutical treatments have affected exercise outcomes despite improvements in other important clinical markers. Supplemental oxygen acutely improves exercise capacity in interstitial lung disease and is recommended for hypoxic patients, although quality of life or survival benefits have not yet been demonstrated. Exercise training improves walking capacity and dyspnoea in short-term trials and is useful to maximize functional capacity. The role of exercise testing in the routine management of patients with interstitial lung disease is not clearly defined. However, given the poor prognosis in patients with idiopathic pulmonary fibrosis and the marked variation in clinical course, assessment of exercise capacity may provide useful information for both clinicians and patients when evaluating the risks and benefits of new treatments. The extent of resting or exercise-induced hypoxia in patients with interstitial lung disease may influence the selection of an appropriate exercise test, and oxygen administration should be standardized on repeat testing. PMID:20056733

Holland, Anne E

2010-01-01

227

Mondor's disease associated with metastatic lung cancer in the breast.  

PubMed Central

We report what we believe is the first recorded case of Mondor's disease associated with metastatic lung cancer presenting in the breast. An association between Mondor's disease and primary breast cancer has been described previously. In patients with Mondor's disease and primary breast cancer has been described previously. In patients with Mondor's disease the possibility of underlying carcinoma, either primary or secondary, must be considered. Images Figure 1 PMID:2559400

Courtney, S. P.; Polacarz, S.; Raftery, A. T.

1989-01-01

228

[Acute lung injury as a consequence of fresh frozen plasma administration in a patient with factor XII deficiency].  

PubMed

Along with the complete blood count, the coagulation tests are those most demanded before a surgical procedure. The activated partial thromboplastin time (APPT) quantifies the intrinsic and common coagulation pathways, including factors XII, XI, IX, VIII, X, V and II. Factor XII deficiency is associated with a prolonged APPT and an increase in thromboembolic phenomena, without increasing the intraoperative bleeding risk. A 20 year old man with factor XII deficiency was receiving two units of fresh frozen plasma because of an APPT of 100 seconds, with the intention of normalizing it before an urgent surgery procedure, and the fear of intraoperative bleeding. An hour after starting the transfusion the patient developed an acute lung injury (ALI) compatible with the diagnosis of a transfusion related acute lung injury (TRALI). The surgery continued without complications, and the patient was admitted to the resuscitation unit for 72h, needing respiratory support. If the APTT is prolonged in the absence of bleeding, the presence of a non-specific circulating anticoagulant, a deficiency of factor XI, XII and VIII (associated to Von Willebrand disease) must be ruled out. Therefore, in the case presented here, the administration of hemoderivatives was unnecessary and can have consequences as serious as the one that the patient presented, a transfusion related acute lung injury. PMID:24252352

San Juan-Álvarez, M; Sánchez-Zamora, P; de la Flor-Robledo, M

2014-10-01

229

Epithelial Cell Death Is an Important Contributor to Oxidant-mediated Acute Lung Injury  

PubMed Central

Rationale: Acute lung injury and the acute respiratory distress syndrome are characterized by increased lung oxidant stress and apoptotic cell death. The contribution of epithelial cell apoptosis to the development of lung injury is unknown. Objectives: To determine whether oxidant-mediated activation of the intrinsic or extrinsic apoptotic pathway contributes to the development of acute lung injury. Methods: Exposure of tissue-specific or global knockout mice or cells lacking critical components of the apoptotic pathway to hyperoxia, a well-established mouse model of oxidant-induced lung injury, for measurement of cell death, lung injury, and survival. Measurements and Main Results: We found that the overexpression of SOD2 prevents hyperoxia-induced BAX activation and cell death in primary alveolar epithelial cells and prolongs the survival of mice exposed to hyperoxia. The conditional loss of BAX and BAK in the lung epithelium prevented hyperoxia-induced cell death in alveolar epithelial cells, ameliorated hyperoxia-induced lung injury, and prolonged survival in mice. By contrast, Cyclophilin D–deficient mice were not protected from hyperoxia, indicating that opening of the mitochondrial permeability transition pore is dispensable for hyperoxia-induced lung injury. Mice globally deficient in the BH3-only proteins BIM, BID, PUMA, or NOXA, which are proximal upstream regulators of BAX and BAK, were not protected against hyperoxia-induced lung injury suggesting redundancy of these proteins in the activation of BAX or BAK. Conclusions: Mitochondrial oxidant generation initiates BAX- or BAK-dependent alveolar epithelial cell death, which contributes to hyperoxia-induced lung injury. PMID:20959557

Budinger, G. R. Scott; Mutlu, Gokhan M.; Urich, Daniela; Soberanes, Saul; Buccellato, Leonard J.; Hawkins, Keenan; Chiarella, Sergio E.; Radigan, Kathryn A.; Eisenbart, James; Agrawal, Hemant; Berkelhamer, Sara; Hekimi, Siegfried; Zhang, Jianke; Perlman, Harris; Schumacker, Paul T.; Jain, Manu; Chandel, Navdeep S.

2011-01-01

230

Quick-Relief Medications for Lung Diseases  

MedlinePLUS

... swelling and help other asthma medicines work better. Inhaled Steroids An inhaled steroid is typically prescribed as a long-term control medicine. An inhaled steroid will not provide quick relief for acute attacks. ...

231

Airbag lung: an unusual case of sarcoid-like granulomatous lung disease after a rollover motor vehicle accident.  

PubMed

Sarcoid-like granulomatous lung disease (SLGLD) is a condition associated with the formation of noncaseating, nonnecrotizing granulomas. The final by-product of airbag deployment is alkaline silicates or glass. Silicates trapped and sequestered in the lung parenchyma are a potential mediator for immune system activation and development of sarcoid-like granulomatous lung disease. PMID:24974560

Waring, Thomas P; Hegde, Poornima; Foley, Raymond J

2014-05-01

232

Functional Genomics of Chlorine-induced Acute Lung Injury in Mice  

PubMed Central

Acute lung injury can be induced indirectly (e.g., sepsis) or directly (e.g., chlorine inhalation). Because treatment is still limited to supportive measures, mortality remains high (?74,500 deaths/yr). In the past, accidental (railroad derailments) and intentional (Iraq terrorism) chlorine exposures have led to deaths and hospitalizations from acute lung injury. To better understand the molecular events controlling chlorine-induced acute lung injury, we have developed a functional genomics approach using inbred mice strains. Various mouse strains were exposed to chlorine (45 ppm × 24 h) and survival was monitored. The most divergent strains varied by more than threefold in mean survival time, supporting the likelihood of an underlying genetic basis of susceptibility. These divergent strains are excellent models for additional genetic analysis to identify critical candidate genes controlling chlorine-induced acute lung injury. Gene-targeted mice then could be used to test the functional significance of susceptibility candidate genes, which could be valuable in revealing novel insights into the biology of acute lung injury. PMID:20601635

Leikauf, George D; Pope-Varsalona, Hannah; Concel, Vincent J.; Liu, Pengyuan; Bein, Kiflai; Brant, Kelly A.; Dopico, Richard A.; Di, Y. Peter; Jang, An-Soo; Dietsch, Maggie; Medvedovic, Mario; Li, Qian; Vuga, Louis J.; Kaminski, Naftali; You, Ming; Prows, Daniel R.

2010-01-01

233

Asialoerythropoietin ameliorates bleomycin-induced acute lung injury in rabbits by reducing inflammation  

PubMed Central

Acute lung injury, a critical illness characterized by acute respiratory failure with bilateral pulmonary infiltrates, remains unresponsive to current treatments. The condition involves injury to the alveolar capillary barrier, neutrophil accumulation and the induction of proinflammatory cytokines followed by lung fibrosis. In the present study, a rabbit model of bleomycin-induced acute lung injury was established to examine the effects of asialoerythropoietin (AEP), an agent with tissue-protective activities, on pulmonary inflammation. Six Japanese white rabbits were randomly divided into two equal groups. Acute lung injury was induced in all rabbits by intratracheally injecting bleomycin. The control group was injected with bleomycin only; the experimental (AEP) group was injected intravenously with AEP (80 ?g/kg) prior to the bleomycin injection. Computed tomography (CT) studies were performed seven days later. The CT inflammatory scores of areas exhibiting abnormal density and the pathological inflammatory scores were recorded as a ratio on a 7×7 mm grid. The CT and pathological inflammatory scores were significantly different between the control and AEP groups [122±10 and 16.3±1.5 (controls) vs. 71±8.5 and 9.7±1.4 (AEP), respectively; P<0.01]. Thus, the present study revealed that AEP prevents bleomycin-induced acute lung injury in rabbits. PMID:25289037

SONODA, AKINAGA; NITTA, NORIHISA; TSUCHIYA, KEIKO; OTANI, HIDEJI; WATANABE, SHOBU; MUKAISHO, KENICHI; TOMOZAWA, YUKI; NAGATANI, YUKIHIRO; OHTA, SHINICHI; TAKAHASHI, MASASHI; MURATA, KIYOSHI

2014-01-01

234

Systems biology approaches to identify developmental bases for lung diseases  

PubMed Central

A greater understanding of the regulatory processes contributing to lung development could be helpful to identify strategies to ameliorate morbidity and mortality in premature infants and to identify individuals at risk for congenital and/or chronic lung diseases. Over the past decade, genomics technologies have enabled the production of rich gene expression databases providing information for all genes across developmental time or in diseased tissue. These data sets facilitate systems biology approaches for identifying underlying biological modules and programs contributing to the complex processes of normal development, and those that may be associated with disease states. The next decade will undoubtedly see rapid and significant advances in redefining both lung development and disease at the systems level. PMID:23314295

Bhattacharya, Soumyaroop; Mariani, Thomas J.

2013-01-01

235

Characterization of Lung's Emphysema Distribution: Numerical Assessment of Disease Development  

E-print Network

, Egypt. Abstract--Chronic Obstructive Pulmonary Disease (COPD) refers to a group of lung diseases are the two main conditions that make up COPD, but COPD can also refer to damage caused by chronic asthmatic- Digital image treatments, air density distribution and emphysema characterizations. I. INTRODUCTION

Paris-Sud XI, Université de

236

Physical Therapy for Children with Chronic Lung Disease  

Microsoft Academic Search

Chronic lung disease is a major health problem among children. Estimates suggest that one child in six has a chronic respiratory condition. This article reviews three common chronic respiratory conditions occurring in childhood for which physical therapy is usually recommended. The cause, pathophysiology, and medical treatment are explained for asthma, respiratory complications of chronic neuromuscular disease, and cystic fibrosis. The

JAN STEPHEN TECKLIN

237

Lung Cancer Diseases Diagnostic Asistance Using Gray Color Analysis  

Microsoft Academic Search

Errors in diagnosing the disease is a critical risk that must be faced by any person giving treatment to the hospital. Medical treatment can not always be done with perfect accuracy. Lung cancer is one of the most deadly disease that prone to misdiagnose. In general, some practitioners tend to “read” cancer in x-ray rontgen image as tumor this could

P. Paulus; F. L. Gaol

2010-01-01

238

Angiogenesis in the pathogenesis of inflammatory joint and lung diseases  

Microsoft Academic Search

This paper reviews hypotheses about roles of angiogenesis in the pathogenesis of inflammatory disease in two organs, the synovial joint and the lung. Neovascularisation is a fundamental process for growth and tissue repair after injury. Nevertheless, it may contribute to a variety of chronic inflammatory diseases, including rheumatoid arthritis, osteoarthritis, asthma, and pulmonary fibrosis. Inflammation can promote angiogenesis, and new

David A Walsh; Claire I Pearson

2001-01-01

239

Acute admissions of patients with sickle cell disease who live in Britain.  

PubMed Central

All acute admissions of patients with sickle cell disease who lived in the London borough of Brent and attended this hospital were analysed for a period of one year. Sixty three of the 211 patients who were followed up by the haematology department required 161 acute admissions during the year. Most admissions (126) were for the 42 patients with homozygous sickle cell disease; 147 (91%) were for vaso-occlusive episodes, 142 of which were for painful crises, three for cerebrovascular accidents, and two for renal papillary necrosis. Preschool children with sickle cell disease were admitted predominantly with limb pain, whereas in schoolchildren and adults the incidence of trunk pain was higher. Twenty four of the 93 episodes of trunk pain culminated in an episode of severe visceral sequestration usually affecting the lungs, the liver, or the mesenteric circulation. Two patients died: an 18 month old baby with an acute splenic sequestration crisis and a 19 year old man with a severe girdle syndrome (sickling in the mesenteric circulation, liver, and lungs). Infective episodes were rare (11 episodes) but severe: one haemophilus meningitis, two salmonella infections, and three aplastic crises due to parvovirus infections. The average duration of the hospital stay was 7.4 days per admission. It is concluded that because sickle cell disease causes appreciable morbidity in older children, adolescents, and adults a systematic approach to management is needed to deal with acute episodes such as sequestration syndromes. PMID:3109583

Brozovic, M; Davies, S C; Brownell, A I

1987-01-01

240

Lung function measurement in prematurely born preschool children with and without chronic lung disease  

Microsoft Academic Search

Objective:Prematurely born infants often have recurrent wheeze and long-term respiratory morbidity at follow-up. Assessment of airways obstruction in preschool children is feasible using the interrupter resistance (Rint) but has rarely been examined in preterm children with and without chronic lung disease (CLD). The objective of this study was to determine lung function measured by the interrupter technique, its feasibility in

V R Kairamkonda; J Richardson; N Subhedar; P D Bridge; N J Shaw

2008-01-01

241

Human umbilical cord mesenchymal stem cells reduce systemic inflammation and attenuate LPS-induced acute lung injury in rats  

PubMed Central

Background Mesenchymal stem cells (MSCs) possess potent immunomodulatory properties and simultaneously lack the ability to illicit immune responses. Hence, MSCs have emerged as a promising candidate for cellular therapeutics for inflammatory diseases. Within the context of this study, we investigated whether human umbilical cord-derived mesenchymal stem cells (UC-MSCs) could ameliorate lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in a rat model. Methods ALI was induced via injection of LPS. Rats were divided into three groups: (1) saline group(control), (2) LPS group, and (3) MSC + LPS group. The rats were sacrificed at 6, 24, and 48 hours after injection. Serum, bronchoalveolar lavage fluid (BALF), and lungs were collected for cytokine concentration measurements, assessment of lung injury, and histology. Results UC-MSCs increased survival rate and suppressed LPS-induced increase of serum concentrations of pro-inflammatory mediators TNF-?, IL-1?, and IL-6 without decreasing the level of anti-inflammatory cytokine IL-10. The MSC + LPS group exhibited significant improvements in lung inflammation, injury, edema, lung wet/dry ratio, protein concentration, and neutrophil counts in the BALF, as well as improved myeloperoxidase (MPO) activity in the lung tissue. Furthermore, UC-MSCs decreased malondialdehyde (MDA) production and increased Heme Oxygenase-1 (HO-1) protein production and activity in the lung tissue. Conclusion UC-MSCs noticeably increased the survival rate of rats suffering from LPS-induced lung injury and significantly reduced systemic and pulmonary inflammation. Promoting anti-inflammatory homeostasis and reducing oxidative stress might be the therapeutic basis of UC-MSCs. PMID:22974286

2012-01-01

242

Human CD56+ Cytotoxic Lung Lymphocytes Kill Autologous Lung Cells in Chronic Obstructive Pulmonary Disease  

PubMed Central

CD56+ natural killer (NK) and CD56+ T cells, from sputum or bronchoalveolar lavage of subjects with chronic obstructive pulmonary disease (COPD) are more cytotoxic to highly susceptible NK targets than those from control subjects. Whether the same is true in lung parenchyma, and if NK activity actually contributes to emphysema progression are unknown. To address these questions, we performed two types of experiments on lung tissue from clinically-indicated resections (n?=?60). First, we used flow cytometry on fresh single-cell suspension to measure expression of cell-surface molecules (CD56, CD16, CD8, NKG2D and NKp44) on lung lymphocytes and of the 6D4 epitope common to MICA and MICB on lung epithelial (CD326+) cells. Second, we sequentially isolated CD56+, CD8+ and CD4+ lung lymphocytes, co-cultured each with autologous lung target cells, then determined apoptosis of individual target cells using Annexin-V and 7-AAD staining. Lung NK cells (CD56+ CD3?) and CD56+ T cells (CD56+ CD3+) were present in a range of frequencies that did not differ significantly between smokers without COPD and subjects with COPD. Lung NK cells had a predominantly “cytotoxic” CD56+ CD16+ phenotype; their co-expression of CD8 was common, but the percentage expressing CD8 fell as FEV1 % predicted decreased. Greater expression by autologous lung epithelial cells of the NKG2D ligands, MICA/MICB, but not expression by lung CD56+ cells of the activating receptor NKG2D, correlated inversely with FEV1 % predicted. Lung CD56+ lymphocytes, but not CD4+ or CD8+ conventional lung T cells, rapidly killed autologous lung cells without additional stimulation. Such natural cytotoxicity was increased in subjects with severe COPD and was unexplained in multiple regression analysis by age or cancer as indication for surgery. These data show that as spirometry worsens in COPD, CD56+ lung lymphocytes exhibit spontaneous cytotoxicity of autologous structural lung cells, supporting their potential role in emphysema progression. Trial Registration ClinicalTrials.gov NCT00281229 PMID:25078269

Freeman, Christine M.; Stolberg, Valerie R.; Crudgington, Sean; Martinez, Fernando J.; Han, MeiLan K.; Chensue, Stephen W.; Arenberg, Douglas A.; Meldrum, Catherine A.; McCloskey, Lisa; Curtis, Jeffrey L.

2014-01-01

243

Acute Lung Injury Complicating Blood Transfusion in Post-Partum Hemorrhage: Incidence and Risk Factors  

PubMed Central

Background We retrospectively investigated the incidence and risk factors for transfusion-related acute lung injury (TRALI) among patients transfused for post-partum hemorrhage (PPH). Methods We identified a series of 71 consecutive patients with PPH requiring the urgent transfusion of three or more red blood cell (RBC) units, with or without transfusion of fresh frozen plasma (FFP) and/or platelets (PLT). Clinical records were then retrieved and examined for respiratory distress events. According to the 2004 consensus definition, cases of new-onset hypoxemia, within 6 hours after transfusion, with bilateral pulmonary changes, in the absence of cardiogenic pulmonary edema were identified as TRALI. If an alternative risk factor for acute lung injury was present, possible TRALI was diagnosed. Results Thirteen cases of TRALI and 1 case of possible TRALI were identified (overall incidence 19.7%). At univariate analysis, patients with TRALI received higher number of RBC, PLT and FFP units and had a longer postpartum hospitalization. Among the diseases occurring in pregnancy- and various pre-existing comorbidities, only gestational hypertension and pre-eclampsia, significantly increased the risk to develop TRALI (p = 0.006). At multivariate analysis including both transfusion- and patient-related risk factors, pregnancy-related, hypertensive disorders were confirmed to be the only predictors for TRALI, with an odds ratio of 27.7 ( 95% CI 1.27–604.3, p=0.034). Conclusions Patients suffering from PPH represent a high-risk population for TRALI. The patients with gestational hypertension and pre-eclampsia, not receiving anti-hypertensive therapy, have the highest risk. Therefore, a careful monitoring of these patients after transfusions is recommended. PMID:25408855

Teofili, Luciana; Bianchi, Maria; Zanfini, Bruno A.; Catarci, Stefano; Sicuranza, Rossella; Spartano, Serena; Zini, Gina; Draisci, Gaetano

2014-01-01

244

Dual Oxidase 2 in Lung Epithelia Is Essential for Hyperoxia-Induced Acute Lung Injury in Mice  

PubMed Central

Abstract Aims: Acute lung injury (ALI) induced by excessive hyperoxia has been employed as a model of oxidative stress imitating acute respiratory distress syndrome. Under hyperoxic conditions, overloading quantities of reactive oxygen species (ROS) are generated in both lung epithelial and endothelial cells, leading to ALI. Some NADPH oxidase (NOX) family enzymes are responsible for hyperoxia-induced ROS generation in lung epithelial and endothelial cells. However, the molecular mechanisms of ROS production in type II alveolar epithelial cells (AECs) and ALI induced by hyperoxia are poorly understood. Results: In this study, we show that dual oxidase 2 (DUOX2) is a key NOX enzyme that affects hyperoxia-induced ROS production, particularly in type II AECs, leading to lung injury. In DUOX2 mutant mice (DUOX2thyd/thyd) or mice in which DUOX2 expression is knocked down in the lungs, hyperoxia-induced ALI was significantly lower than in wild-type (WT) mice. DUOX2 was mainly expressed in type II AECs, but not endothelial cells, and hyperoxia-induced ROS production was markedly reduced in primary type II AECs isolated from DUOX2thyd/thyd mice. Furthermore, DUOX2-generated ROS are responsible for caspase-mediated cell death, inducing ERK and JNK phophorylation in type II AECs. Innovation: To date, no role for DUOX2 has been defined in hyperoxia-mediated ALI despite it being a NOX homologue and major ROS source in lung epithelium. Conclusion: Here, we present the novel finding that DUOX2-generated ROS induce AEC death, leading to hyperoxia-induced lung injury. Antioxid. Redox Signal. 21, 1803–1818. PMID:24766345

Kim, Min-Ji; Ryu, Jae-Chan; Kwon, Younghee; Lee, Suhee; Bae, Yun Soo; Yoon, Joo-Heon

2014-01-01

245

Inhaled aerosolized insulin ameliorates hyperglycemia-induced inflammatory responses in the lungs in an experimental model of acute lung injury  

PubMed Central

Introduction Previous studies have shown that patients with diabetes mellitus appear to have a lower prevalence of acute lung injury. We assumed that insulin prescribed to patients with diabetes has an anti-inflammatory property and pulmonary administration of insulin might exert beneficial effects much more than intravenous administration. Methods Twenty-eight mechanically ventilated rabbits underwent lung injury by saline lavage, and then the animals were allocated into a normoglycemia group (NG), a hyperglycemia group (HG), an HG treated with intravenous insulin (HG-VI) group or an HG treated with aerosolized insulin (HG-AI) group with continuous infusion of different fluid solutions and treatments: normal saline, 50% glucose, 50% glucose with intravenous insulin, or 50% glucose with inhaled aerosolized insulin, respectively. After four hours of treatment, the lungs and heart were excised en bloc, and then high-mobility group B1 concentration in bronchoalveolar lavage fluid, interleukin-8 and toll-like receptor 4 mRNA expression in bronchoalveolar lavage fluid cells, and lung myeloperoxidase activity were measured. Results Treatment with both aerosolized insulin and intravenous insulin attenuated toll-like receptor 4 mRNA expressions in the bronchoalveolar lavage fluid cells. Interleukin-8 and toll-like receptor 4 mRNA expression was significantly lower in the HG-AI group than in the HG-IV group. The lung myeloperoxidase activity in the normal healthy group showed significantly lower levels compared to the NG group but not different compared to those of the HG, HG-VI and HG-AI groups. Conclusions The results suggest that insulin attenuates inflammatory responses in the lungs augmented by hyperglycemia in acute lung injury and the insulin's efficacy may be better when administered by aerosol. PMID:23622115

2013-01-01

246

CT of chronic infiltrative lung disease: Prevalence of mediastinal lymphadenopathy  

SciTech Connect

Our goal was to determine the prevalence of mediastinal lymph node enlargement at CT in patients with diffuse infiltrative lung disease. The study was retrospective and included 175 consecutive patients with diffuse infiltrative lung diseases. Diagnoses included idiopathic pulmonary fibrosis (IPF) (n = 61), usual interstitial pneumonia associated with collagen vascular disease (CVD) (n = 20), idiopathic bronchiolitis obliterans organizing pneumonia (BOOP) (n = 22), extrinsic allergic alveolitis (EAA) (n = 17), and sarcoidosis (n = 55). Fifty-eight age-matched patients with CT of the chest performed for unrelated conditions served as controls. The presence, number, and sites of enlarged nodes (short axis {ge}10 mm in diameter) were recorded. Enlarged mediastinal nodes were present in 118 of 175 patients (67%) with infiltrative lung disease and 3 of 58 controls (5%) (p < 0.001). The prevalence of enlarged nodes was 84% (46 of 55) in sarcoidosis, 67% (41 of 61) in IPF, 70% (14 of 20) in CVD, 53% (9 of 17) in EAA, and 36% (8 of 22) in BOOP. The mean number of enlarged nodes was higher in sarcoidosis (mean 3.2) than in the other infiltrative diseases (mean 1.2) (p < 0.001). Enlarged nodes were most commonly present in station 10R, followed by 7, 4R, and 5. Patients with infiltrative lung disease frequently have enlarged mediastinal lymph nodes. However, in diseases other than sarcoid, usually only one or two nodes are enlarged and their maximal short axis diameter is <15 mm. 11 refs., 2 figs., 1 tab.

