834 results match your criteria Proceedings of the American Thoracic Society[Journal]


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Proc Am Thorac Soc 2012 Dec;9(5)

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http://dx.doi.org/10.1513/pats.9.5.iDOI Listing
December 2012
4 Reads

Adaptation, evaluation, and updating of guidelines: article 14 in Integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):304-10

Introduction: Professional societies, like many other organizations, have recognized the need to use more rigorous processes to ensure that health care recommendations are informed by the best available research evidence. This is the last of a series of 14 articles that methodologists and researchers from around the world have prepared to advise guideline developers in respiratory and other diseases on how to achieve this. We updated a review of the literature on guideline adaptation, evaluation, and updating, focusing on four key questions. Read More

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http://dx.doi.org/10.1513/pats.201208-067STDOI Listing
December 2012
10 Reads

Disseminating and implementing guidelines: article 13 in Integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):298-303

Background: Professional societies, like many other organizations around the world, have recognized the need to use rigorous processes to ensure that health care recommendations are informed by the best available research evidence. This is the thirteenth of a series of 14 articles that were prepared to advise guideline developers in respiratory and other diseases. This article focuses on current concepts and research evidence about how to disseminate and implement guidelines optimally on a national and international level to improve quality of care. Read More

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http://www.atsjournals.org/doi/abs/10.1513/pats.201208-066ST
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http://dx.doi.org/10.1513/pats.201208-066STDOI Listing
December 2012
3 Reads

Reporting and publishing guidelines: article 12 in Integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):293-7

Introduction: Professional societies, like many other organizations around the world, have recognized the need to use rigorous processes to ensure that health care recommendations are informed by the best available research evidence. This is the twelfth of a series of 14 articles that were prepared to advise guideline developers in respiratory and other diseases. This article discusses the reporting and publishing of guidelines. Read More

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http://dx.doi.org/10.1513/pats.201208-065STDOI Listing
December 2012
24 Reads

Moving from evidence to developing recommendations in guidelines: article 11 in Integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):282-92

Introduction: Professional societies, like many other organizations around the world, have recognized the need to use more rigorous processes to ensure that healthcare recommendations are informed by the best available research evidence. This is the 11th of a series of 14 articles that methodologists and researchers from around the world prepared to advise guideline developers for respiratory and other diseases on how to achieve this goal. For this article, we developed five key questions and updated a review of the literature on moving from evidence to recommendations. Read More

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http://www.atsjournals.org/doi/abs/10.1513/pats.201208-064ST
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http://dx.doi.org/10.1513/pats.201208-064STDOI Listing
December 2012
25 Reads

How to integrate multiple comorbidities in guideline development: article 10 in Integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):274-81

Background: Professional societies, like many other organizations around the world, have recognized the need to use more rigorous processes to ensure that health care recommendations are informed by the best available research evidence. This is the 10th of a series of 14 articles that were prepared to advise guideline developers in respiratory and other diseases. This article deals with how multiple comorbidities (co-existing chronic conditions) may be more effectively integrated into guidelines. Read More

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http://dx.doi.org/10.1513/pats.201208-063STDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5820992PMC
December 2012
8 Reads

Stakeholder involvement: how to do it right: article 9 in Integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):269-73

Introduction: Professional societies, like many other organizations around the world, have recognized the need to use more rigorous processes to ensure that healthcare recommendations are informed by the best available research evidence with input from appropriate stakeholders. This is the ninth of a series of 14 articles that were prepared by an international panel to advise guideline developers in respiratory and other diseases on approaches for guideline development. We updated a review of the literature on stakeholder involvement, focusing on six key questions. Read More

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http://dx.doi.org/10.1513/pats.201208-062STDOI Listing
December 2012
5 Reads

Integrating values and consumer involvement in guidelines with the patient at the center: article 8 in Integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):262-8

Introduction: Professional societies, like many other organizations around the world, have recognized the need to use rigorous processes to ensure that healthcare recommendations are informed by the best available research evidence. They are also realizing the need to involve consumers of healthcare (patients, caregivers, and the public) and integrate their values and preferences in clinical guideline development. This is the eighth of a series of 14 articles that were prepared to advise guideline developers in respiratory and other diseases. Read More

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http://dx.doi.org/10.1513/pats.201208-061STDOI Listing
December 2012
4 Reads

