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Acute Lung Injury

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Michael A Matthay – One of the best experts on this subject based on the ideXlab platform.

  • Treatment of Acute Lung Injury
    , 2012
    Co-Authors: Michael A Matthay
    Abstract:

    This presentation at the 2007 Aspen Lung Injury and Repair Conference provided a brief historical perspective from the 1998 Aspen Conference on Acute Lung Injury, highlighting the discussion of clinical definitions. There was also a review of the National Heart, Lung, and Blood Institute ARDS Network clinical trials, with an emphasis on the success of the Lung-protective ventilation strategy in reducing mortality. In addition, there was a discussion of the recently completed fluid and catheter treatment trial, which demonstrated no benefit for pulmonary arterial catheterization over central venous catheterization for monitoring patients with Acute Lung Injury (ALI). The trial demonstrated an increase in ventilator-free days with a fluid-conservative protocol. Finally, there was a discussion of recent experimental studies that show promise for cell-based therapy with mesenchymal stem cells for the treatment of endotoxin-induced ALI in mice. There were three objectives for this presentation at the 2007 Lung

  • Biomarkers in Acute Lung Injury: Insights into the Pathogenesis of Acute Lung Injury
    Critical Care Clinics, 2011
    Co-Authors: Lj Mark Cross, Michael A Matthay
    Abstract:

    Studies of potential biomarkers in experimental models of Acute Lung Injury (ALI) and from clinical samples from patients with ALI have provided extensive information relating to the pathophysiology of the mechanisms of Lung Injury and repair. The utility of biomarkers remains still solely part of the research tools to investigate Lung Injury and repair mechanisms and due to lack of sensitivity and specificity cannot yet be used as a clinical decision tool in patients with either Acute Lung Injury or ARDS. We have reviewed known biomarkers in context of their major biological activity such as inflammatory mediators, coagulation/fibrinolytic mediators, growth factors and the emerging use of proteomics. The continued interest in identifying and studying biomarkers is relevant as it continues to provide important information regarding the mechanisms involved in Lung Injury and repair and how this may be helpful in the identification and design of future therapeutic targets and strategies as well as hopefully to identify a sensitive and specific biomarker that would be of clinical relevance.

  • Alveolar edema fluid clearance and Acute Lung Injury
    Respiratory Physiology & Neurobiology, 2007
    Co-Authors: Yves Berthiaume, Michael A Matthay
    Abstract:

    Although Lung-protective ventilation strategies have substantially reduced mortality of Acute Lung Injury patients there is still a need for new therapies that can further decrease mortality in patients with Acute Lung Injury. Studies of epithelial ion and fluid transport across the distal pulmonary epithelia have provided important new concepts regarding potential new therapies for Acute Lung Injury. Overall, there is convincing evidence that the alveolar epithelium is not only a tight epithelial barrier that resists the movement of edema fluid into the alveoli, but it is also actively involved in the transport of ions and solutes, a process that is essential for edema fluid clearance and the resolution of Acute Lung Injury. The objective of this article is to consider some areas of recent progress in the field of alveolar fluid transport under normal and pathologic conditions. Vectorial ion transport across the alveolar and distal airway epithelia is the primary determinant of alveolar fluid clearance. The general paradigm is that active Na+ and Cl− transport drives net alveolar fluid clearance, as demonstrated in several different species, including the human Lung. Although these transport processes can be impaired in severe Lung Injury, multiple experimental studies suggest that upregulation of Na+ and Cl− transport might be an effective therapy in Acute Lung Injury. We will review mechanisms involved in pharmacological modulation of ion transport in Lung Injury with a special focus on the use of β-adrenergic agonists which has generated considerable interest and is a promising therapy for clinical Acute Lung Injury.

Sebastián Méndez-Álvarez – One of the best experts on this subject based on the ideXlab platform.

  • Genetic susceptibility to Acute Lung Injury.
    Critical Care Medicine, 2003
    Co-Authors: Jesús Villar, Carlos Flores, Sebastián Méndez-Álvarez
    Abstract:

    Objective: To review the complex interactions of markers of genetic susceptibility for critical illness and Acute Lung Injury. These may affect the responses of critically ill patients to Acute Lung Injury and Acute respiratory distress syndrome and may affect outcome. Data Sources and Study Selection: Published research and review articles related to genetic factors associated with susceptibility to critical illnesses and pulmonary disease. Data Extraction and Synthesis: Critical illness in adults often is followed by Acute Lung Injury, a phenomenon of Acute diffuse Lung inflammation. Physicians have long known that each patient responds differently to drugs and has a different risk for a particular event or outcome. Now, there is some evidence that cellular and humoral immune responses are subject to polymorphic genetic control, which explains the well-known diversity of clinical manifestations and outcomes in critically ill patients with the same disease. By revealing altered expression of relatively few genes involved in the responses to Lung Injury and repair, some investigators have found that these responses, and susceptibility to Acute Lung Injury, are heritable. In the last 5 yrs, we have discovered that an individual’s risks and cellular responses can be related to his or her own unique DNA. Conclusions: The search for an association between functional variants of a gene and clinical phenotype may help to identify key pathophysiological processes of disease. In the future, we will know much about which therapy is best for each individual patient in the intensive care unit.