Niimi, Hiroshi; Kang, Eun-Young; Kwong, S. [Univ. of British Columbia and Vancouver Hospital and Health Sciences Centre (Canada)] [and others] [Univ. of British Columbia and Vancouver Hospital and Health Sciences Centre (Canada); and others

1996-03-01

247

Fatal Acute Chagas Disease in a Chimpanzee  

PubMed Central

Background Chagas disease (CD) or American trypanosomiasis is caused by a hemoflagellate protozoan, Trypanosoma cruzi (TC). This organism has been isolated from more than 100 mammalian species and several insect vectors demonstrating a wide host distribution and low host specificity. Methods A 23 year old male chimpanzee died acutely and a complete necropsy was performed to evaluate gross and microscopic pathologic changes. After observation of trypanosomal amastigotes in the myocardium, PCR and immunohistochemistry was employed to confirm the diagnosis of TC. Results Gross findings were consistent with mild congestive heart failure. Microscopic findings included multifocal myocardial necrosis associated with severe lymphocytic to mixed inflammatory infiltrates, edema, and mild chronic interstitial fibrosis. Multifocal intracytoplasmic amastigotes morphologically consistent with TC were observed in cardiac myofibers. TC was confirmed by PCR and immunohistochemistry. Conclusion We report, to the best of our knowledge, the first fatal spontaneous case of TC infection in a chimpanzee. PMID:19281482

Bommineni, Yugendar R.; Dick, Edward J.; Estep, J. Scot; Van de Berg, John L.; Hubbard, Gene B.

2009-01-01

248

A Case of Sarcoidosis with Interstitial Lung Disease Mimicking Clinically Amyopathic Dermatomyositis and Rapidly Progressive Interstitial Lung Disease  

PubMed Central

Here, we report a patient with sarcoidosis who developed edematous erythema and interstitial lung disease. At the initial visit, clinically amyopathic dermatomyositis (CADM) with rapidly progressive interstitial lung disease (RP-ILD) was suspected because he had progressive dyspnea but no muscle weakness. The presence of anti-CADM-140/MDA5 autoantibodies was immediately assessed to facilitate a precise diagnosis, with negative results. Thereafter, skin and transbronchial lung biopsies revealed noncaseating granuloma with Langhans giant cells in both specimens, leading to a diagnosis of sarcoidosis. In this case, clinical features of skin and lung were unable to distinguish DM (including CADM) from sarcoidosis, but the lack of anti-CADM-140/MDA5 antibody was useful for differentiating CADM with RP-ILD mimicking sarcoidosis from bona fide sarcoidosis.

Nogi, Shinichi; Sasaki, Noriko; Chinen, Naofumi; Honda, Kiri; Saito, Eiko; Wakabayashi, Takayuki; Yamada, Chiho; Suzuki, Yasuo

2014-01-01

249

Toll-like receptor 4 implicated in acute lung injury induced by paraquat poisoning in mice  

PubMed Central

Objective: To investigate the possible relationship and mechanism of Toll-like receptor 4 (TLR4) and acute lung injury induced by paraquat (PQ) poisoning. Methods: Male wild type mice and male TLR4-knockout mice were used in this study. After paraquat treatment for 24 hours, mice were euthanized and pathology, TLR4 expression and pro-inflammatory cytokines were evaluated. Results: Wild type mice showed deteriorated lung injury, pathological damages and increased TLR4 expression and pulmonary TNF-?, IL-1? and NF-?B p65 levels after PQ treatment. TLR4-deficient mice were significantly resistant to paraquat-induced lung injury. Conclusion: TLR4 may be required as a mediator and may play an important role in acute lung injury induced by paraquat.

Liu, Wei; Shan, Li-Ping; Dong, Xue-Song; Liu, Zhi

2014-01-01

250

What Are the Signs and Symptoms of Asbestos-Related Lung Diseases?  

MedlinePLUS

... and coughing up blood. Other symptoms of lung cancer include frequent lung infections, fatigue (tiredness), and weight loss without a known ... Lung Diseases Clinical Trials Clinical trials are research ...

251

Airway pressure release ventilation in morbidly obese surgical patients with acute lung injury and acute respiratory distress syndrome.  

PubMed

Morbidly obese patients with body mass index greater than 40 kg/m(2) and respiratory failure requiring critical care services are increasingly seen in trauma and acute care surgical centers. Baseline respiratory pathophysiology including decreased pulmonary compliance with dependent atelectasis and abnormal ventilation-perfusion relationships predisposes these patients to acute lung injury (ALI) and adult respiratory distress syndrome (ARDS) as well as prolonged stays in the intensive care unit. Airway pressure release ventilation (APRV) is an increasingly used alternative mode for salvage therapy in patients with hypoxemic respiratory failure that also provides lung protection from ventilator-induced lung injury. APRV provides the conceptual advantage of an "open lung" approach to ventilation that may be extended to the morbidly obese patient population with ALI and ARDS. We discuss the theoretical benefits and a recent clinical experience of APRV ventilation in the morbidly obese patient with respiratory failure at a Level I trauma, surgical critical care, and acute care surgery center. PMID:23461947

Testerman, George M; Breitman, Igal; Hensley, Sarah

2013-03-01

252

Acute lung injury isolated to an in situ lung preparation causes sustained reflex cardiovascular depression in dogs.  

PubMed

We tested the hypothesis that acute lung injury (ALI) isolated to a perfused in situ left lung preparation results in sustained reflex cardiovascular depression. Phorbol myristate acetate (PMA), an agent that activates neutrophils, administered into the isolated lung preparation of chloralose-anesthetized dogs resulted in ALI, as assessed by wet-to-dry weight ratios and histopathology, and significant decreases in heart rate (43%), mean arterial pressure (27%), aortic blood flow (29%) and maximum rate of change in left ventricular pressure (30%). Significant reflex effects occurred by 20 min after PMA administration and were sustained for 40 min (n = 7). Hemodynamic variables recovered when the left lung was denervated 60 min after PMA administration. Indomethacin administered into the isolated circulation before PMA (n = 5) did not significantly influence the ALI or reflex effects. Systemic atropinization (n = 6) prevented only the bradycardia. Left lung denervation before ALI (n = 3) prevented all reflex effects. We conclude that PMA administration into an isolated in situ lung preparation results in ALI and sustained reflex cardiovascular depression that is most likely elicited by pulmonary C-fiber stimulation and mediated by withdrawal of sympathetic efferent nerve activity. PMID:7836209

Allen, D A; Schertel, E R; Weisbrode, S E; Myerowitz, P D

1994-10-01

253

Titanium Dioxide Exposure Induces Acute Eosinophilic Lung Inflammation in Rabbits  

PubMed Central

Titanium dioxide (TiO2) is increasingly widely used in industrial, commercial and home products. TiO2 aggravates respiratory symptoms by induction of pulmonary inflammation although the mechanisms have not been well investigated. We aimed to investigate lung inflammation in rabbits after intratracheal instillation of P25 TiO2. One ml of 10, 50 and 250 µg of P25 TiO2 was instilled into one of the lungs of rabbits, chest computed-tomography was performed, and bronchoalveolar lavage (BAL) fluid was collected before, at 1 and 24 h after P25 TiO2 exposure. Changes in inflammatory cells in the BAL fluids were measured. Lung pathological assay was also carried out at 24 h after P25 TiO2 exposure. Ground glass opacities were noted in both lungs 1 h after P25 TiO2 and saline (control) instillation. Although the control lung showed complete resolution at 24 h, the lung exposed to P25 TiO2 showed persistent ground glass opacities at 24 h. The eosinophil counts in BAL fluid were significantly increased after P25 TiO2 exposure. P25 TiO2 induced a dose dependent increase of eosinophils in BAL fluid but no significant differences in neutrophil and lymphocyte cell counts were detected. The present findings suggest that P25 TiO2 induces lung inflammation in rabbits which is associated with eosinophilic inflammation. PMID:24705802

CHOI, Gil Soon; OAK, Chulho; CHUN, Bong-Kwon; WILSON, Donald; JANG, Tae Won; KIM, Hee-Kyoo; JUNG, Mannhong; TUTKUN, Engin; PARK, Eun-Kee

2014-01-01

254

Pattern of inspiratory gas delivery affects CO 2 elimination in health and after acute lung injury  

Microsoft Academic Search

Objective  To avoid ventilator induced lung injury, tidal volume should be low in acute lung injury (ALI). Reducing dead space may be\\u000a useful, for example by using a pattern of inspiration that prolongs the time available for gas distribution and diffusion\\u000a within the respiratory zone, the mean distribution time (MDT). A study was conducted to investigate how MDT affects CO2 elimination in pigs

Elisabet Åström; Leif Uttman; Lisbet Niklason; Jerome Aboab; Laurent Brochard; Björn Jonson

2008-01-01

255

Transfusion related acute lung injury with massive pulmonary secretion during cardiac surgery. A case report  

PubMed Central

A Indo-Caribbean patient undergoing cardiac surgery developed Transfusion Related Acute Lung Injury (TRALI) with massive endobronchial secretion of clear fluid mimicking severe pulmonary edema. Hypoxemia and lung stiffness were so severe that didn’t allow closure of the sternum on completion of surgery. The patient was treated with invasive ventilation, high positive pressure and % FiO2 and aggressive endotracheal suction. After several hours, secretions reduced spontaneously and the patient made an uneventful recovery. PMID:24694086

2014-01-01

256

Acute Lung Injury-Induced Collagen Deposition is Associated with Elevated Asymmetric Dimethylarginine and Arginase Activity  

PubMed Central

Evidence suggests that lung structure and function is partly maintained by a balance between the competing arginine-metabolizing enzymes arginase and nitric oxide synthase. Asymmetric dimethylarginine is an endogenous inhibitor of nitric oxide synthase. It is metabolized by dimethylarginine dimethylaminohydrolase-2, which is oxidant-sensitive. The mechanism that induces excess lung collagen deposition in burned patients has not yet been explored. Our objective is to investigate the role of asymmetric dimethylarginine and the arginase pathway in acute lung injury. An ovine model for burn and smoke inhalation injury was used to assess excess lung collagen deposition. Sheep were deeply anesthetized during the injury, mechanically ventilated, resuscitated with fluid, and sacrificed after either 2 or 3 weeks. Lungs were assessed histologically and biochemically for collagen content, arginase activity, lipid peroxidation product and antioxidant concentration, and protein concentrations. Plasma was assessed for amino acid and nitrate/nitrite concentrations. Burn and inhalation injury resulted in significantly reduced pulmonary function and increased lung collagen deposition. These physiological changes were associated with significantly increased lung arginase activity, collagen synthesis precursor ornithine aminotransferase, and ornithine decarboxylase, which is associated with cell proliferation. Significant decreases in plasma nitrate/nitrite after injury were associated with increased lung asymmetric dimethylarginine concentrations and decreased dimethylarginine dimethylaminohydrolase-2 expression. The decreased dimethylarginine dimethylaminohydrolase-2 expression was associated with significantly increased lipid peroxidation product and decreased antioxidant content in the lung. This data supports that excess lung collagen deposition and reduced pulmonary function in acute lung injury following burn and inhalation injury is mediated through the arginase pathway. PMID:20938379

Sousse, Linda E.; Yamamoto, Yusuke; Enkhbaatar, Perenlei; Rehberg, Sebastian W.; Wells, Sandra M.; Leonard, Scott; Traber, Maret G.; Yu, Yong-Ming; Cox, Robert A.; Hawkins, Hal K.; Traber, Lillian D.; Herndon, David N.; Traber, Daniel L.

2011-01-01

257

Treatment for sulfur mustard lung injuries; new therapeutic approaches from acute to chronic phase  

PubMed Central

Objective Sulfur mustard (SM) is one of the major potent chemical warfare and attractive weapons for terrorists. It has caused deaths to hundreds of thousands of victims in World War I and more recently during the Iran-Iraq war (1980–1988). It has ability to develop severe acute and chronic damage to the respiratory tract, eyes and skin. Understanding the acute and chronic biologic consequences of SM exposure may be quite essential for developing efficient prophylactic/therapeutic measures. One of the systems majorly affected by SM is the respiratory tract that numerous clinical studies have detailed processes of injury, diagnosis and treatments of lung. The low mortality rate has been contributed to high prevalence of victims and high lifetime morbidity burden. However, there are no curative modalities available in such patients. In this review, we collected and discussed the related articles on the preventive and therapeutic approaches to SM-induced respiratory injury and summarized what is currently known about the management and therapeutic strategies of acute and long-term consequences of SM lung injuries. Method This review was done by reviewing all papers found by searching following key words sulfur mustard; lung; chronic; acute; COPD; treatment. Results Mustard lung has an ongoing pathological process and is active disorder even years after exposure to SM. Different drug classes have been studied, nevertheless there are no curative modalities for mustard lung. Conclusion Complementary studies on one hand regarding pharmacokinetic of drugs and molecular investigations are mandatory to obtain more effective treatments. PMID:23351279

2012-01-01

258

Mitogen-activated Protein Kinase Kinase Kinase 1 Protects against Nickel-induced Acute Lung Injury  

PubMed Central

Nickel compounds are environmental and occupational hazards that pose serious health problems and are causative factors of acute lung injury. The c-jun N-terminal kinases (JNKs) are regulated through a mitogen-activated protein (MAP) 3 kinase-MAP2 kinase cascade and have been implicated in nickel toxicity. In this study, we used genetically modified cells and mice to investigate the involvement of two upstream MAP3Ks, MAP3K1 and 2, in nickel-induced JNK activation and acute lung injury. In mouse embryonic fibroblasts, levels of JNK activation and cytotoxicity induced by nickel were similar in the Map3k2-null and wild-type cells but were much lower in the Map3k1/Map3k2 double-null cells. Conversely, the levels of JNK activation and cytotoxicity were unexpectedly much higher in the Map3k1-null cells. In adult mouse tissue, MAP3K1 was widely distributed but was abundantly expressed in the bronchiole epithelium of the lung. Accordingly, MAP3K1 ablation in mice resulted in severe nickel-induced acute lung injury and reduced survival. Based on these findings, we propose a role for MAP3K1 in reducing JNK activation and protecting the mice from nickel-induced acute lung injury. PMID:18467339

Mongan, Maureen; Tan, Zongqing; Chen, Liang; Peng, Zhimin; Dietsch, Maggie; Su, Bing; Leikauf, George; Xia, Ying

2008-01-01

259

Lung Disease Including Asthma and Adult Vaccination  

MedlinePLUS

... and have not gotten this vaccine or have immunity to these diseases Varicella vaccine to protect against ... gotten two doses of this vaccine or have immunity to this disease Learn about adult vaccination and ...

260

Supplementation of parenteral nutrition with fish oil attenuates acute lung injury in a rat model  

PubMed Central

Fish oil rich in n-3 polyunsaturated fatty acids has diverse immunomodulatory properties and attenuates acute lung injury when administered in enternal nutrition. However, enteral nutrition is not always feasible. Therefore, we investigated the ability of parenteral nutrition supplemented with fish oil to ameliorate acute lung injury. Rats were infused with parenteral nutrition solutions (without lipids, with soybean oil, or with soybean oil and fish oil) for three days. Lipopolysaccharide (15 mg/kg) was then administered intratracheally to induce acute lung injury, characterized by impaired lung function, polymorphonuclear leukocyte recruitment, parenchymal tissue damage, and upregulation of mRNAs for inflammatory mediators. Administration of parenteral nutrition supplemented with fish oil prior to lung insult improved gas exchange and inhibited neutrophil recruitment and upregulation of mRNAs for inflammatory mediators. Parenteral nutrition supplemented with fish oil also prolonged survival. To investigate the underlying mechanisms, leukotriene B4 and leukotriene B5 secretion was measured in neutrophils from the peritoneal cavity. The neutrophils from rats treated with fish oil-rich parenteral nutrition released significantly more leukotriene B5, an anti-inflammatory eicosanoid, than neutrophils isolated from rats given standard parenteral nutrition. Parenteral nutrition with fish oil significantly reduced lipopolysaccharide-induced lung injury in rats in part by promoting the synthesis of anti-inflammatory eicosanoids. PMID:24688221

Kohama, Keisuke; Nakao, Atsunori; Terashima, Mariko; Aoyama-Ishikawa, Michiko; Shimizu, Takayuki; Harada, Daisuke; Nakayama, Mitsuo; Yamashita, Hayato; Fujiwara, Mayu; Kotani, Joji

2014-01-01

261

Supplementation of parenteral nutrition with fish oil attenuates acute lung injury in a rat model.  

PubMed

Fish oil rich in n-3 polyunsaturated fatty acids has diverse immunomodulatory properties and attenuates acute lung injury when administered in enternal nutrition. However, enteral nutrition is not always feasible. Therefore, we investigated the ability of parenteral nutrition supplemented with fish oil to ameliorate acute lung injury. Rats were infused with parenteral nutrition solutions (without lipids, with soybean oil, or with soybean oil and fish oil) for three days. Lipopolysaccharide (15 mg/kg) was then administered intratracheally to induce acute lung injury, characterized by impaired lung function, polymorphonuclear leukocyte recruitment, parenchymal tissue damage, and upregulation of mRNAs for inflammatory mediators. Administration of parenteral nutrition supplemented with fish oil prior to lung insult improved gas exchange and inhibited neutrophil recruitment and upregulation of mRNAs for inflammatory mediators. Parenteral nutrition supplemented with fish oil also prolonged survival. To investigate the underlying mechanisms, leukotriene B4 and leukotriene B5 secretion was measured in neutrophils from the peritoneal cavity. The neutrophils from rats treated with fish oil-rich parenteral nutrition released significantly more leukotriene B5, an anti-inflammatory eicosanoid, than neutrophils isolated from rats given standard parenteral nutrition. Parenteral nutrition with fish oil significantly reduced lipopolysaccharide-induced lung injury in rats in part by promoting the synthesis of anti-inflammatory eicosanoids. PMID:24688221

Kohama, Keisuke; Nakao, Atsunori; Terashima, Mariko; Aoyama-Ishikawa, Michiko; Shimizu, Takayuki; Harada, Daisuke; Nakayama, Mitsuo; Yamashita, Hayato; Fujiwara, Mayu; Kotani, Joji

2014-03-01

262

Modeling the dynamics of recruitment and derecruitment in mice with acute lung injury  

PubMed Central

Lung recruitment and derecruitment contribute significantly to variations in the elastance of the respiratory system during mechanical ventilation. However, the decreases in elastance that occur with deep inflation are transient, especially in acute lung injury. Bates and Irvin (8) proposed a model of the lung that recreates time-varying changes in elastance as a result of progressive recruitment and derecruitment of lung units. The model is characterized by distributions of critical opening and closing pressures throughout the lung and by distributions of speeds with which the processes of opening and closing take place once the critical pressures have been achieved. In the present study, we adapted this model to represent a mechanically ventilated mouse. We fit the model to data collected in a previous study from control mice and mice in various stages of acid-induced acute lung injury (3). Excellent fits to the data were obtained when the normally distributed critical opening pressures were about 5 cmH2O above the closing pressures and when the hyperbolically distributed opening velocities were about an order of magnitude greater than the closing velocities. We also found that, compared with controls, the injured mice had markedly increased opening and closing pressures but no change in the velocities, suggesting that the key biophysical change wrought by acid injury is dysfunction of surface tension at the air-liquid interface. Our computational model of lung recruitment and derecruitment dynamics is thus capable of accurately mimicking data from mice with acute lung injury and may provide insight into the altered biophysics of the injured lung. PMID:18948446

Massa, Christopher B.; Allen, Gilman B.; Bates, Jason H. T.

2008-01-01

263

Perinatal Factors in Neonatal and Pediatric Lung Diseases  

PubMed Central

Wheezing and asthma are significant clinical problems for infants and young children, particularly following premature birth. Recurrent wheezing in infants can progress to persistent asthma. As in adults, altered airway structure (remodeling) and function (increased bronchoconstriction) are also important in neonatal and pediatric airway diseases. Accumulating evidence suggests that airway disease in children is influenced by perinatal factors including perturbations in normal fetal lung development, postnatal interventions in the intensive care unit, and environmental and other insults in the neonatal period. Here, in addition to genetics, maternal health, environmental processes, innate immunity, and impaired lung development/function can all influence pathogenesis of airway disease in children. We summarize current understanding of how prenatal and postnatal factors can contribute to development of airway diseases in neonates and children. Understanding these mechanisms will help identify and develop novel therapies for childhood airway diseases. PMID:24090092

Britt, Rodney D.; Faksh, Arij; Vogel, Elizabeth; Martin, Richard J.; Pabelick, Christina M.; Prakash, Y.S.

2014-01-01

264

Inhibition of NADPH oxidase prevents acute lung injury in obese rats following severe trauma.  

PubMed

Lung capillary filtration coefficient (Kf) and impacts of oxidative stress have not been determined in the setting of severe trauma, especially in obese patients who exhibit increased lung injury. We hypothesized that severe trauma leads to a greater increase in lung Kf in obesity due to exacerbated production of and/or vulnerability to oxidative stress. Severe trauma was induced in lean and obese Zucker rats by muscle injury, fibula fracture, and bone component injection to both hindlimbs, with or without 24-h treatments of apocynin, a NADPH oxidase (NOX) inhibitor. Lung wet/dry weight ratios, lung vascular Kf, lung neutrophil counts, lung NOX and myeloperoxidase (MPO) activity, and plasma IL-6 levels were measured 24 h after trauma. In an additional study, lungs were isolated from nontrauma lean and obese rats to determine the acute effect of phenazime methosulfate, a superoxide donor, on pulmonary vascular Kf. After trauma, compared with lean rats, obese rats exhibited greater increases in lung capillary Kf, neutrophil accumulation, NOX and MPO activity, and plasma IL-6. The lung wet/dry weight ratio was increased in obese rats but not in lean rats. Apocynin treatment decreased lung Kf, neutrophil counts, NOX and MPO activities, wet/dry weight ratio, and plasma IL-6 in obese rats. Phenazime methosulfate treatment resulted in a greater increase in lung Kf in nontrauma obese rats compared with nontrauma lean rats. These results suggest that obese rats are susceptible to lung injury following severe trauma due to increased production of and responsiveness to pulmonary oxidative stress. PMID:24414071

Xiang, Lusha; Lu, Silu; Mittwede, Peter N; Clemmer, John S; Hester, Robert L

2014-03-01

265

Classification of diffuse lung diseases: why and how.  

PubMed

The understanding of complex lung diseases, notably the idiopathic interstitial pneumonias and small airways diseases, owes as much to repeated attempts over the years to classify them as to any single conceptual breakthrough. One of the many benefits of a successful classification scheme is that it allows workers, within and between disciplines, to be clear that they are discussing the same disease. This may be of particular importance in the recruitment of individuals for a clinical trial that requires a standardized and homogeneous study population. Different specialties require fundamentally different things from a classification: for epidemiologic studies, a classification that requires categorization of individuals according to histopathologic pattern is not usually practicable. Conversely, a scheme that simply divides diffuse parenchymal disease into inflammatory and noninflammatory categories is unlikely to further the understanding about the pathogenesis of disease. Thus, for some disease groupings, for example, pulmonary vasculopathies, there may be several appropriate classifications, each with its merits and demerits. There has been an interesting shift in the past few years, from the accepted primacy of histopathology as the sole basis on which the classification of parenchymal lung disease has rested, to new ways of considering how these entities relate to each other. Some inventive thinking has resulted in new classifications that undoubtedly benefit patients and clinicians in their endeavor to improve management and outcome. The challenge of understanding the logic behind current classifications and their shortcomings are explored in various examples of lung diseases. PMID:23970508

Hansell, David M

2013-09-01

266

Inhaled activated protein C: a novel therapy for acute lung injury?  

PubMed

Acute lung injury (ALI) is characterized by the presence of dysregulated coagulation and inflammation. Therefore, Waerhaug and colleagues hypothesized that administration of activated protein C (APC) via the inhaled route would be a novel and effective treatment for ALI. They demonstrated that inhaled APC improved oxygenation and lung aeration in a sheep model of lipopolysaccharide-induced ALI, but did not alter lung water or hemodynamics. Future studies are needed to determine plasma and airspace APC levels when administered by the inhaled route, and to determine if inhaled APC has a similar effect in other models of ALI. PMID:19519935

Liu, Kathleen D; Looney, Mark R; Matthay, Michael A

2009-01-01

267

Acute renal failure leads to dysregulation of lung salt and water channels  

Microsoft Academic Search

Acute renal failure leads to dysregulation of lung salt and water channels.BackgroundRenal ischemia\\/reperfusion (I\\/R) injury and the acute respiratory distress syndrome (ARDS) frequently coexist in the intensive care setting, and this combination is associated with a high mortality. Recent experimental data demonstrate that renal I\\/R injury leads to an increase in pulmonary vascular permeability, similar to that observed in ARDS.