Synthesis, grading, and presentation of evidence in guidelines: article 7 in Integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):256-61

Introduction: Professional societies, like many other organizations around the world, have recognized the need to use more rigorous processes to ensure that health care recommendations are informed by the best available research evidence. This is the seventh of a series of 14 articles that were prepared to advise guideline developers in respiratory and other diseases on approaches for guideline development. This article focuses on synthesizing, rating, and presenting evidence in guidelines. Read More

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http://dx.doi.org/10.1513/pats.201208-060STDOI Listing
December 2012
15 Reads

Incorporating considerations of cost-effectiveness, affordability, and resource implications in guideline development: article 6 in Integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):251-5

Introduction: Professional societies, like many other organizations around the world, have recognized the need to use rigorous processes to ensure that health care recommendations are based on the best available research evidence. This is the sixth of a series of 14 articles prepared to advise guideline developers for respiratory and other diseases on how to achieve this goal. In this article, we focused on integrating cost and resource information in guideline development and formulating recommendations focusing on four key questions. Read More

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http://dx.doi.org/10.1513/pats.201208-059STDOI Listing
December 2012
6 Reads

Deciding what type of evidence and outcomes to include in guidelines: article 5 in Integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):243-50

Introduction: Professional societies, like many other organizations around the world, have recognized the need to use more rigorous processes to ensure that health care recommendations are informed by the best available research evidence. This is the fifth of a series of 14 articles that were prepared by an international panel to advise guideline developers in respiratory and other diseases on approaches for guideline development. This article focuses on what type of evidence and outcomes to include in guidelines. Read More

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http://dx.doi.org/10.1513/pats.201208-058STDOI Listing
December 2012
10 Reads

Guideline funding and conflicts of interest: article 4 in Integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):234-42

Introduction: Professional societies, like many other organizations around the world, have recognized the need to use more rigorous processes to ensure that healthcare recommendations are informed by the best available research evidence. This is the fourth of a series of 14 articles prepared to advise guideline developers in respiratory and other disease. It focuses on commercial funding of guidelines and managing conflict of interest effectively in the context of guidelines. Read More

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http://dx.doi.org/10.1513/pats.201208-057STDOI Listing
December 2012
3 Reads

Guideline group composition and group processes: article 3 in Integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):229-33

Background: Professional societies, like many other organizations around the world, have recognized the need to use more rigorous processes to ensure that health care recommendations are informed by the best available research evidence. This is the third of a series of 14 articles that were prepared to advise guideline developers in respiratory and other diseases on considerations for group compositions and group processes in guideline development, and how this can be effectively integrated in the context of respiratory disease guidelines on a national and international level.

Methods: We updated a review of the literature addressing group composition and group process, focusing on the following questions: 1. Read More

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http://dx.doi.org/10.1513/pats.201208-056STDOI Listing
December 2012
7 Reads

Priority setting in guideline development: article 2 in Integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):225-8

Introduction: Professional societies, like many other organizations around the world, have recognized the need to use more rigorous processes to ensure that health care recommendations are informed by the best available research evidence. Priority setting is an essential component of developing clinical practice guidelines informed by the best available research evidence. It ensures that resources and attention are devoted to those areas in which clinical recommendations will provide the greatest benefit to patients, clinicians, and policy makers. Read More

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http://dx.doi.org/10.1513/pats.201208-055STDOI Listing
December 2012
28 Reads

Identifying target audiences: who are the guidelines for? : article 1 in Integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):219-24

Background: Professional societies, like many other organizations around the world, have recognized the need to use rigorous processes to ensure that health care recommendations are informed by the best available research evidence. Different clinical practice guidelines addressing the management of the same disease may vary widely in the evidence used and the format of the recommendations, with the result that not all are appropriate for all audiences. This is the first of a series of 14 articles that clinicians, methodologists, and researchers from around the world prepared to advise those developing guidelines in respiratory and other diseases about the potential impact of identifying the target audiences for their clinical practice guidelines. Read More

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http://dx.doi.org/10.1513/pats.201208-054STDOI Listing
December 2012
37 Reads

A guide to guidelines for professional societies and other developers of recommendations: introduction to integrating and coordinating efforts in COPD guideline development. An official ATS/ERS workshop report.