  • Genetic susceptibility to Acute Lung Injury.
    Critical Care Medicine, 2003
    Co-Authors: Jesús Villar, Carlos Flores, Sebastián Méndez-Álvarez
    Abstract:

    Objective: To review the complex interactions of markers of genetic susceptibility for critical illness and Acute Lung Injury. These may affect the responses of critically ill patients to Acute Lung Injury and Acute respiratory distress syndrome and may affect outcome. Data Sources and Study Selection: Published research and review articles related to genetic factors associated with susceptibility to critical illnesses and pulmonary disease. Data Extraction and Synthesis: Critical illness in adults often is followed by Acute Lung Injury, a phenomenon of Acute diffuse Lung inflammation. Physicians have long known that each patient responds differently to drugs and has a different risk for a particular event or outcome. Now, there is some evidence that cellular and humoral immune responses are subject to polymorphic genetic control, which explains the well-known diversity of clinical manifestations and outcomes in critically ill patients with the same disease. By revealing altered expression of relatively few genes involved in the responses to Lung Injury and repair, some investigators have found that these responses, and susceptibility to Acute Lung Injury, are heritable. In the last 5 yrs, we have discovered that an individual’s risks and cellular responses can be related to his or her own unique DNA. Conclusions: The search for an association between functional variants of a gene and clinical phenotype may help to identify key pathophysiological processes of disease. In the future, we will know much about which therapy is best for each individual patient in the intensive care unit.

  • Genetic susceptibility to Acute Lung Injury.
    Critical care medicine, 2003
    Co-Authors: Jesús Villar, Carlos Flores, Sebastián Méndez-Álvarez
    Abstract:

    To review the complex interactions of markers of genetic susceptibility for critical illness and Acute Lung Injury. These may affect the responses of critically ill patients to Acute Lung Injury and Acute respiratory distress syndrome and may affect outcome. Published research and review articles related to genetic factors associated with susceptibility to critical illnesses and pulmonary disease. Critical illness in adults often is followed by Acute Lung Injury, a phenomenon of Acute diffuse Lung inflammation. Physicians have long known that each patient responds differently to drugs and has a different risk for a particular event or outcome. Now, there is some evidence that cellular and humoral immune responses are subject to polymorphic genetic control, which explains the well-known diversity of clinical manifestations and outcomes in critically ill patients with the same disease. By revealing altered expression of relatively few genes involved in the responses to Lung Injury and repair, some investigators have found that these responses, and susceptibility to Acute Lung Injury, are heritable. In the last 5 yrs, we have discovered that an individual’s risks and cellular responses can be related to his or her own unique DNA. The search for an association between functional variants of a gene and clinical phenotype may help to identify key pathophysiological processes of disease. In the future, we will know much about which therapy is best for each individual patient in the intensive care unit.

Jesús Villar – One of the best experts on this subject based on the ideXlab platform.

  • Genetic susceptibility to Acute Lung Injury.
    Critical Care Medicine, 2003
    Co-Authors: Jesús Villar, Carlos Flores, Sebastián Méndez-Álvarez
    Abstract:

    Objective: To review the complex interactions of markers of genetic susceptibility for critical illness and Acute Lung Injury. These may affect the responses of critically ill patients to Acute Lung Injury and Acute respiratory distress syndrome and may affect outcome. Data Sources and Study Selection: Published research and review articles related to genetic factors associated with susceptibility to critical illnesses and pulmonary disease. Data Extraction and Synthesis: Critical illness in adults often is followed by Acute Lung Injury, a phenomenon of Acute diffuse Lung inflammation. Physicians have long known that each patient responds differently to drugs and has a different risk for a particular event or outcome. Now, there is some evidence that cellular and humoral immune responses are subject to polymorphic genetic control, which explains the well-known diversity of clinical manifestations and outcomes in critically ill patients with the same disease. By revealing altered expression of relatively few genes involved in the responses to Lung Injury and repair, some investigators have found that these responses, and susceptibility to Acute Lung Injury, are heritable. In the last 5 yrs, we have discovered that an individual’s risks and cellular responses can be related to his or her own unique DNA. Conclusions: The search for an association between functional variants of a gene and clinical phenotype may help to identify key pathophysiological processes of disease. In the future, we will know much about which therapy is best for each individual patient in the intensive care unit.