Hamid Rabb; Zhaohui Wang; Takashi Nemoto; John Hotchkiss; Naoko Yokota; Manoocher Soleimani

2003-01-01

268

Effect of Prone Position on Regional Shunt, Aeration and Perfusion in Experimental Acute Lung Injury  

Microsoft Academic Search

Rationale: The prone position is used to improve gas exchange in patients with acute respiratory distress syndrome. However, the regional mechanism by which the prone position improves gas ex- change in acutely injured lungs is still incompletely defined. Methods:Weusedpositronemissiontomographyimagingof( 13 N)nitro- gen to assess the regional distribution of pulmonary shunt, aeration, perfusion, and ventilation in seven surfactant-depleted sheep in supineandpronepositions.Results:Inthesupineposition,thedorsal

Torsten Richter; Giacomo Bellani; R. Scott Harris; Marcos F. Vidal Melo; Tilo Winkler; Jose G. Venegas; Guido Musch

2005-01-01

269

Parasite Burden and CD36-Mediated Sequestration Are Determinants of Acute Lung Injury in an Experimental Malaria Model  

Microsoft Academic Search

Although acute lung injury (ALI) is a common complication of severe malaria, little is known about the underlying molecular basis of lung dysfunction. Animal models have provided powerful insights into the pathogenesis of severe malaria syndromes such as cerebral malaria (CM); however, no model of malaria-induced lung injury has been definitively established. This study used bronchoalveolar lavage (BAL), histopathology and

Fiona E. Lovegrove; Sina A. Gharib; Lourdes Peña-Castillo; Samir N. Patel; John T. Ruzinski; Timothy R. Hughes; W. Conrad Liles; Kevin C. Kain

2008-01-01

270

Indoor air pollution from solid fuel use, chronic lung diseases and lung cancer in Harbin, Northeast China  

Microsoft Academic Search

In some areas of China, indoor air pollution (IAP) originating principally from the combustion of solid fuels has a relevant role in lung cancer. Most previous studies focused on the female population and only a few on both the sexes. We analyzed the relationship between IAP from solid fuel use and selected chronic lung diseases and lung cancer risk in

Carlotta Galeone; Claudio Pelucchi; Carlo La Vecchia; Eva Negri; Cristina Bosetti; Jinfu Hu

2008-01-01

271

Lung injury in mice and rats acutely exposed to beryllium  

SciTech Connect

The effect of lung injury, in rats and mice, exposed to an aerosol of beryllium sulfate (BE) for one hour, through nose-only inhalation, was evaluated by the methods of bronchoalveolar lavage (BAL) and lung cell kinetics. The BAL in rats, sacrificed over a 21 day period following exposure, showed lactate dehydrogenase (LDH) and alkaline phosphatase (Alk Pase) activities as the most sensitive indicators of lung damage. LDH activity peaked at day 8 while Alk Pase activity peaked at day 5, both being 30 times greater than comparable control values. Acid phosphatase activity and albumin levels were also increased, but not to the same extent as LDH and Alk Pase. The BAL of mice showed LDH activity as the most sensitive indicator of lung damage, with a maximum response 3 times greater than controls at day 5. In another series of experiments, animals were treated with three agents capable of inducing fibrosis: beryllium sulfate, bleomycin, and butylated hydroxytoluene (BHT). Cy A completely inhibited the fibrogenic effects of BHT in mice, as measured through total lung hydroxyproline content. Bleomycin-induced fibrosis was significantly reduced by Cy A treatment in rats, but showed no effect in mice. Additionally, the effect of iron salt administration to rats decreased the intravenous LD/sub 50/ dose, and significantly reduced the inhalation toxicity, of beryllium sulfate. The protective mechanism of iron salt administration, through the induction of ferritin synthesis, is postulated.

Sendelbach, L.E. Jr.

1985-01-01

272

An overview of the pathogenesis of cystic fibrosis lung disease  

Microsoft Academic Search

The pathogenesis of cystic fibrosis (CF) lung disease is reviewed, focusing on an overview of the physiologic mechanisms that regulate mucus transport. A major emphasis is placed on the active transport systems that regulate the airway surface liquid (ASL) volume and, particularly, regulate the volume of the periciliary liquid (PCL) layer. A sequence is developed for CF whereby there is

R. C Boucher

2002-01-01

273

DOES CHRONIC OZONE EXPOSURE LEAD TO LUNG DISEASE?  

EPA Science Inventory

The potential role of ozone in the induction of chronic lung diseases remains unclear. sing an ambient profile adopted from aerometric data from the Southwest Air Basin, rats were exposed to O3 for up to 18 months before assessments of pulmonary structure, function and biochemist...

274

Rare Infiltrative Lung Diseases: A Challenge for Clinicians  

Microsoft Academic Search

Rare diffuse infiltrative lung diseases are a challenge for clinicians, radiologists, and pathologists for at least three reasons: (a) their low incidence and prevalence hamper the acquisition of expertise and frequently the diagnosis is delayed; (b) therapeutic actions are mainly empirical and based on steroid use, and (c) pathogenetic events are difficult to explain and only recently new therapeutic measures

Venerino Poletti; Ulrich Costabel; Gian Luca Casoni; Caterina Bigliazzi; Marjolein Drent; Dario Olivieri

2004-01-01

275

Relative importance of cigarette smoking in occupational lung disease  

Microsoft Academic Search

Since 1900 respiratory disease has remained a constant serious cause of chronic ill health and premature death in Britain. The falling importance of tuberculosis and pneumonia has been off-set by the rise in lung cancer. Bronchitis morbidity and mortality have fallen only slightly since 1935. To produce any real improvement in the future existing information as to cause must be

P C Elmes

1981-01-01

276

Hodgkin's disease terminating in oat cell carcinoma of the lung.  

PubMed

A 27-year-old woman with Hodgkin's disease, nodular sclerasing type, having received two courses of radiation therapy with one year and nine months interval and a prolonged course of chemotherapy with combinations of COPP, MOPP and CVPP, developed oat cell carcinoma of the lung, four years after the initial diagnosis. PMID:221092

Cehreli, C; Ruacan, S A; Firat, D; Kucuksu, N

1979-04-01

277

in vivo tomographic velocimetry of the lung for the detailed study of lung disease and its treatments  

NASA Astrophysics Data System (ADS)

All lung disease dramatically alters the local motion of the lung during breathing. It stands to reason, therefore, that detailed measurement of lung motion could provide dramatic improvements in assessment of lung function. Using synchrotron-based phase contrast imaging, we have developed and applied tools for lung motion and function measurement. We demonstrate a low-dose alternative to traditional 4D-CT methods, capable of measuring instantaneous 3D tissue motion using only 6 projection images. Additionally, our technique provides estimation of the airflow distribution throughout the bronchial tree during the breathing cycle. The ability to measure lung function at a regional level will provide invaluable information for studies into normal and pathological lung dynamics, and may provide new pathways for diagnosis of regional lung diseases. Although proof-of-concept data were acquired on a synchrotron, the low-dose methodology developed lends itself to clinical scanning and offers translational opportunities.

Dubsky, Stephen; Hooper, Stuart B.; Siu, Karen K. W.; Fouras, Andreas

2012-10-01

278

The Role of Progenitor Cells in Lung Disease Prognosis  

Microsoft Academic Search

\\u000a The number of investigations related to the role of stem and progenitor cells in lung repair has grown exponentially in recent\\u000a years. Bone-marrow-derived cells, including stem cells and progenitors, have emerged as candidate markers to prognosticate\\u000a outcomes during pulmonary disease. The relationship of these cells to prognosis has provided clues regarding the pathophysiologic\\u000a characteristics of pulmonary disease, and direction for

Ellen L. Burnham; Susan Majka; Marc Moss

279

OXIDATIVE STRESS RELATED APOPTOSIS IN SMOKERS AND CHRONIC LUNG DISEASES  

Microsoft Academic Search

Cigarette smoke contains various carcinogens, reactive oxygen species (ROS) and reactive nitrogen species (RNS). It has been found that cigarette smoking causes several chronic lung diseases including chronic obstructive pulmonary diseases (COPD). There are mul- tiple markers used for oxidative damage\\/stress in smokers such as urinary 8- hydroxydeoxyguanosine (8-OHdG), serum hydrogen peroxide (H2O2), interleukin-8 (IL-8) and H2O2 in breath condensate.

Ratana Banjerdpongchai

2006-01-01

280

MATRILYSIN PARTICIPATES IN THE ACUTE LUNG INJURY INDUCED BY OIL COMBUSTION PRODUCTS  

EPA Science Inventory

ROLE OF MATRILYSIN IN THE ACUTE LUNG INJURY INDUCED BY OIL COMBUSTION PARTICLES. K L Dreher1, WY Su2 and C L Wilson3. 1US Environmental Protection Agency, Research Triangle Park, NC; 2Duke University, Durham, NC;3Washington University, St. Louis, MO. Mechanisms by ...

281

Polymer-Surfactant Treatment of Meconium-induced Acute Lung Injury  

Microsoft Academic Search

Substances (for example, serum proteins or meconium) that inter- fere with the activity of pulmonary surfactant in vitro may also be important in the pathogenesis or progression of acute lung injury. Addition of polymers such as dextran or polyethylene glycol (PEG) to surfactants prevents and reverses surfactant inactivation. The purpose of this study was to find out whether surfactant\\/polymer mixtures

KAREN W. LU; H. WILLIAM TAEUSCH; BENGT ROBERTSON; JON GOERKE; JOHN A. CLEMENTS

2000-01-01

282

Gap Junction Channel Modulates Pulmonary Vascular Permeability through Calcium in Acute Lung Injury: An Experimental Study  

Microsoft Academic Search

Background: Increased pulmonary vascular permeability is a hallmark of acute lung injury (ALI). Gap junction channels (GJCs) connect adjacent cells and facilitate ion exchange. It remained unclear whether GJCs modulate pulmonary permeability in ALI through intracellular calcium. Objectives: This study aimed to verify if GJCs in pulmonary microvessel endothelial cells (PMVECs) modulate pulmonary vascular permeability in ALI via intracellular calcium.

Jinzhou Zhang; Wen Wang; Jing Sun; Qiang Li; Jincheng Liu; Hailong Zhu; Tao Chen; Hongbing Wang; Shiqiang Yu; Guocheng Sun; Wensheng Chen; Dinghua Yi

2010-01-01

283

Identification of Patients with Acute Lung Injury from Free-Text Chest X-Ray Reports  

E-print Network

of acute hypoxemic respiratory failure with bilateral pulmonary infiltrates that is associ- ated of a precipitating cause, either due to direct lung injury from trauma or pneumonia or secondary to another insult pulmonary infiltrates on chest radiograph, representing non-cardiac pul- monary edema as evidenced

Yetisgen-Yildiz, Meliha

284

Acute effects of thoracic irradiation on lung function and structure in awake sheep  

SciTech Connect

To investigate the acute physiological and structural changes after lung irradiation, the effects of whole-lung irradiation were investigated in fourteen sheep. Ten sheep were prepared with vascular and chronic lung lymph catheters, then a week later were given 1,500 rad whole-lung radiation and monitored for 2 days. Four sheep were given the same dose of radiation and were killed 4 h later for structural studies. Lung lymph flow increased at 3 h after radiation (14.6 +/- 2.1 ml/h) to twice the base-line flow rate (7.5 +/- 1.3), with a high lymph-to-plasma protein concentration. Pulmonary arterial pressure increased twofold from base line (18 +/- 1.6 cmH2O) at 2 h after radiation (33 +/- 3.8). Cardiac output and systemic pressure in the aorta did not change after lung radiation. Arterial O/sub 2/ tension decreased from 85 +/- 3 to 59 +/- 4 Torr at 1 day after radiation. Lymphocyte counts in both blood and lung lymph decreased to a nadir by 4 h and remained low. Thromboxane B2 concentration in lung lymph increased from base line (0.07 +/- 0.03 ng/ml) to peak at 3 h after radiation (8.2 +/- 3.7 ng/ml). The structural studies showed numerous damaged lymphocytes in the peripheral lung and bronchial associated lymphoid tissue. Quantitative analysis of the number of granulocytes in peripheral lung showed no significant change (base line 6.2 +/- 0.8 granulocytes/100 alveoli, 4 h = 10.3 +/- 2.3). The most striking change involved lung airways. The epithelial lining of the majority of airways from intrapulmonary bronchus to respiratory bronchiolus revealed damage with the appearance of intracellular and intercellular cell fragments and granules. This new large animal model of acute radiation lung injury can be used to monitor physiological, biochemical, and morphological changes after lung radiation. It is relevant to the investigation of diffuse oxidant lung injury as well as to radiobiology per se.

Loyd, J.E.; Bolds, J.M.; Sheller, J.R.; Duke, S.S.; Gillette, A.W.; Malcolm, A.W.; Meyrick, B.O.; Brigham, K.L.

1987-01-01

285

Spred-2 Deficiency Exacerbates Lipopolysaccharide-Induced Acute Lung Inflammation in Mice  

PubMed Central

Background Acute respiratory distress syndrome (ARDS) is a severe and life-threatening acute lung injury (ALI) that is caused by noxious stimuli and pathogens. ALI is characterized by marked acute inflammation with elevated alveolar cytokine levels. Mitogen-activated protein kinase (MAPK) pathways are involved in cytokine production, but the mechanisms that regulate these pathways remain poorly characterized. Here, we focused on the role of Sprouty-related EVH1-domain-containing protein (Spred)-2, a negative regulator of the Ras-Raf-extracellular signal-regulated kinase (ERK)-MAPK pathway, in lipopolysaccharide (LPS)-induced acute lung inflammation. Methods Wild-type (WT) mice and Spred-2?/? mice were exposed to intratracheal LPS (50 µg in 50 µL PBS) to induce pulmonary inflammation. After LPS-injection, the lungs were harvested to assess leukocyte infiltration, cytokine and chemokine production, ERK-MAPK activation and immunopathology. For ex vivo experiments, alveolar macrophages were harvested from untreated WT and Spred-2?/? mice and stimulated with LPS. In in vitro experiments, specific knock down of Spred-2 by siRNA or overexpression of Spred-2 by transfection with a plasmid encoding the Spred-2 sense sequence was introduced into murine RAW264.7 macrophage cells or MLE-12 lung epithelial cells. Results LPS-induced acute lung inflammation was significantly exacerbated in Spred-2?/? mice compared with WT mice, as indicated by the numbers of infiltrating leukocytes, levels of alveolar TNF-?, CXCL2 and CCL2 in a later phase, and lung pathology. U0126, a selective MEK/ERK inhibitor, reduced the augmented LPS-induced inflammation in Spred-2?/? mice. Specific knock down of Spred-2 augmented LPS-induced cytokine and chemokine responses in RAW264.7 cells and MLE-12 cells, whereas Spred-2 overexpression decreased this response in RAW264.7 cells. Conclusions The ERK-MAPK pathway is involved in LPS-induced acute lung inflammation. Spred-2 controls the development of LPS-induced lung inflammation by negatively regulating the ERK-MAPK pathway. Thus, Spred-2 may represent a therapeutic target for the treatment of ALI. PMID:25275324

Xu, Yang; Ito, Toshihiro; Fushimi, Soichiro; Takahashi, Sakuma; Itakura, Junya; Kimura, Ryojiro; Sato, Miwa; Mino, Megumi; Yoshimura, Akihiko; Matsukawa, Akihiro

2014-01-01

286

The effects of Gamijinhae-tang on elastase/lipopolysaccharide-induced lung inflammation in an animal model of acute lung injury  

PubMed Central

Background Gamijinhae-tang (GJHT) has long been used in Korea to treat respiratory diseases. The therapeutic effect of GJHT is likely associated with its anti-inflammatory activity. However, the precise mechanisms underlying its effects are unknown. This study was conducted to evaluate the protective effects of GJHT in a porcine pancreatic elastase (PPE) and lipopolysaccharide(LPS) induced animal model of acute lung injury (ALI). Methods In this study, mice were intranasally exposed to PPE and LPS for 4 weeks to induce chronic obstructive pulmonary disease (COPD)-like lung inflammation. Two hours prior to PPE and LPS administration, the treatment group was administered GJHT extracts via an oral injection. The numbers of neutrophils, lymphocytes, macrophages and total cells in the bronchoalveolar lavage (BAL) fluid were counted, and pro-inflammatory cytokines were also measured. For histologic analysis, hematoxylin and eosin (H&E) stains and periodic acid-Schiff (PAS) stains were evaluated. Results After inducing ALI by treating mice with PPE and LPS for 4 weeks, the numbers of neutrophils, lymphocytes and total cells were significantly lower in the GJHT group than in the ALI group. In addition, the IL-1? and IL-6 levels were significantly decreased in the GJHT group. The histological results also demonstrated the attenuation effect of GJHT on PPE- and LPS-induced lung inflammation. Conclusions The results of this study indicate that GJHT has significantly reduces PPE- and LPS-induced lung inflammation. The remarkable protective effects of GJHT suggest its therapeutic potential in COPD treatment. PMID:23866260

2013-01-01

287

Diesel Exhaust Particles in Lung Acutely Enhance Experimental Peripheral Thrombosis  

Microsoft Academic Search

Background—Pollution by particulates has consistently been associated with increased cardiovascular morbidity and mortality, but a plausible biological basis for this association is lacking. Methods and Results—Diesel exhaust particles (DEPs) were instilled into the trachea of hamsters, and blood platelet activation, experimental thrombosis, and lung inflammation were studied. Doses of 5 to 500 g of DEPs per animal induced neutrophil influx

Abderrahim Nemmar; Peter H. M. Hoet; David Dinsdale; Jozef Vermylen; Marc F. Hoylaerts; Benoit Nemery

2010-01-01

288

Modifications of lung clearance mechanisms by acute influenza A infection  

SciTech Connect

Four volunteers with naturally acquired, culture-proved influenza A infection inhaled a radiolabeled aerosol to permit investigation of lung mucociliary clearance mechanisms during and after symptomatic illness. Mucus transport in the trachea was undetectable when monitored with an external multidetector probe within 48 hours of the onset of the illness, but was found at a normal velocity by 1 week in three of the four subjects. In two volunteers who coughed 23 to 48 times during the 4.5-hour observation period, whole lung clearance was as fast within the first 48 hours of illness as during health 3 months later in spite of the absence of measurable tracheal mucus transport. Conversely, in spite of the return 1 week later of mucus transport at velocities expected in the trachea, whole lung clearance for the 4.5-hour period was slowed in two volunteers who coughed less than once an hour. The data offer evidence that cough is important in maintaining lung clearance for at least several days after symptomatic influenza A infection when other mechanisms that depend on ciliary function are severely deficient.

Levandowski, R.A.; Gerrity, T.R.; Garrard, C.S.

1985-10-01

289

Blood transfusion for the treatment of acute anaemia in inflammatory bowel disease and other digestive diseases  

PubMed Central

Allogeneic blood transfusion (ABT) is frequently used as the first therapeutic option for the treatment of acute anaemia in patients with inflammatory bowel disease (IBD), especially when it developed due to gastrointestinal or perioperative blood loss, but is not risk-free. Adverse effects of ABT include, but are not limited to, acute hemolytic reaction (wrong blood or wrong patient), febrile non-hemolytic transfusional reaction, bacterial contamination, transfusion-related acute lung injury, transfusion associated circulatory overload, transfusion-related immuno-modulation, and transmission of almost all infectious diseases (bacteria, virus, protozoa and prion), which might result in increased risk of morbidity and mortality. Unfortunately, the main physiological goal of ABT, i.e. to increase oxygen consumption by the hypoxic tissues, has not been well documented. In contrast, the ABT is usually misused only to increase the haemoglobin level within a fixed protocol [mostly two by two packed red blood cell (PRC) units] independently of the patient’s tolerance to normovolemic anaemia or his clinical response to the transfusion of PRC units according to a “one-by-one” administration schedule. Evidence-based clinical guidelines may promote best transfusion practices by implementing restrictive transfusion protocols, thus reducing variability and minimizing the avoidable risks of transfusion, and the use of autologous blood and pharmacologic alternatives. In this regard, preoperative autologous blood donation (PABD) consistently diminished the frequency of ABT, although its contribution to ABT avoidance is reduced when performed under a transfusion protocol. In addition, interpretation of utility of PABD in surgical IBD patients is hampered by scarcity of published data. However, the role of autologous red blood cells as drug carriers is promising. Finally, it must be stressed that a combination of methods used within well-constructed protocols will offer better prospects for blood conservation in selected IBD patients undergoing elective surgery. PMID:19787832

Garcia-Erce, Jose Antonio; Gomollon, Fernando; Munoz, Manuel

2009-01-01

290

Severe right heart failure in a patient with chronic obstructive lung disease: a diagnostic challenge.  

PubMed

A 55-year-old male was admitted for evaluation of severe dyspnoea and hypoxaemia. Physical examination upon admission showed elevated jugular venous pressure and an accentuated second heart sound. Chest radiograph showed cardiomegaly with increased bibasilar markings. Arterial blood gas analysis while breathing room air showed marked hypoxaemia. High resolution computed tomography angiography of the chest showed modestly enlarged mediastinal lymph nodes with discrete diffuse ground-glass attenuation especially at the lower lung zones. Positron emission tomography using 18F labelled 2-deoxy-D-glucose (FDG) demonstrated the mediastinal lymph nodes were FDG-avid. Transthoracic echocardiography showed dilated hypokinetic right heart chambers with bulging of the interventricular septum to the left, compatible with acute cor-pulmonale. From the tricuspid regurgitation jet measurement a systolic pulmonary artery pressure (PAP) of 48 mmHg was estimated. Patent foramen ovale was suspected on bubble test. Right heart catheterisation confirmed pulmonary arterial hypertension: mPAP 47 mmHg, pulmonary artery occlusion pressure 5 mmHg, cardiac index 1.1 L/min/m2, pulmonary vascular resistance (PVR) 959 dyne.sec.cm(-5). Pulmonary function tests showed a marked diffusing capacity for carbon monoxide (DLCO) decrease of 32% predicted but no obstructive lung deficit. Before an open lung biopsy could be scheduled the patient developed acute cardiogenic shock. At autopsy pulmonary veno-occlusive disease with marked pulmonary hypertension was diagnosed. PMID:24380224

Meysman, M; Pipeleers-Marichal, M; Geers, C; Ilsen, B; Vincken, W

2013-01-01

291

Errors in the measurement of total lung capacity in chronic obstructive lung disease.  

PubMed

The standard plethysmographic method of measuring total lung capacity (TLC) has been reported to result in spuriously high estimates in patients with severe airway obstruction. The helium-dilution method is known to underestimate TLC in the same patients. To determine the magnitude of these possible errors we measured TLC by four methods in 20 patients with varying degrees of chronic obstructive lung disease and in 11 normal subjects. TLC was measured by (1) helium dilution (TLCHe); (2) a volume-displacement body plethysmograph, box volume being plotted against mouth pressure (TLCm); (3) the same body plethysmograph with volume plotted against pressure measured with an oesophageal balloon (TLCes); and (4) a radiological technique (TLCxr). In normal subjects there was no difference between TCLm (6.57 +/- 1.20) and TLCes (6.51 +/- 1.24). In the patients with chronic obstructive lung disease TLCm gave results significantly higher than those of any other method. If TLCes is taken as the closest estimate of true TLC, TLCm consistently overestimates and TLCHe underestimates TLC. There was no relationship between the degree of airway obstruction and (TLCm - TLCes) but there was between (TLCes - TLCHe) and severity of airway obstruction. We conclude that using mouth pressure in the plethysmographic measurement of TLC in patients with chronic obstructive lung disease results in consistent but slight overestimation of TLC. PMID:6879500

Paré, P D; Wiggs, B J; Coppin, C A

1983-06-01

292

Probiotics in the Management of Lung Diseases  

PubMed Central

The physiology and pathology of the respiratory and gastrointestinal tracts are closely related. This similarity between the two organs may underlie why dysfunction in one organ may induce illness in the other. For example, smoking is a major risk factor for COPD and IBD and increases the risk of developing Crohn's disease. Probiotics have been defined as “live microorganisms which, when administered in adequate amounts, confer health benefits on the host.” In model systems probiotics regulate innate and inflammatory immune responses. Commonly used probiotics include lactic acid bacteria, particularly Lactobacillus, Bifidobacterium, and Saccharomyces, and these are often used as dietary supplements to provide a health benefit in gastrointestinal diseases including infections, inflammatory bowel disease, and colon cancer. In this respect, probiotics probably act as immunomodulatory agents and activators of host defence pathways which suggest that they could influence disease severity and incidence at sites distal to the gut. There is increasing evidence that orally delivered probiotics are able to regulate immune responses in the respiratory system. This review provides an overview of the possible role of probiotics and their mechanisms of action in the prevention and treatment of respiratory diseases. PMID:23737654

Mortaz, Esmaeil; Adcock, Ian M.; Folkerts, Gert; Barnes, Peter J.; Paul Vos, Arjan; Garssen, Johan

2013-01-01

293

A case of venlafaxine-induced interstitial lung disease.  