Proc Am Thorac Soc 2012 Dec;9(5):215-8

Organizations around the world are recognizing that guidelines should be based on the best available evidence, that the development of recommendations needs to be transparent, and that appropriate processes should be followed. In June 2007, we convened an American Thoracic Society (ATS)/European Respiratory Society (ERS)-sponsored workshop with over 60 representatives from 36 international organizations to provide advice to guideline developers about the required steps and processes for guideline development using the management of chronic obstructive pulmonary disease (COPD) as an example. Following the workshop, participants completed a series of 14 review articles that underwent peer review and incorporated key new literature until June 2011 for most articles in this series. Read More

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http://dx.doi.org/10.1513/pats.201208-053STDOI Listing
December 2012
30 Reads

A guide to guidelines for pulmonary, sleep, and critical care medicine clinicians.

Proc Am Thorac Soc 2012 Dec;9(5):211-4

Department of Research and Evaluation, Kaiser Permanente Southern California, 100 S. Los Robles Ave., Pasadena, CA 91101, USA.

Both the Institute of Medicine and the Guidelines International Network have recently published standards for trustworthy guidelines. The standards address multiple aspects of guideline development, including being transparent about funding and methodology, minimizing bias related to conflicts of interest, assembling writing committees with broad stakeholder representation, using rigorous and systematic methods to synthesize evidence and formulate recommendations, and periodically assessing guidelines for currency and updating them as required. In this article, we present the perspective of the Documents Development and Implementation Committee of the American Thoracic Society (ATS) on these and other guideline-related topics of relevance to ATS members. Read More

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http://dx.doi.org/10.1513/pats.201211-103EDDOI Listing
December 2012
1 Read

Clinical year in review IV: HIV, mycobacterial disease, pulmonary hypertension, and interstitial lung disease.

Proc Am Thorac Soc 2012 Oct;9(4):204-9

Department of Medicine, University of California San Francisco, San Francisco, California, USA.

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http://dx.doi.org/10.1513/pats.201207-035TTDOI Listing
October 2012
7 Reads

Clinical year in review III: asthma, chronic obstructive pulmonary disease, environmental and occupational lung disease, and ethics and end-of-life care.

Proc Am Thorac Soc 2012 Oct;9(4):197-203

Division of Pulmonary and Critical Care Medicine, National Jewish Health, 1400 Jackson St., J-201, Denver, CO 80206, USA.

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http://dx.doi.org/10.1513/pats.201206-032TTDOI Listing
October 2012
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Clinical year in review II: mechanical ventilation, acute respiratory distress syndrome, critical care, and lung cancer.

Proc Am Thorac Soc 2012 Oct;9(4):190-6

Interdepartmental Division of Critical Care and Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada.

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http://dx.doi.org/10.1513/pats.201206-033TTDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5820997PMC
October 2012
4 Reads

STAT3: a central mediator of pulmonary fibrosis?

Proc Am Thorac Soc 2012 Jul;9(3):177-82

UBC James Hogg Research Centre, Anesthesiology, Pharmacology, and Therapeutics, 1081 Burrard Street, St. Paul's Hospital, Vancouver, BC, Canada.

Pulmonary fibrosis is a devastating, relentlessly progressive, and lethal disease. There is a significant unmet need for effective treatment since currently no FDA-approved therapies exist. Current thinking suggests that idiopathic pulmonary fibrosis (IPF) is initiated by pathways similar to normal wound healing, but relentless fibrosis occurs secondary to absent or defective inhibitory mechanisms that normally terminate wound healing. Read More

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http://dx.doi.org/10.1513/pats.201201-007AWDOI Listing
July 2012
2 Reads

Epigenetic mechanisms through which Toll-like receptor-9 drives idiopathic pulmonary fibrosis progression.

Proc Am Thorac Soc 2012 Jul;9(3):172-6

Department of Pathology, University of Michigan Medical School, 109 Zina Pitcher Place, Ann Arbor, MI 48103-2200, USA.

Patients with idiopathic pulmonary fibrosis (IPF) survive a median of 3 years after diagnosis, but a high degree of variability in longitudinal disease progression has been observed. Unfortunately, physiology and clinical parameters determined at the time of diagnosis have proven inaccurate in predicting the rate at which IPF ultimately progresses. A mechanistic explanation for disease progression in patients with IPF is presently unclear, but we have recently shown that hypomethylated CpG DNA drives the rapid progression of fibrotic lung disease through the differentiation of pulmonary fibroblasts into myofibroblasts through a TLR9-dependent mechanism. Read More

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http://www.atsjournals.org/doi/abs/10.1513/pats.201201-002AW
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http://dx.doi.org/10.1513/pats.201201-002AWDOI Listing
July 2012
7 Reads

Stem cells and pulmonary fibrosis: cause or cure?