PubMed

A patient treated with venlafaxine for major depression developed an interstitial lung disease (ILD) with the characteristic clinical, radiological and pathological features of chronic hypersensitivity pneumonitis. A high resolution computed tomography scan demonstrated ground glass opacity, mosaic perfusion with air-trapping and traction bronchiectasis in both lungs. The pathological findings were consistent with a nonspecific interstitial pneumonia pattern. Clinical and radiological improvements were noted after the discontinuation of venlafaxine and the administration of a corticosteroid. This report provides further evidence that the anti-depressant venlafaxine can cause ILD. PMID:25237379

Oh, Serim; Cha, Seung-Ick; Kim, Hyera; Kim, Minjung; Choi, Sun Ha; Seo, Hyewon; Park, Tae-In

2014-08-01

294

[Granulomatous lymphocytic interstitial lung disease in common variable immunodeficiency].  

PubMed

Common variable immunodeficiency (CVID) is the most frequent primary immune deficiency. Recurrent infections are classical consequences of CVID, but their impact has been largely reduced by immunoglobulin replacement. CVID is also associated with various inflammatory and autoimmune manifestations resulting from abnormal cellular immunity. The lungs are especially affected by a recently described entity called granulomatous lymphocytic interstitial lung disease (GLILD). GLILD currently constitutes an important cause of morbidity and mortality in these patients. It is distinct from bronchiectasis secondary to recurrent infections, and presents similarities but also striking differences with sarcoidosis. PMID:24354253

Bianchi, M Prella; Letovanec, I; Spertini, F; Nicod, L P; Lazor, R

2013-11-20

295

Regulatory Effects of iNOS on Acute Lung Inflammatory Responses in Mice  

PubMed Central

The role of endogenous NO in the regulation of acute lung injury is not well defined. We investigated the effects of inducible nitric oxide synthase (iNOS) and endothelial NOS (eNOS) on the acute inflammatory response in mouse lungs. Acute lung injury was induced by intratracheal instillation of bacterial lipopolysaccharide (LPS) into wild-type (WT) mice and mice deficient in iNOS (iNOS?/?) or eNOS (eNOS?/?). Endpoints of inflammatory injury were myeloperoxidase (MPO) content and leak of albumin into lung. Inflammatory injury was similar in WT and eNOS?/? mice but was substantially increased in iNOS?/? mice. Bronchoalveolar lavage (BAL) fluids of iNOS?/? and WT mice showed similar levels of CXC chemokines (MIP-2, KC) but enhanced levels of CC chemokines (MCP-1, MCP-3). Increased lung content of MPO in iNOS?/? mice was reduced by anti-MCP-1 to values found in WT mice. In vitro stimulation of microvascular endothelial cells with LPS and IFN? revealed elevated production of CXC and CC chemokines in cells from iNOS?/? mice when compared to endothelial cells from iNOS+/+ mice. Peritoneal macrophages from iNOS?/? donors also revealed increased production of CC chemokines after stimulation with LPS and interferon (IFN?). These data indicate that absence of iNOS causes enhanced lung inflammatory responses in mice which may be related to enhanced production of MCP-1 by endothelial cells and macrophages. It appears that iNOS affects the lung inflammatory response by regulating chemokine production. PMID:14633605

Speyer, Cecilia L.; Neff, Thomas A.; Warner, Roscoe L.; Guo, Ren-Feng; Sarma, J. Vidya; Riedemann, Niels C.; Murphy, Megan E.; Murphy, Hedwig S.; Ward, Peter A.

2003-01-01

296

Processing of CT images for analysis of diffuse lung disease in the lung tissue research consortium  

NASA Astrophysics Data System (ADS)

The goal of Lung Tissue Resource Consortium (LTRC) is to improve the management of diffuse lung diseases through a better understanding of the biology of Chronic Obstructive Pulmonary Disease (COPD) and fibrotic interstitial lung disease (ILD) including Idiopathic Pulmonary Fibrosis (IPF). Participants are subjected to a battery of tests including tissue biopsies, physiologic testing, clinical history reporting, and CT scanning of the chest. The LTRC is a repository from which investigators can request tissue specimens and test results as well as semi-quantitative radiology reports, pathology reports, and automated quantitative image analysis results from the CT scan data performed by the LTRC core laboratories. The LTRC Radiology Core Laboratory (RCL), in conjunction with the Biomedical Imaging Resource (BIR), has developed novel processing methods for comprehensive characterization of pulmonary processes on volumetric high-resolution CT scans to quantify how these diseases manifest in radiographic images. Specifically, the RCL has implemented a semi-automated method for segmenting the anatomical regions of the lungs and airways. In these anatomic regions, automated quantification of pathologic features of disease including emphysema volumes and tissue classification are performed using both threshold techniques and advanced texture measures to determine the extent and location of emphysema, ground glass opacities, "honeycombing" (HC) and "irregular linear" or "reticular" pulmonary infiltrates and normal lung. Wall thickness measurements of the trachea, and its branches to the 3 rd and limited 4 th order are also computed. The methods for processing, segmentation and quantification are described. The results are reviewed and verified by an expert radiologist following processing and stored in the public LTRC database for use by pulmonary researchers. To date, over 1200 CT scans have been processed by the RCL and the LTRC project is on target for recruitment of the 2200 patients with 1800 CT scans in the repository for the 5-year effort. Ongoing analysis of the results in the LTRC database by the LTRC participating institutions and outside investigators are underway to look at the clinical and physiological significance of the imaging features of these diseases and correlate these findings with quality of life and other important prognostic indicators of severity. In the future, the quantitative measures of disease may have greater utility by showing correlation with prognosis, disease severity and other physiological parameters. These imaging features may provide non-invasive alternative endpoints or surrogate markers to alleviate the need for tissue biopsy or provide an accurate means to monitor rate of disease progression or response to therapy.

Karwoski, Ronald A.; Bartholmai, Brian; Zavaletta, Vanessa A.; Holmes, David; Robb, Richard A.

2008-03-01

297

Successful single-lung transplantation for multicentric castleman disease.  

PubMed

We report a rare case of multicentric Castleman disease treated successfully with single-lung transplantation. A 12-year-old patient developed increasing dyspnea. Elevated serum interleukin-6 (177.0 pg/mL) and immunoglobulin G (IgG; 13,900 mg/dL) levels were observed. Steroid therapy was effective but the respiratory condition gradually deteriorated. He underwent single-lung transplantation at 36 years of age. Preoperative interleukin-6 and IgG levels were 0.3 pg/mL and 5,260 mg/dL, respectively. After 6 months he is alive without symptoms. Postoperative IgG levels were restored to normal limits (1,624 mg/dL) and interleukin-6 levels remained within normal limits (1.4 pg/mL). Overinflation of the native left lung also improved. PMID:25193223

Morimura, Yuki; Chen, Fengshi; Kinjo, Tomoaki; Miyagawa-Hayashino, Aya; Kubo, Takeshi; Yamada, Tetsu; Sato, Masaaki; Aoyama, Akihiro; Date, Hiroshi

2014-09-01

298

Building a reference multimedia database for interstitial lung diseases.  

PubMed

This paper describes the methodology used to create a multimedia collection of cases with interstitial lung diseases (ILDs) at the University Hospitals of Geneva. The dataset contains high-resolution computed tomography (HRCT) image series with three-dimensional annotated regions of pathological lung tissue along with clinical parameters from patients with pathologically proven diagnoses of ILDs. The motivations for this work is to palliate the lack of publicly available collections of ILD cases to serve as a basis for the development and evaluation of image-based computerized diagnostic aid. After 38 months of data collection, the library contains 128 patients affected with one of the 13 histological diagnoses of ILDs, 108 image series with more than 41l of annotated lung tissue patterns as well as a comprehensive set of 99 clinical parameters related to ILDs. The database is available for research on request and after signature of a license agreement. PMID:21803548

Depeursinge, Adrien; Vargas, Alejandro; Platon, Alexandra; Geissbuhler, Antoine; Poletti, Pierre-Alexandre; Müller, Henning

2012-04-01

299

Hypertransaminasemia and fatal lung disease: a case report  

PubMed Central

Glycogenosis type II (Pompe disease) is a rare autosomal recessive genetic disorder caused by mutations in the gene encoding the lysosomal enzyme acid ?-glucosidase. The classic form is characterized by severe cardiac involvement, generalized hypotonia and exitus early in life. Presenting symptoms and signs of the disease may be neglected or underestimated, thus delaying the diagnosis. Respiratory manifestations mainly occur because of respiratory muscle weakness. However, additional mechanisms can favor the development of pulmonary complications that result in fatal respiratory failure. We herein describe a case of an infant with glycogenosis type II presenting with hepatomegaly and hypertransaminasemia, who rapidly developed fatal lung disease. PMID:23391190

2013-01-01

300

Hypertransaminasemia and fatal lung disease: a case report.  

PubMed

Glycogenosis type II (Pompe disease) is a rare autosomal recessive genetic disorder caused by mutations in the gene encoding the lysosomal enzyme acid ?-glucosidase. The classic form is characterized by severe cardiac involvement, generalized hypotonia and exitus early in life. Presenting symptoms and signs of the disease may be neglected or underestimated, thus delaying the diagnosis. Respiratory manifestations mainly occur because of respiratory muscle weakness. However, additional mechanisms can favor the development of pulmonary complications that result in fatal respiratory failure. We herein describe a case of an infant with glycogenosis type II presenting with hepatomegaly and hypertransaminasemia, who rapidly developed fatal lung disease. PMID:23391190

Santamaria, Francesca; De Stefano, Sara; Montella, Silvia; Maglione, Marco; Della Casa, Roberto; Acampora, Emma; Pignata, Claudio; Salerno, Mariacarolina; Parenti, Giancarlo

2013-01-01

301

A preclinical rodent model of acute radiation-induced lung injury after ablative focal irradiation reflecting clinical stereotactic body radiotherapy.  

PubMed

In a previous study, we established an image-guided small-animal micro-irradiation system mimicking clinical stereotactic body radiotherapy (SBRT). The goal of this study was to develop a rodent model of acute phase lung injury after ablative irradiation. A radiation dose of 90 Gy was focally delivered to the left lung of C57BL/6 mice using a small animal stereotactic irradiator. At days 1, 3, 5, 7, 9, 11 and 14 after irradiation, the lungs were perfused with formalin for fixation and paraffin sections were stained with hematoxylin and eosin (H&E) and Masson's trichrome. At days 7 and 14 after irradiation, micro-computed tomography (CT) images of the lung were taken and lung functional measurements were performed with a flexiVent™ system. Gross morphological injury was evident 9 days after irradiation of normal lung tissues and dynamic sequential events occurring during the acute phase were validated by histopathological analysis. CT images of the mouse lungs indicated partial obstruction located in the peripheral area of the left lung. Significant alteration in inspiratory capacity and tissue damping were detected on day 14 after irradiation. An animal model of radiation-induced lung injury (RILI) in the acute phase reflecting clinical stereotactic body radiotherapy was established and validated with histopathological and functional analysis. This model enhances our understanding of the dynamic sequential events occurring in the acute phase of radiation-induced lung injury induced by ablative dose focal volume irradiation. PMID:24937781

Hong, Zhen-Yu; Lee, Hae-June; Choi, Won Hoon; Lee, Yoon-Jin; Eun, Sung Ho; Lee, Jung Il; Park, Kwangwoo; Lee, Ji Min; Cho, Jaeho

2014-07-01

302

Antacid Control of Complications from Acute Gastroduodenal Disease After Burns.  

National Technical Information Service (NTIS)

To determine the effectiveness of hydrogen ion neutralization in preventing the clinical complications (hemorrhage and perforation) of acute gastroduodenal disease after thermal injury, 48 patients with burns of greater than 35% total body surface were ev...

J. C. McAlhany, A. J. Czaja, B. A. Pruitt

1976-01-01

303

Gastric Acid Secretion and Acute Gastroduodenal Disease after Burns.  

National Technical Information Service (NTIS)

Total titratable acidity of fasting gastric secretion was determined in 34 hemodynamically stable patients within five days after burn. Acid output was not predictive of disease; acute duodenal ulcers, however, were not discovered in patients with acid se...

A. J. Czaja, J. C. McAlhany, B. A. Pruitt

1975-01-01

304

ROLE OF TACHYKININS IN OZONE-INDUCED ACUTE LUNG INJURY  

EPA Science Inventory

To examine the hypothesis that the acute, reversible changes caused by O3 exposure are mediated by techykinin release, guinea pigs were depleted of tachykinins using repeated capsaicin (CAP) injections prior to O3 exposure, in an attempt to prevent O3-induced functional changes. ...

305

The role of oxygen free radicals in occupational and environmental lung diseases.  

PubMed Central

Oxygen free radicals and their metabolites, collectively described as reactive oxygen species (ROS), have been implicated in the pathogenesis of many diseases. The pulmonary system is particularly vulnerable to ROS-induced injury because of its continuous exposure to toxic pollutants from a wide variety of sources in the ambient air. Additionally, lungs are exposed systemically to ROS generated from xenobiotic compounds and endogenous sources. This review describes the sources of endogenous and exogenous ROS generation in the lung. Special emphasis is given to major sources of ROS in occupational and environmental exposures to asbestos, crystalline silica, coal, chromium, herbicides, bleomycin, and cigarette smoke. ROS-induced lung injury at different target levels may contribute to similar patterns of cell injury and alterations at the molecular level by initiation, propagation, and autocatalytic chain reactions. Intracellular signalling, activation and inactivation of enzymes, stimulation, secretion, and release of proinflammatory cytokines, chemokines, and nuclear factor activation and alterations are also common events. Understanding the interactions of these intricate mechanistic events is important in the prevention and amelioration of lung injury that results from acute and chronic exposures to toxins in ambient air. PMID:9114285

Vallyathan, V; Shi, X

1997-01-01

306

Acute Demyelinating Disease after Oral Therapy with Herbal Extracts  

PubMed Central

Central nervous system demyelinating processes such as multiple sclerosis and acute disseminated encephalomyelitis constitute a group of diseases not completely understood in their physiopathology. Environmental and toxic insults are thought to play a role in priming autoimmunity. The aim of the present report is to describe a case of acute demyelinating disease with fatal outcome occurring 15 days after oral exposure to herbal extracts. PMID:21738505

Kostianovsky, Alex; Maskin, Patricio; Noriega, Maria M.; Soler, Cristina; Bonelli, Ignacio; Riley, Claire S.; O'Connor, Kevin C.; Saubidet, Cristi?n Lopez; Alvarez, Paulino A.

2011-01-01

307

Monitoring of Nonsteroidal Immunosuppressive Drugs in Patients With Lung Disease and Lung Transplant Recipients  

PubMed Central

Objectives: Immunosuppressive pharmacologic agents prescribed to patients with diffuse interstitial and inflammatory lung disease and lung transplant recipients are associated with potential risks for adverse reactions. Strategies for minimizing such risks include administering these drugs according to established, safe protocols; monitoring to detect manifestations of toxicity; and patient education. Hence, an evidence-based guideline for physicians can improve safety and optimize the likelihood of a successful outcome. To maximize the likelihood that these agents will be used safely, the American College of Chest Physicians established a committee to examine the clinical evidence for the administration and monitoring of immunosuppressive drugs (with the exception of corticosteroids) to identify associated toxicities associated with each drug and appropriate protocols for monitoring these agents. Methods: Committee members developed and refined a series of questions about toxicities of immunosuppressives and current approaches to administration and monitoring. A systematic review was carried out by the American College of Chest Physicians. Committee members were supplied with this information and created this evidence-based guideline. Conclusions: It is hoped that these guidelines will improve patient safety when immunosuppressive drugs are given to lung transplant recipients and to patients with diffuse interstitial lung disease. PMID:23131960

Meyer, Keith C; Nathanson, Ian; Angel, Luis; Bhorade, Sangeeta M; Chan, Kevin M; Culver, Daniel; Harrod, Christopher G; Hayney, Mary S; Highland, Kristen B; Limper, Andrew H; Patrick, Herbert; Strange, Charlie; Whelan, Timothy

2012-01-01

308

Activation of PPAR? by Wy-14643 ameliorates systemic lipopolysaccharide-induced acute lung injury  

SciTech Connect

Highlights: •Activation of PPAR? attenuated LPS-mediated acute lung injury. •Pretreatment with Wy-14643 decreased the levels of IFN-? and IL-6 in ALI. •Nitrosative stress and lipid peroxidation were downregulated by PPAR? activation. •PPAR? agonists may be potential therapeutic targets for acute lung injury. -- Abstract: Acute lung injury (ALI) is a major cause of mortality and morbidity worldwide. The activation of peroxisome proliferator-activated receptor-? (PPAR?) by its ligands, which include Wy-14643, has been implicated as a potential anti-inflammatory therapy. To address the beneficial efficacy of Wy-14643 for ALI along with systemic inflammation, the in vivo role of PPAR? activation was investigated in a mouse model of lipopolysaccharide (LPS)-induced ALI. Using age-matched Ppara-null and wild-type mice, we demonstrate that the activation of PPAR? by Wy-14643 attenuated LPS-mediated ALI. This was evidenced histologically by the significant alleviation of inflammatory manifestations and apoptosis observed in the lung tissues of wild-type mice, but not in the corresponding Ppara-null mice. This protective effect probably resulted from the inhibition of LPS-induced increases in pro-inflammatory cytokines and nitroxidative stress levels. These results suggest that the pharmacological activation of PPAR? might have a therapeutic effect on LPS-induced ALI.

Yoo, Seong Ho, E-mail: yoosh@snu.ac.kr [Seoul National University Hospital, Biomedical Research Institute and Institute of Forensic Medicine, Seoul National University College of Medicine, Seoul (Korea, Republic of); Abdelmegeed, Mohamed A. [Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD (United States)] [Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD (United States); Song, Byoung-Joon, E-mail: bj.song@nih.gov [Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD (United States)] [Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD (United States)

2013-07-05

309

Relationship between occupations and asbestosfibre content of the lungs in patients with pleural mesothelioma, lung cancer, and other diseases  

PubMed Central

Whitwell, F., Scott, Jean, and Grimshaw, Myra (1977).Thorax, 32, 377-386. Relationship between occupations and asbestos-fibre content of the lungs in patients with pleural mesothelioma, lung cancer, and other diseases. The light-visible asbestos-fibre content of 300 lung specimens has been measured using a potash-digestion and phase-contrast microscopy technique, and the results have been correlated with the occupations of the patients. Among 100 pleural mesothelioma specimens were 88 where the patients had been exposed to asbestos, and in 73 of these (83%) the lung tissue contained over 100 000 asbestos fibres per gram of dried lung, and only one specimen showed less than 20 000 fibres per gram. When asbestosis was present, the lungs nearly always showed over 3 million fibres per gram. In 100 control lungs (those without industrial disease or lung cancer) there were less than 20 000 fibres per gram of dried lung in 71% of specimens. Lungs from 100 patients with lung cancer but no industrial disease contained less than 20 000 fibres per gram of dried lung in 80% of cases. Patients with parietal pleural plaques nearly all had over 20 000 fibres per gram in their lungs. The number of asbestos fibres found in the lungs was closely related to the occupations of the patients but not to their home environment. Patients who had lived near likely sources of atmospheric asbestos pollution did not have higher asbestos fibre counts than the rest of the patients. It is concluded that there is a definite dose relationship between asbestos exposure and mesothelioma formation but that' `sub-asbestosis' levels of asbestos exposure do not contribute to the formation of lung cancer in those not subjected to industrial asbestos exposure. Images PMID:929482

Whitwell, F.; Scott, Jean; Grimshaw, Myra

1977-01-01

310

Ultrasound-guided lung recruitment in a 3-month-old infant with acute respiratory distress syndrome.  

PubMed

The reversal of lung collapse is one of the challenges of lung injury prevention in pediatric acute respiratory distress syndrome. In this case, lung recruitment maneuver (RM) with positive end-expiratory pressure under computed tomography guidance is the procedure of choice, but cumulative ionizing radiation exposure is a major radiologic concern, especially in infants. Real-time guidance of lung recruitment under bedside lung ultrasound (US) assessment in adults has shown to be an effective procedure for performing RM that avoids ionizing radiation overexposure. We report a case of US-guided lung recruitment procedure applied in an infant with severe acute respiratory distress syndrome and advocate that the lung US-guided RM in infants is a feasible and safe procedure. PMID:25364957

Sameshima, Yoshino Tamaki; de Almeida, João Fernando Lourenço; Silva, Murilo Marques Almeida; Remondini, Renata; Haddad, Luciana Branco; Neto, Miguel José Francisco; Funari, Marcelo Buarque de Gusmão

2014-12-01

311

Self-reported prior lung diseases as risk factors for non-small cell lung cancer in Mexican Americans.  

PubMed

This study was conducted to assess the association between prior history of respiratory disease and lung cancer among Mexican Americans using data from a multi-racial/ethnic lung cancer case-control study. Cases (n = 204) were patients with previously untreated lung cancer. Healthy control participants (n = 325) were recruited from a large physician group practice. Demographics, cigarette use, and history of respiratory disease were collected. Multivariable logistic regression models were used to estimate relative risk. Prior history of COPD (OR = 2.0; 95 % CI 1.2-3.3) and pneumonia (OR = 2.2; 95 % CI 1.3-3.6) were associated with an increased risk of lung cancer. These findings illustrate that prior COPD and pneumonia are associated with an increased risk of lung cancer among Mexican Americans. To our knowledge, this is one of largest case-control analyses assessing the role of respiratory disease and lung cancer risk specifically among Mexican-Americans. PMID:22847640

McHugh, Michelle K; Schabath, Matthew B; Ho, Chung-Han; Liu, Mei; D'Amelio, Anthony M; Greisinger, Anthony J; Delclos, George L; Spitz, Margaret R; Etzel, Carol J

2013-10-01

312

Immunopathogenesis of severe acute respiratory disease in Zaire ebolavirus-infected pigs.  

PubMed

Ebola viruses (EBOV) are filamentous single-stranded RNA viruses of the family Filoviridae. Zaire ebolavirus (ZEBOV) causes severe haemorrhagic fever in humans, great apes and non-human primates (NHPs) with high fatality rates. In contrast, Reston ebolavirus (REBOV), the only species found outside Africa, is lethal to some NHPs but has never been linked to clinical disease in humans despite documented exposure. REBOV was isolated from pigs in the Philippines and subsequent experiments confirmed the susceptibility of pigs to both REBOV and ZEBOV with predilection for the lungs. However, only ZEBOV caused severe lung pathology in 5-6 weeks old pigs leading to respiratory distress. To further elucidate the mechanisms for lung pathology, microarray analysis of changes in gene expression was performed on lung tissue from ZEBOV-infected pigs. Furthermore, systemic effects were monitored by looking at changes in peripheral blood leukocyte subsets and systemic cytokine responses. Following oro-nasal challenge, ZEBOV replicated mainly in the respiratory tract, causing severe inflammation of the lungs and consequently rapid and difficult breathing. Neutrophils and macrophages infiltrated the lungs but only the latter were positive for ZEBOV antigen. Genes for proinflammatory cytokines, chemokines and acute phase proteins, known to attract immune cells to sites of infection, were upregulated in the lungs, causing the heavy influx of cells into this site. Systemic effects included a decline in the proportion of monocyte/dendritic and B cells and a mild proinflammatory cytokine response. Serum IgM was detected on day 5 and 6 post infection. In conclusion, a dysregulation/over-activation of the pulmonary proinflammatory response may play a crucial role in the pathogenesis of ZEBOV infection in 5-6 weeks old pigs by attracting inflammatory cells to the lungs. PMID:23626748

Nfon, Charles K; Leung, Anders; Smith, Greg; Embury-Hyatt, Carissa; Kobinger, Gary; Weingartl, Hana M

2013-01-01

313

Proteinase-activated receptor-1, CCL2, and CCL7 regulate acute neutrophilic lung inflammation.  

PubMed

PAR1 plays a central role in mediating the interplay between coagulation and inflammation, but its role in regulating acute neutrophilic inflammation is unknown. We report that antagonism of PAR1 was highly effective at reducing acute neutrophil accumulation in a mouse model of LPS-induced lung inflammation. PAR1 antagonism also reduced alveolar-capillary barrier disruption in these mice. This protection was associated with a reduction in the expression of the chemokines, CCL2 and CCL7, but not the proinflammatory cytokines, TNF and IL-6, or the classic neutrophil chemoattractants, CXCL1 and CXCL2. Antibody neutralization of CCL2 and CCL7 significantly reduced LPS-induced total leukocyte and neutrophil accumulation, recovered from the bronchoalveolar lavage fluid of challenged mice. Immunohistochemical analysis revealed that CCL2 predominantly localized to alveolar macrophages and pulmonary epithelial cells, whereas CCL7 was restricted to the pulmonary epithelium. In keeping with these observations, the intranasal administration of recombinant CCL2 (rCCL2) and rCCL7 led to the accumulation of neutrophils within the lung airspaces of naive mice in the absence of any underlying inflammation. Flow cytometry analysis further demonstrated an increase in Ly6G(hi) neutrophils expressing the chemokine receptors, CCR1 and CCR2, isolated from mouse lungs compared with circulating neutrophils. Conversely, the expression of CXCR2 decreased on neutrophils isolated from the lung compared with circulating neutrophils. Furthermore, this switch in chemokine receptor expression was accentuated after acute LPS-induced lung inflammation. Collectively, these findings reveal a novel role for PAR1 and the chemokines, CCL2 and CCL7, during the early events of acute neutrophilic inflammation. PMID:23972264

Mercer, Paul F; Williams, Andrew E; Scotton, Christopher J; José, Ricardo J; Sulikowski, Michal; Moffatt, James D; Murray, Lynne A; Chambers, Rachel C

2014-01-01

314

Persistent activation of an innate immune response translates respiratory viral infection into chronic lung disease  

Microsoft Academic Search

To understand the pathogenesis of chronic inflammatory disease, we analyzed an experimental mouse model of chronic lung disease with pathology that resembles asthma and chronic obstructive pulmonary disease (COPD) in humans. In this model, chronic lung disease develops after an infection with a common type of respiratory virus is cleared to only trace levels of noninfectious virus. Chronic inflammatory disease

Edy Y Kim; John T Battaile; Anand C Patel; Yingjian You; Eugene Agapov; Mitchell H Grayson; Loralyn A Benoit; Derek E Byers; Yael Alevy; Jennifer Tucker; Suzanne Swanson; Rose Tidwell; Jeffrey W Tyner; Jeffrey D Morton; Mario Castro; Deepika Polineni; G Alexander Patterson; Reto A Schwendener; John D Allard; Gary Peltz; Michael J Holtzman

2008-01-01

315

Vitamin D Deficiency and the Lung: Disease Initiator or Disease Modifier?  

PubMed Central

Vitamin D deficiency is a global public health problem and has been associated with an increased incidence and severity of many diseases including diseases of the respiratory system. These associations have largely been demonstrated epidemiologically and have formed the basis of the justification for a large number of clinical supplementation trials with a view to improving disease outcomes. However, the trials that have been completed to date and the ongoing experimental studies that have attempted to demonstrate a mechanistic link between vitamin D deficiency and lung disease have been disappointing. This observation raises many questions regarding whether vitamin D deficiency is truly associated with disease pathogenesis, is only important in the exacerbation of disease or is simply an indirect biomarker of other disease mechanisms? In this review, we will briefly summarize our current understanding of the role of vitamin D in these processes with a focus on lung disease. PMID:23896653

Foong, Rachel E.; Zosky, Graeme R.

2013-01-01

316

Translational toxicological research: investigating and preventing acute lung injury in organophosphorus insecticide poisoning.  

PubMed

Poisoning through ingestion of organophosphorus (OP) insecticide is a leading cause of suicide globally. Severe poisoning with OP compounds creates an unconscious, paralysed patient with respiratory failure. These symptoms make pulmonary aspiration of stomach contents highly likely, potentially causing an acute lung injury. To explore this hypothesis, we created a Gottingen minipig pulmonary aspiration model (n=26) to investigate the mechanism and severity of lung injury created through pulmonary instillation of 0.5?mL/kg mixtures of porcine gastric juice (GJ), OP and/or its solvent. Early results show that aspiration of OP and GJ causes pulmonary neutrophil sequestration, alveolar haemorrhage and interstitial oedema, with disruption of the alveolar-capillary membrane. Further measurements will include quantitative CT imaging, histopathology scoring, acute lung injury biomarkers and respiratory function. In order to test the validity of the minipig model, a pilot study in Sri Lanka has been devised to observe signs of lung injury in human patients who have ingested OP insecticide with or without clinical evidence of pulmonary aspiration. Lung injury will be assessed with PaO2/FIO2 ratios and physiological dead space measurement. Blood, bronchoalveolar lavage and urine will be taken at 24 and 48?h after poisoning and at 3-4?h in surgical control patients to measure acute lung injury biomarkers. An unpublished toxicology study from Sri Lanka, 2011-2012, showed that over 40% of unconscious poisoned patients with a GCS <9 were not intubated for ambulance transfer between rural and district hospitals. Delay in intubation leads to aspiration pneumonitis and pneumonia in 38%-45% of unconscious poisoned patients. We hypothesise that non-drug assisted placement of supraglottic airways may be a good tool for use in unconscious poisoned patients requiring transfer from small rural hospitals in Asia. They could confer better airway protection than no airway intervention and reduce both morbidity and mortality. PMID:24351316

Hulse, Elspeth J; Clutton, R E; Drummond, G; Eddleston, M

2014-06-01

317

Inhaled hydrogen sulfide protects against lipopolysaccharide-induced acute lung injury in mice  

PubMed Central

Background Local pulmonary and systemic infections can lead to acute lung injury (ALI). The resulting lung damage can evoke lung failure and multiple organ dysfunction associated with increased mortality. Hydrogen sulfide (H2S) appears to represent a new therapeutic approach to ALI. The gas has been shown to mediate potent anti-inflammatory and organ protective effects in vivo. This study was designed to define its potentially protective role in sepsis-induced lung injury. Methods C57BL/6 N mice received lipopolysaccharide (LPS) intranasally in the absence or presence of 80 parts per million H2S. After 6 h, acute lung injury was determined by comparative histology. Bronchoalveolar lavage (BAL) fluid was analyzed for total protein content and differential cell counting. BAL and serum were further analyzed for interleukin-1?, macrophage inflammatory protein-2, and/or myeloperoxidase glycoprotein levels by enzyme-linked immunosorbent assays. Differences between groups were analyzed by one way analysis of variance. Results Histological analysis revealed that LPS instillation led to increased alveolar wall thickening, cellular infiltration, and to an elevated ALI score. In the presence of H2S these changes were not observed despite LPS treatment. Moreover, neutrophil influx, and pro-inflammatory cytokine release were enhanced in BAL fluid of LPS-treated mice, but comparable to control levels in H2S treated mice. In addition, myeloperoxidase levels were increased in serum after LPS challenge and this was prevented by H2S inhalation. Conclusion Inhalation of hydrogen sulfide protects against LPS-induced acute lung injury by attenuating pro-inflammatory responses. PMID:23025523

2012-01-01

318

Acquired Cell-Mediated Immunodepression in Acute Chagas' Disease  

PubMed Central

In this study two groups of patients with acute Chagas' disease were identified. Group one consisted of five patients with apparent acute Chagas' disease. These patients showed symptoms and signals of an acute illness, such as high fever and enlarged spleen. One of these patients developed severe myocarditis and heart failure. Group two consisted of seven patients with inapparent acute Chagas' disease. This was a nonclinical entity, not perceived by the patient who did not seek medical care. The diagnosis was made by the shift of a serologic test which indicates the presence of immunoglobulin M antibodies to Trypanosoma cruzi. The patients with apparent acute Chagas' disease showed positive delayed-type skin response to T. cruzi antigen. Also, their leukocytes showed significant inhibition of migration in the presence of this antigen. By contrast, the patients with the inapparent acute Chagas' disease did not show positive delayed-type skin response to T. cruzi antigen and no significant inhibition was observed when their cells migrated in the presence of this antigen. Of interest, none of these patients was capable of developing contact sensitivity to 2,4-dinitrochlorobenzene. However, three out of five patients with the apparent acute disease and all the normal control subjects showed positive contact reaction after sensitization to this drug. The results of these experiments would suggest that the thymus-derived (T)-lymphocyte function is depressed in patients with the clinically inapparent acute Chagas' disease. This immunodepression seems to be acquired in the course of the T. cruzi infection because all patients showed positive delayed-type skin response to at least one ubiquitous microbial extract, thus indicating previously normal T-cell function. We hypothesize that T. cruzi antigens may directly stimulate T cells with the concomitant release of factors that might become supressive for T-cell responses. Furthermore, the suppressive effect might interfere with the T-cell response to other antigens, such as to 2,4-dinitrochlorobenzene. Images PMID:107195

Teixeira, Antonio R. L.; Teixeira, Gloria; Macedo, Vanize; Prata, Aluizio

1978-01-01

319

Acquired cell-mediated immunodepression in acute Chagas' disease.  

PubMed

In this study two groups of patients with acute Chagas' disease were identified. Group one consisted of five patients with apparent acute Chagas' disease. These patients showed symptoms and signals of an acute illness, such as high fever and enlarged spleen. One of these patients developed severe myocarditis and heart failure. Group two consisted of seven patients with inapparent acute Chagas' disease. This was a nonclinical entity, not perceived by the patient who did not seek medical care. The diagnosis was made by the shift of a serologic test which indicates the presence of immunoglobulin M antibodies to Trypanosoma cruzi. The patients with apparent acute Chagas' disease showed positive delayed-type skin response to T. cruzi antigen. Also, their leukocytes showed significant inhibition of migration in the presence of this antigen. By contrast, the patients with the inapparent acute Chagas' disease did not show positive delayed-type skin response to T. cruzi antigen and no significant inhibition was observed when their cells migrated in the presence of this antigen. Of interest, none of these patients was capable of developing contact sensitivity to 2,4-dinitrochlorobenzene. However, three out of five patients with the apparent acute disease and all the normal control subjects showed positive contact reaction after sensitization to this drug. The results of these experiments would suggest that the thymus-derived (T)-lymphocyte function is depressed in patients with the clinically inapparent acute Chagas' disease. This immunodepression seems to be acquired in the course of the T. cruzi infection because all patients showed positive delayed-type skin response to at least one ubiquitous microbial extract, thus indicating previously normal T-cell function. We hypothesize that T. cruzi antigens may directly stimulate T cells with the concomitant release of factors that might become supressive for T-cell responses. Furthermore, the suppressive effect might interfere with the T-cell response to other antigens, such as to 2,4-dinitrochlorobenzene. PMID:107195

Teixeira, A R; Teixeira, G; Macêdo, V; Prata, A

1978-12-01

320

Eosinophilic lung disease: immunological studies of blood and alveolar eosinophils.  

PubMed Central

Five patients with eosinophilic lung diseases and blood hypereosinophilia (PIE syndrome) were investigated clinically and by bronchoalveolar lavage (BAL). Comparative studies on blood and alveolar eosinophils were carried out after purification and selection of eosinophil subpopulations according to their density. A predominant 'hypodense' alveolar eosinophil population was found in BAL fluids of active chronic eosinophilic pneumonia (CEP). In addition, supernatants of alveolar macrophages obtained from CEP are able to enhance spontaneously the generation of eosinophil oxygen metabolites. Such eosinophil stimulation emphasizes a probable tissue cell cooperation. In addition, BAL permitted the study of membrane immunological markers on eosinophilic inflammatory cells endowed with migratory properties. An increase in eosinophils carrying surface IgE was demonstrated in alveolar cells from PIE Syndrome particularly with hypodense eosinophils from CEP patients. Although no specific stimulus is known at the present time, this work underlines the potential implication of IgE-mediated hypersensitivity processes in the pathogenesis of eosinophilic lung diseases. PMID:3955885

Prin, L; Capron, M; Gosset, P; Wallaert, B; Kusnierz, J P; Bletry, O; Tonnel, A B; Capron, A

1986-01-01

321

Cytokine levels in pleural fluid as markers of acute rejection after lung transplantation*  

PubMed Central

Our objective was to determine the levels of lactate dehydrogenase, IL-6, IL-8, and VEGF, as well as the total and differential cell counts, in the pleural fluid of lung transplant recipients, correlating those levels with the occurrence and severity of rejection. We analyzed pleural fluid samples collected from 18 patients at various time points (up to postoperative day 4). The levels of IL-6, IL-8, and VEGF tended to elevate in parallel with increases in the severity of rejection. Our results suggest that these levels are markers of acute graft rejection in lung transplant recipients. PMID:25210966

de Camargo, Priscila Cilene Leon Bueno; Afonso, Jose Eduardo; Samano, Marcos Naoyuki; Acencio, Milena Marques Pagliarelli; Antonangelo, Leila; Teixeira, Ricardo Henrique de Oliveira Braga

2014-01-01

322

Mechanisms of Indirect Acute Lung Injury: A Novel Role for the Co-Inhibitory Receptor, Programmed Death-1 (PD-1)  

PubMed Central

Objective To determine the contribution of PD-1 in the morbidity and mortality associated with the development of indirect-acute lung injury Summary Background Data The immune cell interaction(s) leading to indirect-acute lung injury are not completely understood. In this respect, while we have recently shown that the murine cell surface co-inhibitory receptor, Programmed Cell death receptor (PD)-1, has a role in septic morbidity/mortality that is mediated in part through the effects on the innate immune arm. However, it is not know if PD-1 has a role in the development of indirect-acute lung injury and how this may be mediated at a cellular level. Methods PD-1 ?/? mice were used in a murine model of indirect-acute lung injury (hemorrhagic shock followed 24 h after with cecal ligation & puncture-septic challenge) and compared to wild type controls. Groups were initially compared for survival and subsequently for markers of pulmonary inflammation, influx of lymphocytes and neutrophils, and expression of PD-1 and its ligand, PD-L1. In addition, peripheral blood leukocytes of patients with indirect-acute lung injury were examined to assess changes in cellular PD-1 expression relative to mortality. Results PD-1 ?/? mice showed improved survival compared to wild type controls. In the mouse lung, CD4+, CD11c+ and Gr-1+ cells showed increased PD-1 expression in response to indirect-acute lung injury. However, while the rise in BAL fluid protein concentrations, lung IL-6, and lung MCP-1 were similar between PD-1 ?/? and wild type animals subjected to indirect acute lung injury, the PD-1 ?/? animals that were subjected to shock/septic challenge had reduced CD4:CD8 ratios, TNF-? levels, MPO activity, and caspase 3 levels in the lung. Comparatively, we observed that humans, who survived their acute lung injury, had significantly lower expression of PD-1 on T cells. Conclusions PD-1 expression contributes to mortality following the induction of indirect-acute lung injury and this appears to be associated with modifications in the cellular and cytokine profiles in the lung. PMID:21997806

Monaghan, Sean F.; Thakkar, Rajan K.; Heffernan, Daithi S.; Huang, Xin; Chung, Chun-Shiang; Lomas-Neira, Joanne; Cioffi, William G.; Ayala, Alfred

2011-01-01

323

Lung Regional Metabolic Activity and Gas Volume Changes Induced by Tidal Ventilation in Patients with Acute Lung Injury  

PubMed Central

Rationale: During acute lung injury (ALI), mechanical ventilation can aggravate inflammation by promoting alveolar distension and cyclic recruitment–derecruitment. As an estimate of the intensity of inflammation, metabolic activity can be measured by positron emission tomography imaging of [18F]fluoro-2-deoxy-D-glucose. Objectives: To assess the relationship between gas volume changes induced by tidal ventilation and pulmonary metabolic activity in patients with ALI. Methods: In 13 mechanically ventilated patients with ALI and relatively high positive end-expiratory pressure, we performed a positron emission tomography scan of the chest and three computed tomography scans: at mean airway pressure, end-expiration, and end-inspiration. Metabolic activity was measured from the [18F]fluoro-2-deoxy-D-glucose uptake rate. The computed tomography scans were used to classify lung regions as derecruited throughout the respiratory cycle, undergoing recruitment–derecruitment, and normally aerated. Measurements and Main Results: Metabolic activity of normally aerated lung was positively correlated both with plateau pressure, showing a pronounced increase above 26 to 27 cm H2O, and with regional Vt normalized by end-expiratory lung gas volume. This relationship did not appear to be caused by a higher underlying parenchymal metabolic activity in patients with higher plateau pressure. Regions undergoing cyclic recruitment–derecruitment did not have higher metabolic activity than those collapsed throughout the respiratory cycle. Conclusions: In patients with ALI managed with relatively high end-expiratory pressure, metabolic activity of aerated regions was associated with both plateau pressure and regional Vt normalized by end-expiratory lung gas volume, whereas no association was found between cyclic recruitment–derecruitment and increased metabolic activity. PMID:21257791

Bellani, Giacomo; Guerra, Luca; Musch, Guido; Zanella, Alberto; Patroniti, Nicolo; Mauri, Tommaso; Messa, Cristina; Pesenti, Antonio

2011-01-01

324

Lung Dendritic Cells: Targets for Therapy in Allergic Disease  

Microsoft Academic Search

Dendritic cells (DCs) are crucial in determining the functional outcome of allergen encounter in the lung. Antigen presentation\\u000a by myeloid DCs leads to Th2 sensitization typical of allergic disease, whereas antigen presentation by plas-macytoid DCs serves\\u000a to dampen inflammation. It is increasingly clear that DCs have an antigen presenting function beyond sensitisation. DCs therefore\\u000a constitute a novel target for the

Bart N. Lambrecht; Hamida Hammad

325

Childhood Interstitial Lung Diseases: An 18-year Retrospective Analysis  

PubMed Central

OBJECTIVE: Childhood interstitial lung diseases (ILD) occur in a variety of clinical contexts. Advances in the understanding of disease pathogenesis and use of standardized terminology have facilitated increased case ascertainment. However, as all studies have been performed at specialized referral centers, the applicability of these findings to general pulmonary practice has been uncertain. The objective of this study was to determine the historical occurrence of childhood ILD to provide information reflecting general pediatric pulmonary practice patterns. METHODS: Childhood ILD cases seen at Vanderbilt Children’s Hospital from 1994 to 2011 were retrospectively reviewed and classified according to the current pediatric diffuse lung disease histopathologic classification system. RESULTS: A total of 93 cases were identified, of which 91.4% were classifiable. A total of 68.8% (64/93) of subjects underwent lung biopsy in their evaluations. The largest classification categories were disorders related to systemic disease processes (24.7%), disorders of the immunocompromised host (24.7%), and disorders more prevalent in infancy (22.6%). Eight cases of neuroendocrine cell hyperplasia of infancy (NEHI) were identified, including 5 that were previously unrecognized before this review. CONCLUSIONS: Our findings demonstrate the general scope of childhood ILD and that these cases present within a variety of pediatric subspecialties. Retrospective review was valuable in recognizing more recently described forms of childhood ILD. As a significant portion of cases were classifiable based on clinical, genetic, and/or radiographic criteria, we urge greater consideration to noninvasive diagnostic approaches and suggest modification to the current childhood ILD classification scheme to accommodate the increasing number of cases diagnosed without lung biopsy. PMID:24081995

Soares, Jennifer J.; Deutsch, Gail H.; Moore, Paul E.; Fazili, Mohammad F.; Austin, Eric D.; Brown, Rebekah F.; Sokolow, Andrew G.; Hilmes, Melissa A.

2013-01-01

326

Supportive and Palliative Care of Advanced Nonmalignant Lung Disease  

Microsoft Academic Search

Supportive and palliative care is an interdisciplinary challenge with the aims of symptom relief and improvement of quality of life in end-stage patients. Main complaints of patients with advanced nonmalignant lung disease are depression and anxiety, dyspnea, pain, and coughing. The discomfort of many physicians, caregivers, and family members with discussions about end-of-life care is one obstacle for the timely

Michael Kreuter; Felix J. F. Herth

2011-01-01

327

Method Of Treating Silicosis And Other Occupational Lung Diseases  

Cancer.gov

The inhalation of dust containing crystalline silica particles causes silicosis, an incurable lung disease that progresses even after dust exposure ceases. Over a million US workers are exposed to silica dust annually, and thousands worldwide die each year from silicosis. The pulmonary inflammation caused by silica inhalation is characterized by a cellular infiltrate and the accumulation of chemokines, cytokines, and Reactive Oxygen Species (ROS) in bronchoalveolar lavage fluid.

328

Vitamin D to prevent acute lung injury following oesophagectomy (VINDALOO): study protocol for a randomised placebo controlled trial  

PubMed Central

Background Acute lung injury occurs in approximately 25% to 30% of subjects undergoing oesophagectomy. Experimental studies suggest that treatment with vitamin D may prevent the development of acute lung injury by decreasing inflammatory cytokine release, enhancing lung epithelial repair and protecting alveolar capillary barrier function. Methods/Design The ‘Vitamin D to prevent lung injury following oesophagectomy trial’ is a multi-centre, randomised, double-blind, placebo-controlled trial. The aim of the trial is to determine in patients undergoing elective transthoracic oesophagectomy, if pre-treatment with a single oral dose of vitamin D3 (300,000 IU (7.5 mg) cholecalciferol in oily solution administered seven days pre-operatively) compared to placebo affects biomarkers of early acute lung injury and other clinical outcomes. The primary outcome will be change in extravascular lung water index measured by PiCCO® transpulmonary thermodilution catheter at the end of the oesophagectomy. The trial secondary outcomes are clinical markers indicative of lung injury: PaO2:FiO2 ratio, oxygenation index; development of acute lung injury to day 28; duration of ventilation and organ failure; survival; safety and tolerability of vitamin D supplementation; plasma indices of endothelial and alveolar epithelial function/injury, plasma inflammatory response and plasma vitamin D status. The study aims to recruit 80 patients from three UK centres. Discussion This study will ascertain whether vitamin D replacement alters biomarkers of lung damage following oesophagectomy. Trial registration Current Controlled Trials ISRCTN27673620 PMID:23782429

2013-01-01

329

Ulinastatin reduces pathogenesis of phosgene-induced acute lung injury in rats.  

PubMed

Phosgene (CG) is an industrial chemical used to make plastics, rubbers, dyestuff, and pesticides. Although the inhalation of CG is relatively uncommon, its accidental exposure can lead to acute lung injury (ALI). Ulinastatin, a urinary trypsin inhibitor, has been emerged to use for the treatment of acute inflammatory state of a number of organs including the lung. In this study, we examined the pathogenic changes in the lungs after the inhalation of CG gas and also examined the effect of ulinastatin treatment in reversing these changes in rats. We found that the rats exposed to CG gas at a dose of 5.0 g/m(3) for 5 min led to ALI after 6 h. The signs of lung injury include pulmonary edema, hemorrhage, and cellular infiltration in pulmonary alveoli. In addition, interleukin-15 (IL-15) and intercellular adhesion molecule-1 (ICAM-1) were significantly increased in CG-inhaled animals. Ulinastatin administration at 1 h postexposure significantly reduced the intensity of all the pathological changes in the lungs of these CG-exposed animals. Ulinastatin at a dose of 400 U/g was shown to decrease the total number of cells in bronchoalveolar lavage fluid and the levels of IL-15 and ICAM-1 in the serum. We also found that the structure of the lung was protected by ulinastatin treatment. Thus, our data suggest that ulinastatin can be used as an effective drug for the treatment of CG-induced ALI. The serum levels of IL-15 and ICAM-1 can be used as the markers of lung injury after exposure to CG and may also serve as useful therapeutic targets at an early stage. The effects of long-term treatment of ulinastatin and the mechanisms by which ulinastatin decreases the infiltration of blood cells and reduces cytokines need further investigation. PMID:23075575

Shen, Jie; Gan, Zhengyi; Zhao, Jie; Zhang, Liming; Xu, Guoxiong

2014-10-01

330

BURN-INDUCED ACUTE LUNG INJURY REQUIRES A FUNCTIONAL TOLL-LIKE RECEPTOR 4  

PubMed Central

The role of the Toll-like receptor 4 (TLR4), a component of the innate immune system, in the development of burn-induced acute lung injury (ALI) has not been completely defined. Recent data suggested that an intact TLR4 plays a major role in the development of organ injury in sterile inflammation. We hypothesized that burn-induced ALI is a TLR4-dependent process. Male C57BL/6J (TLR4 wild-type [WT]) and C57BL/10ScN (TLR4 knockout [KO]) mice were subjected to a 30% total body surface area steam burn. Animals were killed at 6 and 24 h after the insult. Lung specimens were harvested for histological examination after hematoxylin-eosin staining. In addition, lung myeloperoxidase (MPO) and intercellular adhesion molecule 1 immunostaining was performed. Lung MPO was measured by an enzymatic assay. Total lung keratinocyte-derived chemoattractant (IL-8) content was measured by enzyme-linked immunosorbent assay. Western blot was performed to quantify phosphorylated I?B?, phosphorylated nuclear factor ?B p65 (NF-?Bp65), and high mobility group box 1 expression. Acute lung injury, characterized by thickening of the alveolar-capillary membrane, hyaline membrane formation, intraalveolar hemorrhage, and neutrophil infiltration, was seen in WT but not KO animals at 24 h. Myeloperoxidase and intercellular adhesion molecule 1 immunostaining of KO animals was also similar to sham but elevated in WT animals. In addition, a reduction in MPO enzymatic activity was observed in KO mice as well as a reduction in IL-8 levels compared with their WT counterparts. Burn-induced ALI develops within 24 h after the initial thermal insult in our model. Toll-like receptor 4 KO animals were clearly protected and had a much less severe lung injury. Our data suggest that burn-induced ALI is a TLR4-dependent process. PMID:21330948

Krzyzaniak, Michael; Cheadle, Gerald; Peterson, Carrie; Loomis, William; Putnam, James; Wolf, Paul; Baird, Andrew; Eliceiri, Brian; Bansal, Vishal; Coimbra, Raul

2014-01-01

331

Expression of adhesion molecules in allergic lung diseases.  