Proc Am Thorac Soc 2012 Jul;9(3):164-71

Centre for Respiratory Research, University College London, 5 University Street, London, UK.

Pulmonary fibrosis is a feature of a number of important lung diseases, and alveolar epithelial injury plays a key role in their pathogenesis. Traditionally, type II alveolar epithelial cells have been viewed as the progenitor cells of the alveolar epithelium; however, recent studies have identified a number of other progenitor and stem cell populations that may participate in alveolar epithelial repair. These studies suggest that the injury microenvironment plays a role in regulation of progenitor cell populations. Read More

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http://dx.doi.org/10.1513/pats.201201-010AWDOI Listing
July 2012
2 Reads

Hepatocyte growth factor and lung fibrosis.

Proc Am Thorac Soc 2012 Jul;9(3):158-63

Service de Pneumologie A, Hôpital Bichat, 46 rue Henri Huchard, Paris CEDEX 18, France.

Idiopathic pulmonary fibrosis is currently believed to be driven by alveolar epithelial cells, with abnormally activated alveolar epithelial cells accumulating in an attempt to repair injured alveolar epithelium (1). Thus, targeting the alveolar epithelium to prevent or inhibit the development of pulmonary fibrosis might be an interesting therapeutic option in this disease. Hepatocyte growth factor (HGF) is a growth factor for epithelial and endothelial cells, which is secreted by different cell types, especially fibroblasts and neutrophils. Read More

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http://dx.doi.org/10.1513/pats.201202-018AWDOI Listing
July 2012
40 Reads

Idiopathic pulmonary fibrosis: an altered fibroblast proliferation linked to cancer biology.

Authors:
Carlo Vancheri

Proc Am Thorac Soc 2012 Jul;9(3):153-7

Regional Center for Interstitial and Rare Lung Diseases, Department of Clinical and Experimental Biomedicine, Section of Respiratory Diseases, University of Catania, Via S. Sofia 78, Catania, Italy.

The fibrotic process that characterizes idiopathic pulmonary fibrosis (IPF) is commonly considered the result of a recurrent injury to the alveolar epithelium followed by an uncontrolled proliferation of fibroblasts. However, based on considerable scientific evidence, it has been recently hypothesized that IPF might be considered a neoproliferative disorder of the lung because this disease exhibits several pathogenic features similar to cancer. Indeed, epigenetic and genetic abnormalities, altered cell-to-cell communications, uncontrolled proliferation, and abnormal activation of specific signal transduction pathways are biological hallmarks that characterize the pathogenesis of IPF and cancer. Read More

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http://dx.doi.org/10.1513/pats.201203-025AWDOI Listing
July 2012
1 Read

Genesis of the myofibroblast in lung injury and fibrosis.

Authors:
Sem H Phan

Proc Am Thorac Soc 2012 Jul;9(3):148-52

Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109-2200, USA.

Tissue injury incites a repair response with a key mesenchymal component that provides the essential connective tissue for subsequent regeneration or pathological fibrosis. The fibroblast is the major mesenchymal cell type to be implicated in this connective tissue response, and it is in its activated or differentiated form that it participates in the repair process. The myofibroblast represents such an activated mesenchymal cell and is a key source of extracellular matrix and inflammatory/fibrogenic cytokines as well as participating in wound contraction. Read More

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http://dx.doi.org/10.1513/pats.201201-011AWDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5830705PMC
July 2012
6 Reads

Mechanical aspects of lung fibrosis: a spotlight on the myofibroblast.

Authors:
Boris Hinz

Proc Am Thorac Soc 2012 Jul;9(3):137-47

Laboratory of Tissue Repair and Regeneration, Matrix Dynamics Group, Faculty of Dentistry, University of Toronto, 150 College Street, Toronto, Ontario, Canada.

Contractile myofibroblasts are responsible for the irreversible alterations of the lung parenchyma that hallmark pulmonary fibrosis. In response to lung injury, a variety of different precursor cells can become activated to develop myofibroblast features, most notably formation of stress fibers and expression of α-smooth muscle actin. Starting as an acute and beneficial repair process, myofibroblast secretion of collagen and contraction frequently becomes excessive and persists. Read More

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http://dx.doi.org/10.1513/pats.201202-017AWDOI Listing
July 2012
2 Reads

TGF-β activation and lung fibrosis.