PubMed

Endothelial adherence and migration of leukocytes into tissue is mediated by different sets of adhesion molecules. The expression of these sets might not only preselect the types of leukocytes that enter the inflammatory sites, but also activate these leukocytes, induce adherence to epithelial cells, and cause the release of cytokines. Atopic asthma, extrinsic allergic alveolitis, and sarcoidosis as examples of immunologic lung diseases were investigated for the expression of adhesion molecules. Bronchial biopsies in chronic obstructive lung disease (COPD) and resected lung tissue of juvenile emphysema were chosen for controls. Immunohistochemistry was done on sections from bronchial and transbronchial biopsies and on smears from bronchoalveolar lavage cells. In all three types of immune disorders, lymphocytes expressed the integrins alpha4/beta1 (VLA4) and ICAM3, whereas lymphocytes in COPD bronchitis and in emphysema controls were unreactive. Eosinophils in atopic asthma bronchitis in contrast to COPD bronchitis also expressed both VLA4 and ICAM3. The expression of VCAM1 on endothelial cells was only seen in atopic asthma and was related to disease activity. The expression of other adhesion molecules was nonspecific. Expression of VCAM1 on endothelial cells and its ligand VLA4 on lymphocytes and eosinophils seems to be a specific event in atopic asthma. Expression of VLA4 and ICAM3 on lymphocytes, however, might be a specific event in all three immune reactions. PMID:11964048

Popper, Helmut H; Pailer, Sabine; Wurzinger, Gerd; Feldner, Herwig; Hesse, Christian; Eber, Eva

2002-02-01

332

From Neurogenic Pulmonary Edema to Fat Embolism Syndrome: A Brief Review of Experimental and Clinical Investigations of Acute Lung Injury and Acute Respiratory Distress Syndrome  

Microsoft Academic Search

Acute respiratory distress syndrome (ARDS) is the most devastating form of acute lung injury (ALI) or pulmonary edema (PE). We presented the experimental studies and clinical investigations of two serious forms of ALI. Drastic and severe PE could be induced by intracranial hypertension or cerebral compression (CC). The CC-induced PE was attributed to overactivation of the medullary sympathetic mechanism. Sympathetic

Hsing I Chen

333

The role of the lung microbiome in health and disease. A National Heart, Lung, and Blood Institute workshop report.  

PubMed

Study of the human lung microbiome in the context of pulmonary health and disease is an area of emerging research interest that is being driven by several contributing factors. These factors include increased recognition of the diversity of human-associated microbiota, their roles in health and in diseases associated with chronic inflammation, and advancements in technologies and tools that have facilitated such discoveries about the microbiota in organ systems outside of the lung. Therefore, the overarching goals of lung microbiome research are: to identify and characterize microbial populations associated with the respiratory tract and lungs; to understand their roles in lung health and disease; and, we hope, to allow the development of improved approaches for diagnosing and treating chronic respiratory diseases in which the microbiome has a role. Recent studies of the lung microbiome have yielded a number of interesting findings but also highlighted questions and challenges for researchers and clinicians. In December 2011, the National Heart, Lung, and Blood Institute convened a workshop to identify key issues and areas for further attention or development to advance research on the lung microbiome. Current knowledge and the state of research on the lung and related areas of human microbiome investigation were reviewed and discussed. PMID:23614695

Huang, Yvonne J; Charlson, Emily S; Collman, Ronald G; Colombini-Hatch, Sandra; Martinez, Fernando D; Senior, Robert M

2013-06-15

334

Lung cyst: an unusual manifestation of Niemann-Pick disease.  

PubMed

Niemann-Pick disease is a rare inherited autosomal recessive disorder, currently classified into six subtypes and characterized by the intracellular accumulation of sphingomyelin in the liver, spleen, lungs, bone marrow or brain. The main pulmonary abnormalities described in high-resolution computed tomography (HRCT) of the chest consist of thickening of the interlobular septa and ground-glass opacities. This case report describes a patient with subtype B Niemann-Pick disease characterized by cysts and ground-glass opacities that were detected on HRCT of the chest. PMID:18699809

Baldi, Bruno G; Santana, Alfredo N C; Takagaki, Teresa Y; Fujita, Carmem; Kairalla, Ronaldo A; Carvalho, Carlos R R

2009-01-01

335

Value of Spirometry in Detecting Volume Restriction in Interstitial Lung Disease Patients  

Microsoft Academic Search

Background: Restriction is a typical functional abnormality in interstitial lung disease (ILD) patients, but is not always present, especially in the early stage of the disease. The greater reduction of vital capacity (VC; %pred.) than total lung capacity (TLC; %pred.) is regarded as a typical pattern of lung function disturbances in ILD patients. Study Objectives: To explore the diagnostic value

Piotr W. Boros; Monika Franczuk; Stefan Wesolowski

2004-01-01

336

Functionalized single-walled carbon nanotubes cause reversible acute lung injury and induce fibrosis in mice.  

PubMed

Nanotechnology is one of today's most promising technological developments, but safety concerns raise questions about its development. Risk assessments of nanomaterials during occupational exposure are crucial for their development. Here, we assessed the lung toxicity of functionalized single-walled carbon nanotube (f-SWCNT) exposure in C57BL/6 mice, elucidated the underlying molecular mechanism, and evaluated the self-repair ability and lung fibrosis of the mice. Soluble f-SWCNTs were administered to mice. After 18 h or 14 days, the lung histopathology, bronchoalveolar lavage fluid, lung edema, vascular permeability, and PaO(2) levels were evaluated, and biochemical and immunostaining tests were also performed. We found that some f-SWCNTs could induce acute lung injury (ALI) in mice via proinflammatory cytokine storm signaling through the NF-?B pathway in vivo. We illustrated that corticosteroid treatments could ameliorate the ALI induced by the f-SWCNTs in mice. Surprisingly, the ALI was almost completely reversed within 14 days, while mild to moderate fibrosis, granuloma, and DNA damage remained in the mice at day 14. Our studies indicate potential remedies to address the growing concerns about the safety of nanomaterials. In addition, we notify that the type of functional groups should be considered in nanomedicine application as differently functionalized SWCNTs generated different effects on the lung toxicity. PMID:22878607

Zhang, Yanli; Deng, Jiejie; Zhang, Yanxu; Guo, Feng; Li, Chenggang; Zou, Zhen; Xi, Wen; Tang, Jun; Sun, Yang; Yang, Peng; Han, Zongsheng; Li, Dangsheng; Jiang, Chengyu

2013-01-01

337

Interstitial lung disease in patients with non-small-cell lung cancer treated with epidermal growth factor receptor inhibitors  

Microsoft Academic Search

Interstitial lung disease (ILD) refers to a diverse range of pulmonary fibrotic disorders and may be hard to accurately diagnose,\\u000a as distinguishing it from other pulmonary diseases can be difficult. Estimations of the incidence in populations are confounded\\u000a by the complexity of the different forms of the disorder. In addition, ILD is a comorbid disease of lung cancer and is

Masahiro Tsuboi; Thierry Le Chevalier

2006-01-01

338

Mesenchymal stem cells in acute lung injury: are they ready for translational medicine?  

PubMed Central

Acute lung injury (ALI) is a severe clinical condition responsible for high mortality and the development of multiple organ dysfunctions, because of the lack of specific and effective therapies for ALI. Increasing evidence from pre-clinical studies supports preventive and therapeutic effects of mesenchymal stem cells (MSCs, also called mesenchymal stromal cells) in ALI/ARDS (acute respiratory distress syndrome). Therapeutic effects of MSCs were noticed in various delivery approaches (systemic, local, or other locations), multiple origins (bone marrow or other tissues), or different schedules of administrations (before or after the challenges). MSCs could reduce the over-production of inflammatory mediators, leucocyte infiltration, tissue injury and pulmonary failure, and produce a number of benefit factors through interaction with other cells in the process of lung tissue repair. Thus, it is necessary to establish guidelines, standard operating procedures and evaluation criteria for translating MSC-based therapies into clinical application for patients with ALI. PMID:23834470

Xu, Feng; Hu, Yue; Zhou, Jiebai; Wang, Xiangdong

2013-01-01

339

Cerebrospinal Fluid Proteome of Patients with Acute Lyme Disease  

SciTech Connect

Acute Lyme disease results from transmission of and infection by the bacterium Borrelia burgdorferi following a tick bite. During acute infection, bacteria can disseminate to the central nervous system (CNS) leading to the development of Lyme meningitis. Here we have analyzed pooled cerebrospinal fluid (CSF) allowing for a deep view into the proteome for a cohort of patients with early-disseminated Lyme disease and CSF inflammation leading to the identification of proteins that reflect host responses, which are distinct for subjects with acute Lyme disease. Additionally, we analyzed individual patient samples and quantified changes in protein abundance employing label-free quantitative mass spectrometry based methods. The measured changes in protein abundances reflect the impact of acute Lyme disease on the CNS as presented in CSF. We have identified 89 proteins that differ significantly in abundance in patients with acute Lyme disease. A number of the differentially abundant proteins have been found to be localized to brain synapse and thus constitute important leads for better understanding of the neurological consequence of disseminated Lyme disease.

Angel, Thomas E.; Jacobs, Jon M.; Smith, Robert P.; Pasternack, Mark S.; Elias, Susan; Gritsenko, Marina A.; Shukla, Anil K.; Gilmore, Edward C.; McCarthy, Carol; Camp, David G.; Smith, Richard D.

2012-10-05

340

Mismatches at the HLA-DR and HLA-B Loci Are Risk Factors for Acute Rejection after Lung Transplantation  

Microsoft Academic Search

Early high-grade acute rejections (pathologic grade A2 or A3) in recipients of lung allografts are a major risk factor for the subsequent development of obliterative bronchiolitis (OB). We analyzed the risk factors for high-grade acute rejections in 152 recipients of single (100) or bilateral (52) lung al- lografts transplanted at our institution between 1990 and 1996. Using Kaplan-Meier product limit

LARRY L. SCHULMAN; ALAN D. WEINBERG; CARLTON M C GREGOR; MARK E. GALANTOWICZ; NICOLE M. SUCIU-FOCA; SILVIU ITESCU

1998-01-01

341

Impact of TREM-2 gene silencing on inflammatory response of endotoxin-induced acute lung injury in mice.  

PubMed

Acute lung injury (ALI) is one of the critical clinical respiratory diseases, of which infection is the main cause and the first risk factor. This study investigated the impact of triggering receptor of myeloid cells expression (TREM)-2 gene silencing on inflammatory response of endotoxin-induced ALI in mice. Lentivirus-mediated TREM-2-shRNA was transfected into healthy male C57BL/6 mice, and the lipopolysaccharide-induced ALI model was established. The immunohistochemistry, immunofluorescence, fluorescence quantitative PCR, western blot, and ELISA were applied to detect the pathological changes of lung tissue and expressions of TREM-2, tumor necrosis factor-? (TNF-?), and interleukin 10 (IL-10) in bronchoalveolar lavage fluid. The lentivirus group, saline control group, ALI model group, blank control group, and negative control group were set up at the same time. Results found that, in lentivirus group, the pathological change of lung tissue was significantly lighter than ALI model group (P < 0.05), and the expression of TREM-2 was significantly reduced compared with all control groups (P < 0.05). The levels of TNF-? and IL-10 were significantly increased than all control groups (P < 0.05), while above indexes in negative control group and blank control group showed no significant difference with ALI group (P > 0.05). This study indicates that TREM-2 has a protective effect on inflammatory response of endotoxin-induced ALI in mice, which has provided new potential targets for prevention and treatment of ALI. PMID:24916365

Liu, Dai; Dong, Yanting; Liu, Zhuola; Niu, Bo; Wang, Yaowei; Gao, Xiaoling

2014-09-01

342

Acute infectious bursal disease in poultry: A review  

Microsoft Academic Search

This review is focused on the acute form of infectious bursal disease (IBD) caused by very virulent IBD virus (vvIBDV). First described in Europe about 10 years ago, this new form of the disease has rapidly spread all over the world, causing dramatic losses; after a decade, it still represents a considerable threat to the poultry industry. Emergence of the

Thierry P. Van Den Berg

2000-01-01

343

Anti-apoptotic PTD–FNK protein suppresses lipopolysaccharide-induced acute lung injury in rats  

Microsoft Academic Search

The present study was aimed at clarifying the effects of an anti-apoptotic protein for modulating symptoms in acute lung injury (ALI). From Bcl-xL, a Bcl-2 family member, we constructed an artificial protein (FNK) and fused it with the protein transduction domain (PTD) of the HIV\\/Tat protein (PTD–FNK) to facilitate its permeation into cells. ALI was induced by intratracheal infusion of

He Chen; Lei Zhang; Zhanfeng Jin; Enjing Jin; Masakazu Fujiwara; Mohammad Ghazizadeh; Sadamitsu Asoh; Shigeo Ohta; Oichi Kawanami

2007-01-01

344

Preventive effect of Imperatorin on acute lung injury induced by lipopolysaccharide in mice.  

PubMed

Imperatorin, a linear furanocoumarin, has many pharmacological effects such as antibacterial, anti-inflammatory and antiviral effects. The purpose of this study was to investigate the effect of Imperatorin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. BALB/c mice were pretreated with Imperatorin 1h before LPS challenge. We found that the levels of tumor necrosis factor-? (TNF-?), interleukin-1? (IL-1?) and interleukin-6 (IL-6) in the bronchoalveolar lavage fluid (BALF) were decreased significantly, and the level of interleukin-10 (IL-10) was up-regulated 8h after Imperatorin treatment. Pretreatment with Imperatorin (15 or 30 mg/kg) decreased lung wet-to-dry weight (W/D) ratio, the number of inflammatory cells and myeloperoxidase (MPO) activities. Additionally, Imperatorin attenuated lung histopathological changes and significantly inhibited the phosphorylation of I?B, JNK, ERK and p38/MAPK. These findings demonstrate that Imperatorin protects against LPS-induced ALI in mice. PMID:22878138

Sun, Jingjing; Chi, Gefu; Soromou, Lanan Wassy; Chen, Na; Guan, Mingfeng; Wu, Qianchao; Wang, Dacheng; Li, Hongyu

2012-12-01

345

Acute lung injury following the use of granulocyte-macrophage colony-stimulating factor  

PubMed Central

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a hematopoietic growth factor with immunostimulatory effects that include the activation and priming of neutrophils. Neutrophils are an important part of the human immune system, yet they have been implicated in the pathogenesis of acute lung injury (ALI). GM-CSF has been found to increase the amount of activated neutrophils recruited to the lung tissue as well as to increase the life span of neutrophils leading to substantial lung tissue injury and the development of ALI. While, there have been few cases reported of ALI following GM-CSF, the experience reported here is the first of ALI subsequent to local administration of GM-CSF in a patient with significant pulmonary comorbidities. PMID:24459628

Kudlak, Kristina; DeMuro, Jonas P; Hanna, Adel F; Brem, Harold

2013-01-01

346

Analysis of regional compliance in a porcine model of acute lung injury.  

PubMed

Lung protective ventilation in acute lung injury (ALI) focuses on using low tidal volumes and adequate levels of positive end-expiratory pressure (PEEP). Identifying optimal pressure is difficult because pressure-volume (PV) relations differ regionally. Precise analysis demands local measurements of pressures and related alveolar morphologies. In a porcine model of surfactant depletion (n=24), we combined measuring static pressures with endoscopic microscopy and electrical impedance tomography (EIT) to examine regional PV loops and morphologic heterogeneities between healthy (control group; CON) and ALI lungs ventilated with low (LVT) or high tidal volumes (HVT). Quantification included indices for microscopy (Volume Air Index (VAI), Heterogeneity and Circularity Index), EIT analysis and calculation of regional compliances due to generated PV loops. We found that: (1) VAI decreased in lower lobe after ALI, (2) electrical impedance decreased in dorsal regions and (3) PV loops differed regionally. Further studies should prove the potentials of these techniques on individual respiratory settings and clinical outcome. PMID:22820182

Czaplik, Michael; Biener, Ingeborg; Dembinski, Rolf; Pelosi, Paolo; Soodt, Thomas; Schroeder, Wolfgang; Leonhardt, Steffen; Marx, Gernot; Rossaint, Rolf; Bickenbach, Johannes

2012-10-15

347

USE OF REPEATED BRONCHOALVEOLAR LAVAGE IN RABBITS TO ASSESS POLLUTANT-INDUCED LUNG CHANGES IN AN ANIMAL MODEL OF CARDIOVASCULAR (CV) DISEASE.  

EPA Science Inventory

Animal models of coronary heart disease (e.g., hyperlipidemic rabbits) are being used to investigate epidemiologic associations between higher levels of air pollution and adverse CV consequences. Mechanisms by which pollutant-induced lung or systemic inflammation leads to acute C...

348

Protective effects of aerobic exercise on acute lung injury induced by LPS in mice  

PubMed Central

Introduction The regular practice of physical exercise has been associated with beneficial effects on various pulmonary conditions. We investigated the mechanisms involved in the protective effect of exercise in a model of lipopolysaccharide (LPS)-induced acute lung injury (ALI). Methods Mice were divided into four groups: Control (CTR), Exercise (Exe), LPS, and Exercise + LPS (Exe + LPS). Exercised mice were trained using low intensity daily exercise for five weeks. LPS and Exe + LPS mice received 200 µg of LPS intratracheally 48 hours after the last physical test. We measured exhaled nitric oxide (eNO); respiratory mechanics; neutrophil density in lung tissue; protein leakage; bronchoalveolar lavage fluid (BALF) cell counts; cytokine levels in BALF, plasma and lung tissue; antioxidant activity in lung tissue; and tissue expression of glucocorticoid receptors (Gre). Results LPS instillation resulted in increased eNO, neutrophils in BALF and tissue, pulmonary resistance and elastance, protein leakage, TNF-alpha in lung tissue, plasma levels of IL-6 and IL-10, and IL-1beta, IL-6 and KC levels in BALF compared to CTR (P ?0.02). Aerobic exercise resulted in decreases in eNO levels, neutrophil density and TNF-alpha expression in lung tissue, pulmonary resistance and elastance, and increased the levels of IL-6, IL-10, superoxide dismutase (SOD-2) and Gre in lung tissue and IL-1beta in BALF compared to the LPS group (P ?0.04). Conclusions Aerobic exercise plays important roles in protecting the lungs from the inflammatory effects of LPS-induced ALI. The effects of exercise are mainly mediated by the expression of anti-inflammatory cytokines and antioxidants, suggesting that exercise can modulate the inflammatory-anti-inflammatory and the oxidative-antioxidative balance in the early phase of ALI. PMID:23078757

2012-01-01

349

[Experimental acute lung injury in guinea pigs after aerosol challenge with sonicated Pseudomonas aeruginosa whole cells].  

PubMed

Acute hemorrhagic alveolitis was elicited in the lungs of guinea pigs by aerosol challenge with sonicated P. aeruginosa whole cells. Histological findings showed the severe inflammatory changes, which were characterized by the inflammatory infiltration of alveolar macrophages (AM), polymorphonuclear leukocytes (PMN) and eosinophils in the peribronchial and the alveolar space at 8 hours after the challenge. A marked increase of PMN as well as AM was noted in the bronchial alveolar lavage fluid (BALF) at 8 hours after the challenge and the increase of the numbers of AM and PMN in the BALF remained until 24 hours after challenge. The complement titer (CH50) and C3 component in the serum decreased at the early stage, and CH50 maintained low level and C3 component increased gradually. Polyethyleneglycol precipitation-complement consumption test (PEG-CC) of the BALF showed the existence of immune complexes formed in the airway after aerosol inhalation. These data suggest that the immune complexes of P. aeruginosa activate the complement system in the lungs, which is followed by the infiltration of inflammatory cells. Guinea pigs which were pretreated with cobra venom factor significantly reduced the extent of the inflammatory changes in the lungs. The results suggests that the complement system might act as an important factor of the acute lung injury in this model. PMID:8250724

Kasamatsu, Y; Takemura, S; Nakahara, R; Fukuda, W; Onodera, H; Ueda, M; Deguchi, M; Sugino, T; Kondo, M

1993-10-01

350

Lung ultrasound in acute respiratory failure an introduction to the BLUE-protocol.  

PubMed

Critical ultrasound, apparently a recent field, is in fact the outcome of a slow process, initiated since 1946. The lung was traditionally not considered as part of ultrasound, yet we considered its inclusion as a priority in our definition of critical ultrasound. Acute respiratory failure is one of the most distressing situations for the patient. An ultrasound approach of this disorder - the BLUE-protocol allows rapid diagnosis. Its main features will be described. Each kind of respiratory failure provides a particular ultrasound profile. In this difficult setting, initial mistakes are frequent. The BLUE-protocol proposes a step-by-step approach for making accurate diagnosis. By combining three signs with binary answer (anterior lung sliding, anterior lung-rockets), with venous analysis when required, seven profiles are generated, yielding a 90.5% accuracy. This rate is highly enhanced when simple clinical and laboratory data are considered. The BLUE-protocol can be achieved in three minutes, because the use of an intelligent machine, a universal probe, and standardized points allow major time-saving. Lung ultrasound in the critically ill was long available. In a domain where everything must be fast and accurate, the BLUE-protocol can play a major role in the diagnosis of an acute respiratory failure, usually answering immediately to questions where only sophisticated techniques were hitherto used. PMID:19412150

Lichtenstein, D

2009-05-01

351

Molecular basis of asbestos-induced lung disease.  

PubMed

Asbestos causes asbestosis and malignancies by molecular mechanisms that are not fully understood. The modes of action underlying asbestosis, lung cancer, and mesothelioma appear to differ depending on the fiber type, lung clearance, and genetics. After reviewing the key pathologic changes following asbestos exposure, we examine recently identified pathogenic pathways, with a focus on oxidative stress. Alveolar epithelial cell apoptosis, which is an important early event in asbestosis, is mediated by mitochondria- and p53-regulated death pathways and may be modulated by the endoplasmic reticulum. We review mitochondrial DNA (mtDNA)-damage and -repair mechanisms, focusing on 8-oxoguanine DNA glycosylase, as well as cross talk between reactive oxygen species production, mtDNA damage, p53, OGG1, and mitochondrial aconitase. These new insights into the molecular basis of asbestos-induced lung diseases may foster the development of novel therapeutic targets for managing degenerative diseases (e.g., asbestosis and idiopathic pulmonary fibrosis), tumors, and aging, for which effective management is lacking. PMID:23347351

Liu, Gang; Cheresh, Paul; Kamp, David W

2013-01-24

352

Molecular Basis of Asbestos-Induced Lung Disease  

PubMed Central

Asbestos causes asbestosis and malignancies by molecular mechanisms that are not fully understood. The modes of action underlying asbestosis, lung cancer, and mesothelioma appear to differ depending on the fiber type, lung clearance, and genetics. After reviewing the key pathologic changes following asbestos exposure, we examine recently identified pathogenic pathways, with a focus on oxidative stress. Alveolar epithelial cell apoptosis, which is an important early event in asbestosis, is mediated by mitochondria- and p53-regulated death pathways and may be modulated by the endoplasmic reticulum. We review mitochondrial DNA (mtDNA)-damage and -repair mechanisms, focusing on 8-oxoguanine DNA glycosylase, as well as cross talk between reactive oxygen species production, mtDNA damage, p53, OGG1, and mitochondrial aconitase. These new insights into the molecular basis of asbestos-induced lung diseases may foster the development of novel therapeutic targets for managing degenerative diseases (e.g., asbestosis and idiopathic pulmonary fibrosis), tumors, and aging, for which effective management is lacking. PMID:23347351

Liu, Gang; Cheresh, Paul; Kamp, David W.

2013-01-01

353

Deep Hypothermic Circulatory Arrest with Lung Perfusion/Ventilation in a Patient with Acute Type A Aortic Dissection  

PubMed Central

A 50-year-old black male presented with acute type A aortic dissection. Surgical repair was performed under deep hypothermic circulatory arrest (DHCA) with lung perfusion/ventilation throughout the procedure. Details of the lung perfusion technique and its potential benefits and drawbacks are discussed. PMID:22474459

Rodriguez-Blanco, Yiliam F.; Garcia, Lester; Brice, Tania; Ricci, Marco; Salerno, Tomas A.

2012-01-01

354

Effect of Prone Position on Regional Shunt, Aeration, and Perfusion in Experimental Acute Lung Injury  

PubMed Central

Rationale: The prone position is used to improve gas exchange in patients with acute respiratory distress syndrome. However, the regional mechanism by which the prone position improves gas exchange in acutely injured lungs is still incompletely defined. Methods: We used positron emission tomography imaging of [13N]nitrogen to assess the regional distribution of pulmonary shunt, aeration, perfusion, and ventilation in seven surfactant-depleted sheep in supine and prone positions. Results: In the supine position, the dorsal lung regions had a high shunt fraction, high perfusion, and poor aeration. The prone position was associated with an increase in lung gas content and with a more uniform distribution of aeration, as the increase in aeration in dorsal lung regions was not offset by loss of aeration in ventral regions. Consequently, the shunt fraction decreased in dorsal regions in the prone position without a concomitant impairment of gas exchange in ventral regions, thus leading to a significant increase in the fraction of pulmonary perfusion participating in gas exchange. In addition, the vertical distribution of specific alveolar ventilation became more uniform in the prone position. A biphasic relation between regional shunt fraction and gas fraction showed low shunt for values of gas fraction higher than a threshold, and a steep linear increase in shunt for lower values of gas fraction. Conclusion: In a surfactant-deficient model of lung injury, the prone position improved gas exchange by restoring aeration and decreasing shunt while preserving perfusion in dorsal lung regions, and by making the distribution of ventilation more uniform. PMID:15901611

Richter, Torsten; Bellani, Giacomo; Harris, R. Scott; Melo, Marcos F. Vidal; Winkler, Tilo; Venegas, Jose G.; Musch, Guido

2005-01-01

355

Effects of positive end-expiratory pressure on dead space and its partitions in acute lung injury  

Microsoft Academic Search

Objective. A large tidal volume (VT) and lung collapse and re-expansion may cause ventilator-induced lung injury (VILI) in acute lung injury (ALI). A low VT and a positive end-expiratory pressure (PEEP) can prevent VILI, but the more VT is reduced, the more dead space (VD) compromises gas exchange. We investigated how physiological, airway and alveolar VD varied with PEEP and

L. Beydon; L. Uttman; R. Rawal; B. Jonson

2002-01-01

356

The Lung Tissue Microbiome in Chronic Obstructive Pulmonary Disease  

PubMed Central

Rationale: Based on surface brushings and bronchoalveolar lavage fluid, Hilty and coworkers demonstrated microbiomes in the human lung characteristic of asthma and chronic obstructive pulmonary disease (COPD), which have now been confirmed by others. Objectives: To extend these findings to human lung tissue samples. Methods: DNA from lung tissue samples was obtained from nonsmokers (n = 8); smokers without COPD (n = 8); patients with very severe COPD (Global Initiative for COPD [GOLD] 4) (n = 8); and patients with cystic fibrosis (CF) (n = 8). The latter served as a positive control, with sterile water as a negative control. All bacterial community analyses were based on polymerase chain reaction amplifying 16S rRNA gene fragments. Total bacterial populations were measured by quantitative polymerase chain reaction and bacterial community composition was assessed by terminal restriction fragment length polymorphism analysis and pyrotag sequencing. Measurement and Main Results: Total bacterial populations within lung tissue were small (20–1,252 bacterial cells per 1,000 human cells) but greater in all four sample groups versus the negative control group (P < 0.001). Terminal restriction fragment length polymorphism analysis and sequencing distinguished three distinct bacterial community compositions: one common to the nonsmoker and smoker groups, a second to the GOLD 4 group, and the third to the CF-positive control group. Pyrotag sequencing identified greater than 1,400 unique bacterial sequences and showed an increase in the Firmicutes phylum in GOLD 4 patients versus all other groups (P < 0.003) attributable to an increase in the Lactobacillus genus (P < 0.0007). Conclusions: There is a detectable bacterial community within human lung tissue that changes in patients with very severe COPD. PMID:22427533

Sze, Marc A.; Dimitriu, Pedro A.; Hayashi, Shizu; Elliott, W. Mark; McDonough, John E.; Gosselink, John V.; Cooper, Joel; Sin, Don D.; Mohn, William W.

2012-01-01

357

Occupational Lung Diseases among Soldiers Deployed to Iraq and Afghanistan  

PubMed Central

Military personnel deployed to Iraq and Afghanistan, from 2004 to the present, has served in a setting of unique environmental conditions. Among these are exposures to burning trash in open air “burn pits” lit on fire with jet fuel JP-8. Depending on trash burned--water bottles, styrofoam trays, medical waste, unexploded munitions, and computers--toxins may be released such as dioxins and n-hexane and benzene. Particulate matter air pollution culminates from these fires and fumes. Additional environmental exposures entail sandstorms (Haboob, Shamal, and Sharqi) which differ in direction and relationship to rain. These wars saw the first use of improvised explosive devices (roadside phosphate bombs),as well as vehicle improvised explosive devices (car bombs), which not only potentially aerosolize metals, but also create shock waves to induce lung injury via blast overpressure. Conventional mortar rounds are also used by Al Qaeda in both Iraq and Afghanistan. Outdoor aeroallergens from date palm trees are prevalent in southern Iraq by the Tigris and Euphrates rivers, while indoor aeroallergen aspergillus predominates during the rainy season. High altitude lung disease may also compound the problem, particularly in Kandahar, Afghanistan. Clinically, soldiers may present with new-onset asthma or fixed airway obstruction. Some have constrictive bronchiolitis and vascular remodeling on open lung biopsy - despite having normal spirometry and chest xrays and CT scans of the chest. Others have been found to have titanium and other metals in the lung (rare in nature). Still others have fulminant biopsy-proven sarcoidiosis. We found DNA probe–positive Mycobacterium Avium Complex in lung from a soldier who had pneumonia, while serving near stagnant water and camels and goats outside Abu Gharib. This review highlights potential exposures, clinical syndromes, and the Denver Working Group recommendations on post-deployment health. PMID:24443711

Szema, Anthony M

2013-01-01

358

Depression in pulmonary arterial hypertension and interstitial lung diseases.  

PubMed

Advanced lung diseases such as pulmonary arterial hypertension (PAH) and interstitial lung diseases (ILD) are chronic diseases that cause significantly high morbidity and mortality. As a result, patients can undergo some psychological changes leading to a poor quality of life and depression. Diagnosis of depression is often obscured because fatigue and apathy, two common symptoms of depression, frequently overlap with PAH and ILD. Healthcare providers are sometimes reluctant to ask or mistakenly believe that these symptoms are part of the ongoing disease process, rather than a serious condition like depression. Screening tools are available for physicians to be well positioned in recognizing clinical depression in PAH and ILD. A MedLine/PubMED search was performed identifying all relevant articles with "PAH", "ILD", "screening tools" and/or "Depression" in the title. The aim of this review is to provide a brief description of some of the instruments used to screen patients and classes of psychotropic medications accessible to physicians. While pulmonary rehabilitation programs can have a positive impact on patients, physicians should also utilize cognitive behavioral therapy (CBT) as part of regular care. PMID:25006558

Verma, Sameer; Cardenas-Garcia, Jose; Mohapatra, Prasanta R; Talwar, Arunabh

2014-06-01

359

Depression in Pulmonary Arterial Hypertension and Interstitial Lung Diseases  

PubMed Central

Advanced lung diseases such as pulmonary arterial hypertension (PAH) and interstitial lung diseases (ILD) are chronic diseases that cause significantly high morbidity and mortality. As a result, patients can undergo some psychological changes leading to a poor quality of life and depression. Diagnosis of depression is often obscured because fatigue and apathy, two common symptoms of depression, frequently overlap with PAH and ILD. Healthcare providers are sometimes reluctant to ask or mistakenly believe that these symptoms are part of the ongoing disease process, rather than a serious condition like depression. Screening tools are available for physicians to be well positioned in recognizing clinical depression in PAH and ILD. A MedLine/PubMED search was performed identifying all relevant articles with “PAH”, “ILD”, “screening tools” and/or “Depression” in the title. The aim of this review is to provide a brief description of some of the instruments used to screen patients and classes of psychotropic medications accessible to physicians. While pulmonary rehabilitation programs can have a positive impact on patients, physicians should also utilize cognitive behavioral therapy (CBT) as part of regular care. PMID:25006558

Verma, Sameer; Cardenas-Garcia, Jose; Mohapatra, Prasanta R.; Talwar, Arunabh

2014-01-01

360

Phenotypic, immunologic, and clinical characteristics of patients with nontuberculous mycobacterial lung disease in Korea  

PubMed Central

Background This study aimed to elucidate the phenotypic, immunologic, and clinical characteristics of Korean patients with nontuberculous mycobacterial (NTM) lung disease and compare them with non-NTM bronchiectasis (BE) patients. Methods We prospectively recruited patients between 20 and 80 years of age who had nodular BE type NTM lung disease. Phenotypic, immunologic, and clinical characteristics were evaluated through physical examination, laboratory tests, pulmonary function tests, and radiographic examinations. Questionnaires were also answered. The results of the evaluations were compared with the results of non-NTM BE patients. Results A total of 84 patients with NTM lung disease and 47 non-NTM BE patients participated in the study. Mycobacterium avium complex lung disease and M. abscessus lung disease were most common. Patients with NTM lung disease had lower body mass index than non-NTM BE patients. Scoliosis was observed more frequently in patients with NTM lung disease than in non-NTM BE patients. Conclusions Significant similarities were seen between Korean patients with NTM lung disease and patients from other countries. Differences in phenotypic and clinical characteristics between NTM lung disease and non-NTM BE patients suggest differences in the immunopathogenesis of NTM lung disease and non-NTM BE. Trial registration information ClinicalTrials.gov Registration number; NCT01616745 PMID:24274658

2013-01-01

361

Heart–lung and lung transplantation in grown-up congenital heart disease: long-term single centre experience  

Microsoft Academic Search

Objective: Because of considerable progress in paediatric cardiac surgery life expectancy of patients with congenital heart disease (CHD) has improved significantly over the years. There are a growing number of adults with CHD presenting with progressive decline of cardiopulmonary function and Eisenmenger's syndrome. We analysed our experience with heart–lung and lung transplantation in this patient group. Methods: Since 1988, a

Heidi Goerler; Andre Simon; Bernhard Gohrbandt; Christian Hagl; Petra Oppelt; Juergen Weidemann; Axel Haverich; Martin Strueber

2007-01-01

362

[Echocardiographic diagnosis of pulmonary hypertension in chronic lung diseases].  

PubMed

For the time between 1985 and 1990 we found in the literature 14 reports on 483 patients with chronic lung diseases and 140 healthy controls which were investigated by right ventricular catheter and echocardiographic methods. The critical review about ability of echocardiography to recognise the pulmonary hypertension secondary to chronic lung diseases shows following results: 1. Acceleration time (time to peak velocity) revealed correlations to mean or systolic pulmonary artery pressure (SPAP) of -0.72 to -0.92. The sample volume of pulsed Doppler should be taken near the pulmonary valve and in the middle of pulmonary artery diameter. Correction of acceleration time by heart frequency is necessary in children (Akiba). 2. Tricuspid regurgitation to SPAP: r = 0.65-0.92, but sensitivity to recognise pulmonary hypertension was only 20 (to 91)%. Accurate quantitative measurement is possible only in 24 to 66% of the patients with chronic lung diseases. 3. Isovolemic relaxation time: r = 0.70-0.89, limitations by some cardiac influences--but also the ability to reflect effects of medication (Hatle). 4. End-diastolic diameter of tricuspid valve/m2 of body surface: r = 0.84, in connection with right ventricular end-diastolic diameter r = 0.90. Diameters of pulmonary valve, of right pulmonary artery, of right ventricle and characteristics of the flow in the Vena cava inferior have a smaller diagnostic value. Thickness of right ventricular systolic time intervals are without reliable informations about pulmonary hypertension. In conclusion there are some echocardiographic parameters with high diagnostic value in the noninvasive diagnostic of pulmonary hypertension secondary to chronic pulmonary diseases. A table of practicable values and regression equations completes this review. PMID:1579562

Paditz, E

1992-04-01

363

Diagnosis of Pulmonary Tuberculosis and Nontuberculous Mycobacterial Lung Disease in Korea  

PubMed Central

The recovery of nontuberculous mycobacteria (NTM) from respiratory specimens and the number of patients with NTM lung disease have been rapidly increasing in Korea. An early differential diagnosis of NTM lung disease from pulmonary tuberculosis (TB) is important, as the therapeutic regimen differs from that of pulmonary TB, and it is not necessary to track the contacts of patients with NTM lung disease. However, differentiating NTM lung disease from pulmonary TB remains difficult, because the clinical presentations of the two diseases are similar and a definite diagnosis of NTM lung disease based on sputum culture takes time. This review focuses on the changing epidemiology, clinical and radiographic manifestation, and laboratory diagnosis of pulmonary TB and NTM lung disease in Korea. PMID:25114696

Kwon, Yong Soo

2014-01-01

364

Suspected Transfusion Related Acute Lung Injury Improving following Administration of Tranexamic Acid: A Case Report  

PubMed Central

A 16-year-old woman with craniofacial injury developed severe acute respiratory failure under the primary reconstructive surgical procedure requiring several units of blood and plasma. A transfusion related acute lung injury (TRALI) was suspected and supportive treatment was initiated. Because of the severity of symptoms, acute extracorporeal membrane oxygenation (ECMO) was planned. During preparation for ECMO, a single intravenous dose, 1?g of tranexamic acid, was administered and a remarkable improvement was observed shortly thereafter. The patient was placed on ECMO for 16 hours. The further course was uncomplicated and the patient was discharged from ICU on the 6th day after admission fully and she recovered. A clinical improvement was observed in a timely fashion following the administration of tranexamic acid. The handling of a suspected TRALI and potential benefit from administration of tranexamic acid are discussed in this case report. PMID:24995132

Ryniak, Stan; Harbut, Piotr; Ostlund, Anders; Jakobsson, Jan G.

2014-01-01

365

Lung Transplant  

MedlinePLUS

... the NHLBI on Twitter. What Is a Lung Transplant? A lung transplant is surgery to remove a person's diseased lung ... a healthy lung from a deceased donor. Lung transplants are used for people who are likely to ...

366

Type 2 Deiodinase and Host Responses of Sepsis and Acute Lung Injury  

PubMed Central

The role of thyroid hormone metabolism in clinical outcomes of the critically ill remains unclear. Using preclinical models of acute lung injury (ALI), we assessed the gene and protein expression of type 2 deiodinase (DIO2), a key driver for synthesis of biologically active triiodothyronine, and addressed potential association of DIO2 genetic variants with ALI in a multiethnic cohort. DIO2 gene and protein expression levels in murine lung were validated by microarrays and immunoblotting. Lung injury was assessed by levels of bronchoalveolar lavage protein and leukocytes. Single-nucleotide polymorphisms were genotyped and ALI susceptibility association assessed. Significant increases in both DIO2 gene and D2 protein expression were observed in lung tissues from murine ALI models (LPS- and ventilator-induced lung injury), with expression directly increasing with the extent of lung injury. Mice with reduced levels of DIO2 expression (by silencing RNA) demonstrated reduced thyroxine levels in plasma and increased lung injury (increased bronchoalveolar lavage protein and leukocytes), suggesting a protective role for DIO2 in ALI. The G (Ala) allele of the Thr92Ala coding single-nucleotide polymorphism (rs225014) was protective in severe sepsis and severe sepsis–associated ALI after adjustments for age, sex, and genetic ancestry in a logistic regression model in European Americans. Our studies indicate that DIO2 is a novel ALI candidate gene, the nonsynonymous Thr92Ala coding variant of which confers ALI protection. Increased DIO2 expression may dampen the ALI inflammatory response, thereby strengthening the premise that thyroid hormone metabolism is intimately linked to the integrated response to inflammatory injury in critically ill patients. PMID:21685153

Ma, Shwu-Fan; Xie, Lishi; Pino-Yanes, Maria; Sammani, Saad; Wade, Michael S.; Letsiou, Eleftheria; Siegler, Jessica; Wang, Ting; Infusino, Giovanni; Kittles, Rick A.; Flores, Carlos; Zhou, Tong; Prabhakar, Bellur S.; Moreno-Vinasco, Liliana; Villar, Jesus; Jacobson, Jeffrey R.; Dudek, Steven M.

2011-01-01

367

Pulmonary Natural Killer T Cells Play an Essential Role in Mediating Hyperoxic Acute Lung Injury  

PubMed Central

Critically ill patients are routinely exposed to high concentrations of supplemental oxygen for prolonged periods of time, which can be life-saving in the short term, but such exposure also causes severe lung injury and increases mortality. To address this therapeutic dilemma, we studied the mechanisms of the tissue-damaging effects of oxygen in mice. We show that pulmonary invariant natural killer T (iNKT) cells are unexpectedly crucial in the development of acute oxygen-induced lung injury. iNKT cells express high concentrations of the ectonucleotidase CD39, which regulates their state of activation. Both iNKT cell–deficient (J?18?/?) and CD39-null mice tolerate hyperoxia, compared with wild-type control mice that exhibit severe lung injury. An adoptive transfer of wild-type iNKT cells into J?18?/? mice results in hyperoxic lung injury, whereas the transfer of CD39-null iNKT cells does not. Pulmonary iNKT cell activation and proliferation are modulated by ATP-dependent purinergic signaling responses. Hyperoxic lung injury can be induced by selective P2X7-receptor blockade in CD39-null mice. Our data indicate that iNKT cells are involved in the pathogenesis of hyperoxic lung injury, and that tissue protection can be mediated through ATP-induced P2X7 receptor signaling, resulting in iNKT cell death. In conclusion, our data suggest that iNKT cells and purinergic signaling should be evaluated as potential novel therapeutic targets to prevent hyperoxic lung injury. PMID:23349052

Nowak-Machen, Martina; Schmelzle, Moritz; Hanidziar, Dusan; Junger, Wolfgang; Exley, Mark; Otterbein, Leo; Wu, Yan; Csizmadia, Eva; Doherty, Glen; Sitkovsky, Michail

2013-01-01

368

HIF1A Reduces Acute Lung Injury by Optimizing Carbohydrate Metabolism in the Alveolar Epithelium  

PubMed Central

Background While acute lung injury (ALI) contributes significantly to critical illness, it resolves spontaneously in many instances. The majority of patients experiencing ALI require mechanical ventilation. Therefore, we hypothesized that mechanical ventilation and concomitant stretch-exposure of pulmonary epithelia could activate endogenous pathways important in lung protection. Methods and Findings To examine transcriptional responses during ALI, we exposed pulmonary epithelia to cyclic mechanical stretch conditions—an in vitro model resembling mechanical ventilation. A genome-wide screen revealed a transcriptional response similar to hypoxia signaling. Surprisingly, we found that stabilization of hypoxia-inducible factor 1A (HIF1A) during stretch conditions in vitro or during ventilator-induced ALI in vivo occurs under normoxic conditions. Extension of these findings identified a functional role for stretch-induced inhibition of succinate dehydrogenase (SDH) in mediating normoxic HIF1A stabilization, concomitant increases in glycolytic capacity, and improved tricarboxylic acid (TCA) cycle function. Pharmacologic studies with HIF activator or inhibitor treatment implicated HIF1A-stabilization in attenuating pulmonary edema and lung inflammation during ALI in vivo. Systematic deletion of HIF1A in the lungs, endothelia, myeloid cells, or pulmonary epithelia linked these findings to alveolar-epithelial HIF1A. In vivo analysis of 13C-glucose metabolites utilizing liquid-chromatography tandem mass-spectrometry demonstrated that increases in glycolytic capacity, improvement of mitochondrial respiration, and concomitant attenuation of lung inflammation during ALI were specific for alveolar-epithelial expressed HIF1A. Conclusions These studies reveal a surprising role for HIF1A in lung protection during ALI, where normoxic HIF1A stabilization and HIF-dependent control of alveolar-epithelial glucose metabolism function as an endogenous feedback loop to dampen lung inflammation. PMID:24086109

Bonney, Megan; Packard, Thomas; Han, Jun; Borchers, Christoph H.; Mariani, Thomas J.; Kominsky, Douglas J.; Mittelbronn, Michel; Eltzschig, Holger K.

2013-01-01

369

Enhanced Hsp70 expression protects against acute lung injury by modulating apoptotic pathways.  

PubMed

The Acute respiratory distress syndrome (ARDS) is a highly lethal inflammatory lung disorder. Apoptosis plays a key role in its pathogenesis. We showed that an adenovirus expressing the 70 kDa heat shock protein Hsp70 (AdHSP) protected against sepsis-induced lung injury. In this study we tested the hypothesis that AdHSP attenuates apoptosis in sepsis-induced lung injury. Sepsis was induced in rats via cecal ligation and double puncture (2CLP). At the time of 2CLP PBS, AdHSP or AdGFP (an adenoviral vector expressing green fluorescent protein) were injected into the tracheas of septic rats. 48 hours later, lungs were isolated. One lung was fixed for TUNEL staining and immunohistochemistry. The other was homogenized to isolate cytosolic and nuclear protein. Immunoblotting, gel filtration and co-immunoprecipitation were performed in these extracts. In separate experiments MLE-12 cells were incubated with medium, AdHSP or AdGFP. Cells were stimulated with TNF?. Cytosolic and nuclear proteins were isolated. These were subjected to immunoblotting, co-immunoprecipitation and a caspase-3 activity assay. TUNEL assay demonstrated that AdHSP reduced alveolar cell apoptosis. This was confirmed by immunohistochemical detection of caspase 3 abundance. In lung isolated from septic animals, immunoblotting, co-immunoprecipitation and gel filtration studies revealed an increase in cytoplasmic complexes containing caspases 3, 8 and 9. AdHSP disrupted these complexes. We propose that Hsp70 impairs apoptotic cellular pathways via interactions with caspases. Disruption of large complexes resulted in stabilization of lower molecular weight complexes, thereby, reducing nuclear caspase-3. Prevention of apoptosis in lung injury may preserve alveolar cells and aid in recovery. PMID:22132083

Aschkenasy, Gabriella; Bromberg, Zohar; Raj, Nichelle; Deutschman, Clifford S; Weiss, Yoram G

2011-01-01

370

Heart and lung, a dangerous liaison-Tako-tsubo cardiomyopathy and respiratory diseases: A systematic review  

PubMed Central

AIM: To investigate the possible association between Tako-tsubo cardiomyopathy (TTC)-a reversible clinical condition mimicking an acute myocardial infarction characterized by multifactorial pathophysiologic mechanisms- and respiratory system diseases. METHODS: We systematically searched PubMed and EMBASE medical information sources, to identify the different triggering causes, limiting our search to articles in English. The search keywords were: “tako-tsubo cardiomyopathy”, “takotsubo”, “takotsubo cardiomyopathy”, “broken heart syndrome”, “stress-induced cardiomyopathy”, “apical ballooning syndrome”, and “ampulla cardiomyopathy in combination with respiratory diseases, lung, pulmonary disease. For each kind of disease, we registered: author, year and country of study, patient sex, age, concurring situation, and outcome. RESULTS: Out of a total of 1725 articles found, we selected 37 papers reporting a total of 38 patients. As expected, most patients were women (81.6%), mean age was 65 ± 10 years. Outcome was favorable in 100% of cases, and all the patients have been discharged uneventfully in a few days. CONCLUSION: An association between respiratory diseases and TTC is likely to exist. Patients with severe respiratory diseases, due to the high dosages of ?2-agonists used or to the need of invasive procedures, are highly exposed to the risk of developing TTC. PMID:24944763

Manfredini, Roberto; Fabbian, Fabio; Giorgi, Alfredo De; Pala, Marco; Menegatti, Alessandra Mallozzi; Parisi, Claudia; Misurati, Elisa; Tiseo, Ruana; Gallerani, Massimo; Salmi, Raffaella; Bossone, Eduardo

2014-01-01

371

Macrophage damage in relation to the pathogenesis of lung diseases.  