Proc Am Thorac Soc 2012 Jul;9(3):130-6

Nottingham Respiratory Biomedical Research Unit, Nottingham University Hospitals, University of Nottingham, Hucknall Road, Nottingham, UK.

Lung fibrosis can affect the parenchyma and the airways, classically giving rise to idiopathic pulmonary fibrosis (IPF) in the parenchyma or airway remodeling in asthma and chronic obstructive pulmonary disease. TGF-β activation has been implicated in the fibrosis of both IPF and airway remodeling. However, the mechanisms of TGF-β activation appear to differ depending on the cellular and anatomical compartments, with implications on disease pathogenesis. Read More

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http://dx.doi.org/10.1513/pats.201201-003AWDOI Listing
July 2012
3 Reads

Modulation of acute lung injury by integrins.

Authors:
Dean Sheppard

Proc Am Thorac Soc 2012 Jul;9(3):126-9

University of California-San Francisco, CA 94143-2922, USA.

Acute lung injury is a common disorder with a high mortality rate, but previous efforts to develop drugs to treat this disorder have been unsuccessful. In an effort to develop more effective treatments, we have been studying the molecular pathways that regulate the dysfunction of alveolar epithelial cells and endothelial cells that serve as a final common pathway leading to alveolar flooding. Using integrin subunit knockout mice and antibodies we developed by immunizing these mice, we have found important and distinct roles for the αvβ6 integrin on epithelial cells and the αvβ5 integrin on endothelial cells in mediating increases in alveolar permeability in multiple models of acute lung injury. Read More

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http://dx.doi.org/10.1513/pats.201112-052AWDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5830704PMC
July 2012
3 Reads

The genetic and environmental causes of pulmonary fibrosis.

Proc Am Thorac Soc 2012 Jul;9(3):120-5

University of Colorado, 12631 East 17th Avenue, Aurora, CO 80045, USA.

Although substantial progress has been made in understanding the clinical, radiological, and pathological manifestations of fibrosing interstitial lung diseases (ILD), it remains difficult for the clinician to predict the clinical course or the response to therapy for the subtypes of ILD, even from individual to individual with the same diagnosis. This article reviews the genetic and environmental causes of pulmonary fibrosis, specifically focusing on genetic and epigenetic variants of MUC5B and several types of ILD, to discuss why only some individuals with the MUC5B promoter polymorphism develop pulmonary fibrosis. Once we discover how these genetic and epigenetic risks lead to the development of ILD, we and others can apply these discoveries to: (1) identify individuals at risk of developing ILD, (2) diagnose the condition at an earlier stage, (3) identify novel mechanisms that cause ILD, and (4) eventually develop personalized therapeutic strategies for intervention. Read More

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http://dx.doi.org/10.1513/pats.201112-055AWDOI Listing
July 2012
4 Reads

Modulating the alveolar milieu to enhance resolution of fibrotic lung injury.

Proc Am Thorac Soc 2012 Jul;9(3):117-9

Developmental Biology and Regenerative Medicine Program, The Saban Research Institute, Children's Hospital Los Angeles, 4650 Sunset Boulevard, Los Angeles, CA 90027, USA.

Fibrotic lung injury is often attributed to a myriad of factors, including environmental exposure, age, genetic predisposition, epigenetics, coexisting conditions, acute lung injury, and viral infection. No effective therapies, other than lung transplantation, have proven effective against lung fibrosis. Loss of cellular homeostasis mechanisms in alveolar epithelial type I cells and any inability of type II progenitor cells to resist and repair epithelial injury are indicators that impaired response to injury and regeneration is a critical component of this disorder. Read More

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http://dx.doi.org/10.1513/pats.201201-013AWDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5830702PMC
July 2012
18 Reads

The impact of TGF-β on lung fibrosis: from targeting to biomarkers.

Proc Am Thorac Soc 2012 Jul;9(3):111-6

Comprehensive Pneumology Center, Ludwig Maximilians University Munich and Helmholtz Zentrum München, Max-Lebsche-Platz 31, Munich, Germany.

Transforming growth factor-β (TGF-β) is extensively involved in the development of fibrosis in different organs. Overproduction or potentiation of its profibrotic effects leads to an aberrant wound healing response during the initiation of fibrotic processes. Idiopathic pulmonary fibrosis (IPF) is a chronic, devastating disease, in which TGF-β\x{2013}induced disturbances of the homeostatic microenvironment are critical to promote cell activation, migration, invasion, or hyperplastic changes. Read More

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http://dx.doi.org/10.1513/pats.201203-023AWDOI Listing
July 2012
3 Reads

Role of the lysophospholipid mediators lysophosphatidic acid and sphingosine 1-phosphate in lung fibrosis.

Proc Am Thorac Soc 2012 Jul;9(3):102-10

Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, 149 13th Street, Charlestown, MA 02129, USA.

Aberrant wound healing responses to lung injury are believed to contribute to fibrotic lung diseases, such as idiopathic pulmonary fibrosis (IPF). The lysophospholipids lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P), by virtue of their ability to mediate many basic cellular functions, including survival, proliferation, migration, and contraction, can influence many of the biological processes involved in wound healing. Accordingly, recent investigations indicate that LPA and S1P may play critical roles in regulating the development of lung fibrosis. Read More

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http://dx.doi.org/10.1513/pats.201201-005AWDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5455616PMC
July 2012
3 Reads

Coagulation cascade proteinases in lung injury and fibrosis.

Proc Am Thorac Soc 2012 Jul;9(3):96-101

Centre for Respiratory Research, University College London, 5 University Street, London, UK.

The primary function of the coagulation cascade is to promote hemostasis and limit blood loss in response to tissue injury. In addition, there is now considerable evidence that coagulation plays pivotal roles in orchestrating inflammatory and tissue repair responses via both the generation of fibrin and activation of the family of proteinase-activated receptors (PARs). Consequently, uncontrolled coagulation and PAR signaling responses have been shown to contribute to excessive inflammatory and fibroproliferative responses in the context of a broad range of conditions, including acute lung injury and fibrotic lung disease. Read More

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http://dx.doi.org/10.1513/pats.201201-006AWDOI Listing
July 2012
5 Reads

Epithelial responses to lung injury: role of the extracellular matrix.

Authors:
Harold A Chapman

Proc Am Thorac Soc 2012 Jul;9(3):89-95

Pulmonary and Critical Care Division, University of California at San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143-0130, USA.

The key role of extracellular matrices in alveolar epithelial cell (AEC) biology is highlighted by the phenotypes of primary AECs cultured on a soft laminin gel contrasted with that on a stiff, fibronectin matrix. On laminin, AECs maintain an epithelial phenotype, and progenitor cells within this population proliferate. In contrast, on fibronectin, AECs rapidly lose surfactant expression and spread extensively, changes that depend on activation of latent TGF-β1 by engagement of fibronectin-binding integrins. Read More

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http://dx.doi.org/10.1513/pats.201112-053AWDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5830703PMC
July 2012
4 Reads

Chair's summary: lung injury and repair: role of extracellular matrix.

Proc Am Thorac Soc 2012 Jul;9(3):88

Centre for Respiratory Research, University College London, Department of Medicine, Rayne Institute, 5 University Street, UK.

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http://dx.doi.org/10.1513/pats.201203-022AWDOI Listing
July 2012
1 Read

Chronic obstructive pulmonary disease and lung cancer: common pathogenesis, shared clinical challenges.

Proc Am Thorac Soc 2012 May;9(2):74-9

Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Environmental inhaled noxious particles have been known to play a role in several lung diseases, including chronic obstructive pulmonary disease (COPD) and lung cancer, the deadliest malignancy in the world in both sexes. Of the known noxious agents, tobacco smoking is the leading preventable cause of death worldwide and is a recognized risk for the development of both diseases. The association between COPD and lung cancer has been demonstrated in population-based studies, lung cancer screening programs, epidemiological surveys, and case control and biological mechanistic studies. Read More

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http://dx.doi.org/10.1513/pats.201107-039MSDOI Listing
May 2012
3 Reads

New approaches to targeted therapy in lung cancer.

Authors:
William Pao

Proc Am Thorac Soc 2012 May;9(2):72-3

Vanderbilt-Ingram Cancer Center, 2220 Pierce Avenue 777 PRB, Nashville, TN 37232, USA.