PubMed Central

Pulmonary macrophages are important since their migratory patterns and behavior are often pivotal events in the pathogenesis of pulmonary disease. Alveolar macrophages act to decrease the probability of particle penetration through epithelial barriers, and their phagocytic and lytic potentials provide most of the known bactericadal properties of the lung. Macrophages are also involved in immune responses and in defense against neoplasms. Increased inert or infectious particles stimulate the recruitment of additional macrophages. Most free cells containing particles eventually reach the airways and are quickly carried to the pharynx and swallowed. In addition, evidence has now accumulated that macrophages play a part in the pathogenesis of pulmonary diseases. For example, the ingestion of some particles by macrophages causes a release of lysosomal enzymes into the macrophage cytoplasm. These enzymes may kill the macrophage, and dead or dying macrophages release a substance with attracts fibroblasts that elicit fibrogenic responses. Other toxic particles, such as cigarette smoke, my lead to a release of proteases and other toxic enzymes. All particles are capable of competitive inhibition of phagocytosis in macrophages and many may be cytotoxic and further depress phagocytosis. In addition, connective tissue macrophages may contribute to lung disease by concentrating and storing potent carcinogens or other toxic particles close to a reactive bronchial epithelium for long periods. Thus, even through macrophages serve as a first line of defense for the alveolar surface, they may also be capable of injuring the host while exercising their defensive role. PMID:6997029

Brain, J D

1980-01-01

372

A NOVEL WEARABLE PUMP-LUNG DEVICE: IN-VITRO AND ACUTE IN-VIVO STUDY  

PubMed Central

Background To provide long-term ambulatory cardiopulmonary and respiratory support for adult patients, a novel wearable artificial pump-lung device has been developed. The design features, in-vitro and acute in-vivo performance of this device are reported in this paper. Methods This device features a uniquely designed hollow fiber membrane bundle integrated with a magnetically levitated impeller together to form one ultra-compact pump-lung device, which can be placed like current paracorporeal ventricular assist devices to allow ambulatory support. The device is 117 mm in length and 89 mm in diameter and has a priming volume of 115 ml. In-vitro hydrodynamic, gas transfer and biocompatibility experiments were carried out in mock flow loops using ovine blood. Acute in-vivo characterization was conducted in ovine by surgically implanting the device between right atrium and pulmonary artery. Results The in-vitro results showed that the device with a membrane surface area of 0.8 m2 was capable of pumping blood from 1 to 4 L/min against a wide range of pressures and transferring oxygen at a rate of up to 180 ml/min at a blood flow of 3.5 L/min. Standard hemolysis tests demonstrated low hemolysis at the targeted operating condition. The acute in-vivo results also confirmed that the device can provide sufficient oxygen transfer with excellent biocompatibility. Conclusions Base on the in-vitro and acute in-vivo study, this highly integrated wearable pump-lung device can provide efficient respiratory support with good biocompatibility and it is ready for long-term evaluation. PMID:22014451

Zhang, Tao; Wei, Xufeng; Bianchi, Giacomo; Wong, Philip M.; Biancucci, Brian; Griffith, Bartley P.; Wu, Zhongjun J.

2011-01-01

373

Altered Pulmonary Lymphatic Development in Infants with Chronic Lung Disease  

PubMed Central

Pulmonary lymphatic development in chronic lung disease (CLD) has not been investigated, and anatomy of lymphatics in human infant lungs is not well defined. Hypothesis. Pulmonary lymphatic hypoplasia is present in CLD. Method. Autopsy lung tissues of eighteen subjects gestational ages 22 to 40 weeks with and without history of respiratory morbidity were stained with monoclonal antipodoplanin and reviewed under light microscopy. Percentage of parenchyma podoplanin stained at the acinar level was determined using computerized image analysis; 9 CLD and 4 control subjects gestational ages 27 to 36 weeks were suitable for the analysis. Results. Distinct, lymphatic-specific staining with respect to other vascular structures was appreciated in all gestations. Infants with and without respiratory morbidity had comparable lymphatic distribution which extended to the alveolar ductal level. Podoplanin staining per parenchyma was increased and statistically significant in the CLD group versus controls at the alveolar ductal level (0.06% ± 0.02% versus 0.04% ± 0.01%, 95% CI ?0.04% to ?0.002%, P < 0.03). Conclusion. Contrary to our hypothesis, the findings show that there is an increase in alveolar lymphatics in CLD. It is suggested that the findings, by expanding current knowledge of CLD pathology, may offer insight into the development of more effective therapies to tackle CLD. PMID:24527433

McNellis, Emily M.; Mabry, Sherry M.; Taboada, Eugenio; Ekekezie, Ikechukwu I.

2014-01-01

374

EMT and Interstitial Lung Disease: A Mysterious Relationship  

PubMed Central

Purpose of review Pathogenesis of interstitial lung diseases (ILD) has largely been investigated in the context of the most frequent ILD, idiopathic pulmonary fibrosis (IPF). We review studies of epithelial to mesenchymal transition (EMT) and discuss its potential contribution to collagen-producing (myo)fibroblasts in IPF. Recent findings Endoplasmic reticulum (ER) stress leading to epithelial apoptosis has been reported as a potential etiologic factor in fibrosis. Recent studies further suggest EMT as a link between ER stress and fibrosis. Combinatorial interactions among Smad3, ?-catenin and other transcriptional co-activators at the ?-smooth muscle actin (?-SMA) promoter provide direct evidence for crosstalk between transforming growth factor-? (TGF?) and ?-catenin pathways during EMT. Lineage tracing yielded conflicting results, with two recent studies supporting and one opposing a role for EMT in lung fibrosis. Summary Advances have been made in elucidating causes and mechanisms of EMT, potentially leading to new treatment options, although contributions of EMT to lung fibrosis in vivo remain controversial. In addition to EMT providing a direct source of (myo)fibroblasts, expression of mesenchymal markers may reflect epithelial injury, in which case inhibition of EMT might be deleterious. EMT-derived cells may also contribute to aberrant epithelial-mesenchymal crosstalk that promotes fibrogenesis. PMID:22854509

Kage, Hidenori; Borok, Zea

2014-01-01

375

VITAMIN D EFFECTS ON LUNG IMMUNITY AND RESPIRATORY DISEASES  

PubMed Central

SUMMARY Our understanding of vitamin D metabolism and biological effects has grown exponentially in recent years and it has become clear that vitamin D has extensive immunomodulatory effects. The active vitamin D generating enzyme, 1?-hydroxylase, is expressed by the airway epithelium, alveolar macrophages, dendritic cells and lymphocytes indicating that active vitamin D can be produced locally within the lungs. Vitamin D generated in tissues is responsible for many of the immunomodulatory actions of vitamin D. The effects of vitamin D within the lungs include increased secretion of the antimicrobial peptide cathelicidin, decreased chemokine production, inhibition of dendritic cell activation and alteration of T cell activation. These cellular effects are important for host responses against infection and the development of allergic lung diseases like asthma. Epidemiological studies do suggest that vitamin D deficiency predisposes to viral respiratory tract infections and mycobacterial infections and that vitamin D may play a role in the development and treatment of asthma. Randomized, placebo controlled trials are lacking but ongoing. PMID:21419273

Hansdottir, Sif; Monick, Martha M.

2013-01-01

376

Biphasic positive airway pressure minimizes biological impact on lung tissue in mild acute lung injury independent of etiology  

PubMed Central

Introduction Biphasic positive airway pressure (BIVENT) is a partial support mode that employs pressure-controlled, time-cycled ventilation set at two levels of continuous positive airway pressure with unrestricted spontaneous breathing. BIVENT can modulate inspiratory effort by modifying the frequency of controlled breaths. Nevertheless, the optimal amount of inspiratory effort to improve respiratory function while minimizing ventilator-associated lung injury during partial ventilatory assistance has not been determined. Furthermore, it is unclear whether the effects of partial ventilatory support depend on acute lung injury (ALI) etiology. This study aimed to investigate the impact of spontaneous and time-cycled control breaths during BIVENT on the lung and diaphragm in experimental pulmonary (p) and extrapulmonary (exp) ALI. Methods This was a prospective, randomized, controlled experimental study of 60 adult male Wistar rats. Mild ALI was induced by Escherichia coli lipopolysaccharide either intratracheally (ALIp) or intraperitoneally (ALIexp). After 24 hours, animals were anesthetized and further randomized as follows: (1) pressure-controlled ventilation (PCV) with tidal volume (Vt) = 6 ml/kg, respiratory rate = 100 breaths/min, PEEP = 5 cmH2O, and inspiratory-to-expiratory ratio (I:E) = 1:2; or (2) BIVENT with three spontaneous and time-cycled control breath modes (100, 75, and 50 breaths/min). BIVENT was set with two levels of CPAP (Phigh = 10 cmH2O and Plow = 5 cmH2O). Inspiratory time was kept constant (Thigh = 0.3 s). Results BIVENT was associated with reduced markers of inflammation, apoptosis, fibrogenesis, and epithelial and endothelial cell damage in lung tissue in both ALI models when compared to PCV. The inspiratory effort during spontaneous breaths increased during BIVENT-50 in both ALI models. In ALIp, alveolar collapse was higher in BIVENT-100 than PCV, but decreased during BIVENT-50, and diaphragmatic injury was lower during BIVENT-50 compared to PCV and BIVENT-100. In ALIexp, alveolar collapse during BIVENT-100 and BIVENT-75 was comparable to PCV, while decreasing with BIVENT-50, and diaphragmatic injury increased during BIVENT-50. Conclusions In mild ALI, BIVENT had a lower biological impact on lung tissue compared to PCV. In contrast, the response of atelectasis and diaphragmatic injury to BIVENT differed according to the rate of spontaneous/controlled breaths and ALI etiology. PMID:24103805

2013-01-01

377

Cyclic arginine-glycine-aspartate attenuates acute lung injury in mice after intestinal ischemia/reperfusion  

PubMed Central

Introduction Intestinal ischemia is a critical problem resulting in multiple organ failure and high mortality of 60 to 80%. Acute lung injury (ALI) is a common complication after intestinal ischemia/reperfusion (I/R) injuries and contributes to the high mortality rate. Moreover, activated neutrophil infiltration into the lungs is known to play a significant role in the progression of ALI. Integrin-mediated interaction is involved in neutrophil transmigration. Synthetic peptides containing an arginine-glycine-aspartate sequence compete with adhesive proteins and inhibit integrin-mediated interaction and signaling. Thus, we hypothesized that the administration of a cyclic arginine-glycine-aspartate peptide (cRGD) inhibited neutrophil infiltration and provided protection against ALI induced by intestinal I/R. Methods Ischemia in adult male C57BL/6 mice was induced by fastening the superior mesenteric artery with 4-0 suture. Forty-five minutes later, the vascular suture was released to allow reperfusion. cRGD (5 mg/kg body weight) or normal saline (vehicle) was administered by intraperitoneal injection 1 hour prior to ischemia. Blood, gut, and lung tissues were collected 4 hours after reperfusion for various measurements. Results Intestinal I/R caused severe widespread injury to the gut and lungs. Treatment with cRGD improved the integrity of microscopic structures in the gut and lungs, as judged by histological examination. Intestinal I/R induced the expression of ?1, ?2 and ?3 integrins, intercellular adhesion molecule-1, and fibronectin. cRGD significantly inhibited myeloperoxidase activity in the gut and lungs, as well as neutrophils and macrophages infiltrating the lungs. cRGD reduced the levels of TNF-? and IL-6 in serum, in addition to IL-6 and macrophage inflammatory protein-2 in the gut and lungs. Furthermore, the number of TUNEL-staining cells and levels of cleaved caspase-3 in the lungs were significantly lowered in the cRGD-treated mice in comparison with the vehicle mice. Conclusions Treatment with cRGD effectively protected ALI and gut injury, lowered neutrophil infiltration, suppressed inflammation, and inhibited lung apoptosis after intestinal I/R. Thus, there is potential for developing cRGD as a treatment for patients suffering from ALI caused by intestinal I/R. PMID:23360591

2013-01-01

378

Immunomodulatory Effect of Chinese Herbal Medicine Formula Sheng-Fei-Yu-Chuan-Tang in Lipopolysaccharide-Induced Acute Lung Injury Mice  

PubMed Central

Traditional Chinese medicine formula Sheng-Fei-Yu-Chuan-Tang (SFYCT), consisting of 13 medicinal plants, was used to treat patients with lung diseases. This study investigated the immunoregulatory effect of SFYCT on intratracheal lipopolysaccharides- (LPS-) challenged acute lung injury (ALI) mice. SFYCT attenuated pulmonary edema, macrophages, and neutrophils infiltration in the airways. SFYCT decreased inflammatory cytokines, including tumor necrosis factor-? (TNF?), interleukin-1?, and interleukin-6 and inhibited nitric oxide (NO) production but increased anti-inflammatory cytokines, interleukin-4, and interleukin-10, in the bronchoalveolar lavage fluid of LPS-challenged mice. TNF? and monocyte chemotactic protein-1 mRNA expression in the lung of LPS-challenged mice as well as LPS-stimulated lung epithelial cell and macrophage were decreased by SFYCT treatment. SFYCT treatment also decreased the inducible nitric oxide synthase expression and phosphorylation of nuclear factor-?B (NF-?B) in the lung of mice and macrophage with LPS stimulation. SFYCT treatment dose dependently decreased the LPS-induced NO and reactive oxygen species generation in LPS-stimulated macrophage. In conclusion, SFYCT attenuated lung inflammation during LPS-induced ALI through decreasing inflammatory cytokines production while increasing anti-inflammatory cytokines production. The immunoregulatory effect of SFYCT is related to inhibiting NF-?B phosphorylation. PMID:23997804

Lin, Chia-Hung; Yeh, Ching-Hua; Wang, Shulhn-Der; Wang, Jen-Shu; Kao, Shung-Te

2013-01-01

379

Rhinovirus Exacerbates House-Dust-Mite Induced Lung Disease in Adult Mice  

PubMed Central

Human rhinovirus is a key viral trigger for asthma exacerbations. To date, murine studies investigating rhinovirus-induced exacerbation of allergic airways disease have employed systemic sensitisation/intranasal challenge with ovalbumin. In this study, we combined human-rhinovirus infection with a clinically relevant mouse model of aero-allergen exposure using house-dust-mite in an attempt to more accurately understand the links between human-rhinovirus infection and exacerbations of asthma. Adult BALB/c mice were intranasally exposed to low-dose house-dust-mite (or vehicle) daily for 10 days. On day 9, mice were inoculated with human-rhinovirus-1B (or UV-inactivated human-rhinovirus-1B). Forty-eight hours after inoculation, we assessed bronchoalveolar cellular inflammation, levels of relevant cytokines/serum antibodies, lung function and responsiveness/sensitivity to methacholine. House-dust-mite exposure did not result in a classical TH2-driven response, but was more representative of noneosinophilic asthma. However, there were significant effects of house-dust-mite exposure on most of the parameters measured including increased cellular inflammation (primarily macrophages and neutrophils), increased total IgE and house-dust-mite-specific IgG1 and increased responsiveness/sensitivity to methacholine. There were limited effects of human-rhinovirus-1B infection alone, and the combination of the two insults resulted in additive increases in neutrophil levels and lung parenchymal responses to methacholine (tissue elastance). We conclude that acute rhinovirus infection exacerbates house-dust-mite-induced lung disease in adult mice. The similarity of our results using the naturally occurring allergen house-dust-mite, to previous studies using ovalbumin, suggests that the exacerbation of allergic airways disease by rhinovirus infection could act via multiple or conserved mechanisms. PMID:24632596

Phan, Jennifer A.; Kicic, Anthony; Berry, Luke J.; Fernandes, Lynette B.; Zosky, Graeme R.; Sly, Peter D.; Larcombe, Alexander N.

2014-01-01

380

Rhinovirus exacerbates house-dust-mite induced lung disease in adult mice.  

PubMed

Human rhinovirus is a key viral trigger for asthma exacerbations. To date, murine studies investigating rhinovirus-induced exacerbation of allergic airways disease have employed systemic sensitisation/intranasal challenge with ovalbumin. In this study, we combined human-rhinovirus infection with a clinically relevant mouse model of aero-allergen exposure using house-dust-mite in an attempt to more accurately understand the links between human-rhinovirus infection and exacerbations of asthma. Adult BALB/c mice were intranasally exposed to low-dose house-dust-mite (or vehicle) daily for 10 days. On day 9, mice were inoculated with human-rhinovirus-1B (or UV-inactivated human-rhinovirus-1B). Forty-eight hours after inoculation, we assessed bronchoalveolar cellular inflammation, levels of relevant cytokines/serum antibodies, lung function and responsiveness/sensitivity to methacholine. House-dust-mite exposure did not result in a classical TH2-driven response, but was more representative of noneosinophilic asthma. However, there were significant effects of house-dust-mite exposure on most of the parameters measured including increased cellular inflammation (primarily macrophages and neutrophils), increased total IgE and house-dust-mite-specific IgG1 and increased responsiveness/sensitivity to methacholine. There were limited effects of human-rhinovirus-1B infection alone, and the combination of the two insults resulted in additive increases in neutrophil levels and lung parenchymal responses to methacholine (tissue elastance). We conclude that acute rhinovirus infection exacerbates house-dust-mite-induced lung disease in adult mice. The similarity of our results using the naturally occurring allergen house-dust-mite, to previous studies using ovalbumin, suggests that the exacerbation of allergic airways disease by rhinovirus infection could act via multiple or conserved mechanisms. PMID:24632596

Phan, Jennifer A; Kicic, Anthony; Berry, Luke J; Fernandes, Lynette B; Zosky, Graeme R; Sly, Peter D; Larcombe, Alexander N

2014-01-01

381

Integrated training in Lung Biology and Diseases Sponsored by the Division of Pulmonary and Critical Care Medicine  

E-print Network

Integrated training in Lung Biology and Diseases Sponsored by the Division of Pulmonary Obstructive Pulmonary Disease (COPD, Emphysema) 3 Pulmonary Infections 4 Lung Cancer 5 Cystic Fibrosis 6 Lung Transplantation 7 Pulmonary Hypertension 8 Pulmonary Embolism 9 Occupational Lung Diseases 10 Airway Allergic

Gleeson, Joseph G.

382

Therapeutic prospects to treat skeletal muscle wasting in COPD (chronic obstructive lung disease)  

Microsoft Academic Search

Chronic obstructive pulmonary disease (COPD) is an incurable group of lung diseases characterised by progressive airflow limitation and loss of lung function, which lead to profound disability. It is mostly caused by cigarette smoke. Although COPD is one of the most prevalent diseases worldwide and its incidence is increasing, current therapies do little to improve the condition. Much current research

Michelle J. Hansen; Rosa C. Gualano; Steve Bozinovski; Ross Vlahos; Gary P. Anderson

2006-01-01

383

Circulating biomarkers of interstitial lung disease in systemic sclerosis.  

PubMed

Interstitial lung disease (ILD) is a major cause of morbidity and mortality in patients with systemic sclerosis (SSc). Although a large proportion of SSc patients have only limited interstitial involvement with an indolent course, in a significant minority ILD is progressive, requiring prompt treatment and careful monitoring. One of the main challenges for the clinician treating this highly variable disease is the early identification of patients at risk of progressive ILD, while avoiding potentially toxic treatments in those whose disease is inherently stable. Easily available and repeatable biomarkers that allow estimation of the risk of ILD progression and early response to treatment are highly desirable. In this paper, we review the evidence for circulating biomarkers with potential roles in diagnosis, monitoring of disease activity, or determining prognosis. Peripheral blood biomarkers offer the advantages of being readily obtained, non-invasive, and serially monitored. Several possible candidates have emerged from studies performed so far, including SP-D, KL-6, and CCL18. Presently however, there are few prospective studies evaluating the predictive ability of prospective biomarkers after adjustment for disease severity. Future carefully designed, prospective studies of well characterised patients with ILD, with optimal definition of disease severity and outcome measures are needed. PMID:22988462

Lota, Harpreet K; Renzoni, Elisabetta A

2012-01-01

384

Circulating Biomarkers of Interstitial Lung Disease in Systemic Sclerosis  

PubMed Central

Interstitial lung disease (ILD) is a major cause of morbidity and mortality in patients with systemic sclerosis (SSc). Although a large proportion of SSc patients have only limited interstitial involvement with an indolent course, in a significant minority ILD is progressive, requiring prompt treatment and careful monitoring. One of the main challenges for the clinician treating this highly variable disease is the early identification of patients at risk of progressive ILD, while avoiding potentially toxic treatments in those whose disease is inherently stable. Easily available and repeatable biomarkers that allow estimation of the risk of ILD progression and early response to treatment are highly desirable. In this paper, we review the evidence for circulating biomarkers with potential roles in diagnosis, monitoring of disease activity, or determining prognosis. Peripheral blood biomarkers offer the advantages of being readily obtained, non-invasive, and serially monitored. Several possible candidates have emerged from studies performed so far, including SP-D, KL-6, and CCL18. Presently however, there are few prospective studies evaluating the predictive ability of prospective biomarkers after adjustment for disease severity. Future carefully designed, prospective studies of well characterised patients with ILD, with optimal definition of disease severity and outcome measures are needed. PMID:22988462

Lota, Harpreet K.; Renzoni, Elisabetta A.

2012-01-01

385

Clinical experience with pirfenidone in five patients with scleroderma-related interstitial lung disease.  

PubMed

Interstitial lung disease is the most common complication and cause of death among patients with scleroderma. Scleroderma-related interstitial lung disease has usually been treated with cyclophosphamide; however, its effect was evaluated to be modest and long-term administration of this drug is associated with adverse effects. Herein, we report our clinical experience of administering pirfenidone, which is an antifibrotic agent, in five patients with scleroderma-related interstitial lung disease. All patients demonstrated an increase in vital capacity. PMID:25363224

Miura, Yukiko; Saito, Takefumi; Fujita, Kazutaka; Tanaka, Toru; Tsunoda, Yoshiya; Azuma, Arata; Nei, Takahito; Yatagai, Yohei; Rin, Shigen; Sekine, Akimasa; Hayashihara, Kenji

2014-01-01

386

The aurora sign: an ultrasonographic sign suggesting parenchymal lung disease.  

PubMed

The objective of this study was to clarify the cause and clinical significance of a large number of ring-down artefact (RA) observed on the dorsal side of the right hepatic lobe on abdominal ultrasound (US). 2000 abdominal US examinations were evaluated to investigate the frequency and number of RA behind the right lobe of the liver. In this study, RA observed by subcostal or intercostal US were described as the "aurora sign" when they were numerous. US findings were correlated with high resolution CT or three-dimensional CT of the right lung base. Experimental study was also performed to investigate the mechanism of the aurora sign. The results were as follows. (1). Aurora sign was noted in 43 patients. In 37 of these 43 patients (86.0%), chest CT or plain radiography revealed diffuse interstitial changes in the right lower lung field. Three-dimensional CT of the lung and the experimental model revealed that the aurora sign derived from the irregularity of air spaces immediately below the pleura associated with interstitial pulmonary disorders. (2). One or more bands of RA were observed in 907 of the 2000 patients (45.4%). Of 177 patients with fatty liver, RA was observed in 14 (7.9%), while of the 1823 patients with no fatty liver, RA was observed in 893 (49.0%). The frequency of RA was significantly different (p<0.001) between the patients with and without fatty liver. In conclusion, parenchymal lung disease should be suspected when the aurora sign is noted on the dorsal side of the right hepatic lobe. However, RAs are rare in patients with fatty liver. PMID:12857701

Kohzaki, S; Tsurusaki, K; Uetani, M; Nakanishi, K; Hayashi, K

2003-07-01

387

Acute chagas disease: new global challenges for an old neglected disease.  

PubMed

Chagas disease is caused by infection with the protozoan Trypanosoma cruzi, and although over 100 years have passed since the discovery of Chagas disease, it still presents an increasing problem for global public health. A plethora of information concerning the chronic phase of human Chagas disease, particularly the severe cardiac form, is available in the literature. However, information concerning events during the acute phase of the disease is scarce. In this review, we will discuss (1) the current status of acute Chagas disease cases globally, (2) the immunological findings related to the acute phase and their possible influence in disease outcome, and (3) reactivation of Chagas disease in immunocompromised individuals, a key point for transplantation and HIV infection management. PMID:25077613

Andrade, Daniela V; Gollob, Kenneth J; Dutra, Walderez O

2014-07-01