This brief report summarizes Dr. Pao's talk at the 54th Annual Meeting of the Thomas L. Petty Aspen Lung Conference, in Aspen, Colorado, on June 11, 2011. Read More

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http://dx.doi.org/10.1513/pats.201112-054MSDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359104PMC
May 2012
1 Read

Equilibria of humans and our indigenous microbiota affecting asthma.

Authors:
Martin J Blaser

Proc Am Thorac Soc 2012 May;9(2):69-71

Department of Medicine, New York University Langone Medical Center, 550 First Avenue, OBV A606, New York, NY 10016, USA.

It is becoming increasingly clear that our residential microbes, the key constituents in the human microbiome, are centrally involved in many aspects of our physiology. In particular, the ancient and dominant gastric bacteria Helicobacter pylori are highly interactive with human physiology. In modern times, H. Read More

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http://dx.doi.org/10.1513/pats.201108-048MSDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359112PMC
May 2012
3 Reads

Endogenous modifiers of cigarette smoke exposure within the lung.

Proc Am Thorac Soc 2012 May;9(2):66-8

University of Pittsburgh School of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, Pittsburgh, PA 15261, USA.

Cigarette smoke exposure generates both acute and chronic inflammatory cell infiltrates that are operative in numerous pulmonary disorders. Cigarette smoke induces a complex signaling cascade within the lung mediated by epithelial cells, lymphocytes, macrophages, and others. The net result is a destructive and self-perpetuating inflammatory environment that is capable of creating lung diseases such as emphysema, while simultaneously fueling lung tumor growth using both matrix-dependent and -independent means. Read More

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http://dx.doi.org/10.1513/pats.201108-046MSDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359106PMC
May 2012
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The cancer epigenome: its origins, contributions to tumorigenesis, and translational implications.

Authors:
Stephen B Baylin

Proc Am Thorac Soc 2012 May;9(2):64-5

The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21287, USA.

Epigenetic abnormalities in lung and other cancers continue to be defined at a rapid pace. We are coming to appreciate that cancers have an "epigenetic landscape" wherein genes vulnerable to abnormalities, such as promoter DNA hypermethylation and associated gene silencing, tend to reside in defined nuclear positions and chromosome domains and relationships to chromatin regulation, which facilitates states of stem cell renewal. These same genes and domains are also vulnerable to epigenetic abnormalities induced by factors to which cells are exposed during cancer risk states, such as chronic inflammation. Read More

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http://dx.doi.org/10.1513/pats.201201-001MSDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359110PMC
May 2012
7 Reads

Senescence in chronic obstructive pulmonary disease.

Proc Am Thorac Soc 2012 May;9(2):62-3

Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado, USA.

There is a growing realization that chronic obstructive pulmonary disease involves several processes present in aging and cellular senescence. The impact of these processes in the pathogenesis of the main manifestations is multiple, particularly in the propagation of a proinflammatory phenotype, loss of reparative potential, and amplification of oxidative stress, all ultimately leading to tissue damage. This review highlights salient aspects related to senescence discussed in the 2011 Aspen Lung Conference. Read More

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http://dx.doi.org/10.1513/pats.201201-012MSDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359109PMC
May 2012
3 Reads

Chitinase-like proteins in lung injury, repair, and metastasis.

Proc Am Thorac Soc 2012 May;9(2):57-61

Department of Internal Medicine, Yale School of Medicine, New Haven, CT 06520-8056, USA.

This report explains how our studies of asthma and Th2 inflammation led us to investigate the roles of chitinase-like proteins (CLPs) in lung injury and repair and puts forth an overall hypothesis that can explain the roles that these moieties play in biology and a hypothesis regarding the ways that dysregulated CLP expression may contribute to the pathogenesis of a variety of diseases. We test this hypothesis by assessing the contributions of the CLP breast regression protein (BRP)-39 in the pathogenesis of malignant melanoma metastasis to the lung. Read More

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http://www.atsjournals.org/doi/abs/10.1513/pats.201112-056MS
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http://dx.doi.org/10.1513/pats.201112-056MSDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359113PMC
May 2012
5 Reads

Lung cancer chemoprevention.

Authors:
Robert L Keith

Proc Am Thorac Soc 2012 May;9(2):52-6

Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, Veterans Affairs Eastern Colorado Healthcare System, University of Colorado at Denver–School of Medicine, Denver, Colorado, USA.

Lung cancer is the leading cause of cancer death in the United States, and the majority of diagnoses are made in former smokers. Although avoidance of tobacco abuse and smoking cessation clearly will have the greatest impact on lung cancer development, effective chemoprevention could prove to be more effective than treatment of established, advanced-stage disease. Chemoprevention is the use of dietary or pharmaceutical agents to reverse or block the carcinogenic process and has been successfully applied to common malignancies other than lung (including recent reports on the prevention of breast cancer in high-risk individuals). Read More

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http://dx.doi.org/10.1513/pats.201107-038MSDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359111PMC
May 2012
4 Reads

Experimental therapeutics of Nrf2 as a target for prevention of bacterial exacerbations in COPD.

Proc Am Thorac Soc 2012 May;9(2):47-51

Department of Environmental Health Sciences, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA.

A growing body of evidence indicates that oxidative stress plays a central role in the progression of chronic obstructive pulmonary disease (COPD). Chronic oxidative stress caused by cigarette smoke generates damage-associated molecular patterns (DAMPs), such as oxidatively or nitrosatively modified proteins and extracellular matrix fragments, which induce abnormal airway inflammation by activating innate and adaptive immune responses. Furthermore, oxidative stress-induced histone deacetylase 2 (HDAC2) inactivity is implicated in amplifying inflammatory responses and corticosteroid resistance in COPD. Read More

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http://dx.doi.org/10.1513/pats.201201-009MSDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359107PMC
May 2012
4 Reads

Systemic inflammation and comorbidities in chronic obstructive pulmonary disease.

Proc Am Thorac Soc 2012 May;9(2):43-6

Institut del Tòrax, Hospital Clínic, Villarroel 170, Escala 3, Planta 5, 08036 Barcelona, Spain.

The relationship between systemic inflammation and comorbidities in patients with chronic obstructive pulmonary disease (COPD) is unclear. This article discusses (1) the prevalence and clinical impact of comorbidities in COPD; (2) the current knowledge on definition, prevalence, consequences, and treatment of systemic inflammation in COPD; and (3) the relationship of systemic inflammation and lung cancer in COPD. Read More

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http://dx.doi.org/10.1513/pats.201108-050MSDOI Listing
May 2012
3 Reads

Field cancerization in non-small cell lung cancer: implications in disease pathogenesis.

Proc Am Thorac Soc 2012 May;9(2):38-42

Department of Thoracic/Head and Neck Medical Oncology , University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Unit 085, Houston, TX 77030, USA.

Lung cancer, of which non-small cell lung cancer (NSCLC) composes the majority, is the leading cause of cancer-related deaths in the United States and worldwide. NSCLCs are tumors with complex biology that we have recently started to understand with the advent of various histological, transcriptomic, genomic, and proteomic technologies. However, the histological and molecular pathogenesis of this malignancy, in particular of adenocarcinomas, is still largely unknown. Read More

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http://dx.doi.org/10.1513/pats.201201-004MSDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5821032PMC
May 2012
1 Read

Lung epithelial healing: a modified seed and soil concept.

Proc Am Thorac Soc 2012 May;9(2):27-37

Department of Pediatrics, National Jewish Health, Denver, CO 80206, USA.

Airway epithelial healing is defined as restoration of health or soundness; to cure. Our research indicates that two types of progenitor cells participate in this process: the tissue-specific stem cell (TSC) and the facultative basal progenitor (FBP). The TSC restores the epithelium to its normal structure and function. Read More

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http://dx.doi.org/10.1513/pats.201201-008MSDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5821031PMC
May 2012
2 Reads

Genetic epidemiology of cigarette smoke-induced lung disease.

Authors:
Ann G Schwartz

Proc Am Thorac Soc 2012 May;9(2):22-6

Karmanos Cancer Institute, 4100 John R, Detroit, MI 48201, USA.

Chronic obstructive pulmonary disease (COPD) and lung cancer represent two diseases that share a strong risk factor in smoking, and COPD increases risk of lung cancer even after adjusting for the effects of smoking. These diseases not only occur jointly within an individual but also there is evidence of shared occurrence within families. Understanding the genetic contributions to these diseases, both individually and jointly, is needed to identify the highest risk group for screening and targeted prevention, as well as aiding in the development of targeted treatments. Read More

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http://dx.doi.org/10.1513/pats.201106-037MSDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359114PMC
May 2012
2 Reads