  • Genetic susceptibility to Acute Lung Injury.
    Critical Care Medicine, 2003
    Co-Authors: Jesús Villar, Carlos Flores, Sebastián Méndez-Álvarez
    Abstract:

    Objective: To review the complex interactions of markers of genetic susceptibility for critical illness and Acute Lung Injury. These may affect the responses of critically ill patients to Acute Lung Injury and Acute respiratory distress syndrome and may affect outcome. Data Sources and Study Selection: Published research and review articles related to genetic factors associated with susceptibility to critical illnesses and pulmonary disease. Data Extraction and Synthesis: Critical illness in adults often is followed by Acute Lung Injury, a phenomenon of Acute diffuse Lung inflammation. Physicians have long known that each patient responds differently to drugs and has a different risk for a particular event or outcome. Now, there is some evidence that cellular and humoral immune responses are subject to polymorphic genetic control, which explains the well-known diversity of clinical manifestations and outcomes in critically ill patients with the same disease. By revealing altered expression of relatively few genes involved in the responses to Lung Injury and repair, some investigators have found that these responses, and susceptibility to Acute Lung Injury, are heritable. In the last 5 yrs, we have discovered that an individual’s risks and cellular responses can be related to his or her own unique DNA. Conclusions: The search for an association between functional variants of a gene and clinical phenotype may help to identify key pathophysiological processes of disease. In the future, we will know much about which therapy is best for each individual patient in the intensive care unit.

  • Genetic susceptibility to Acute Lung Injury.
    Critical care medicine, 2003
    Co-Authors: Jesús Villar, Carlos Flores, Sebastián Méndez-Álvarez
    Abstract:

    To review the complex interactions of markers of genetic susceptibility for critical illness and Acute Lung Injury. These may affect the responses of critically ill patients to Acute Lung Injury and Acute respiratory distress syndrome and may affect outcome. Published research and review articles related to genetic factors associated with susceptibility to critical illnesses and pulmonary disease. Critical illness in adults often is followed by Acute Lung Injury, a phenomenon of Acute diffuse Lung inflammation. Physicians have long known that each patient responds differently to drugs and has a different risk for a particular event or outcome. Now, there is some evidence that cellular and humoral immune responses are subject to polymorphic genetic control, which explains the well-known diversity of clinical manifestations and outcomes in critically ill patients with the same disease. By revealing altered expression of relatively few genes involved in the responses to Lung Injury and repair, some investigators have found that these responses, and susceptibility to Acute Lung Injury, are heritable. In the last 5 yrs, we have discovered that an individual’s risks and cellular responses can be related to his or her own unique DNA. The search for an association between functional variants of a gene and clinical phenotype may help to identify key pathophysiological processes of disease. In the future, we will know much about which therapy is best for each individual patient in the intensive care unit.

George D. Leikauf – One of the best experts on this subject based on the ideXlab platform.

  • Functional Genomics of Chlorine-induced Acute Lung Injury in Mice
    Proceedings of the American Thoracic Society, 2010
    Co-Authors: George D. Leikauf, Hannah Pope-varsalona, Vincent J. Concel, Pengyuan Liu, Kiflai Bein, Kelly A. Brant, Richard A. Dopico, An-soo Jang, Maggie Dietsch
    Abstract:

    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 ( approximately 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 x 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.

  • Differential Gene Expression in the Initiation and Progression of Nickel-Induced Acute Lung Injury
    American journal of respiratory cell and molecular biology, 2000
    Co-Authors: Susan A. Mcdowell, Kelly Gammon, Cindy J. Bachurski, Jonathan S. Wiest, John E. Leikauf, Daniel R. Prows, George D. Leikauf
    Abstract:

    Acute Lung Injury, an often fatal condition, can result from a wide range of insults leading to a complex series of biologic responses. Despite extensive research, questions remain about the interplay of the factors involved and their role in Acute Lung Injury. We proposed that assessing the temporal and functional relationships of differentially expressed genes after pulmonary insult would reveal novel interactions in the progression of Acute Lung Injury. Specifically, 8,734 sequence-verified murine complementary DNAs were analyzed in mice throughout the initiation and progression of Acute Lung Injury induced by particulate nickel sulfate. This study revealed the expression patterns of genes previously associated with Acute Lung Injury in relationship to one another and also uncovered changes in expression of a number of genes not previously associated with Acute Lung Injury. The overall pattern of gene expression was consistent with oxidative stress, hypoxia, cell proliferation, and extracellular matrix repair, followed by a marked decrease in pulmonary surfsurfactant proteins. Also, expressed sequence tags (ESTs), with nominal homology to known genes, displayed similar expression patterns to those of known genes, suggesting possible roles for these ESTs in the pulmonary response to Injury. Thus, this analysis of the progression and response to Acute Lung Injury revealed novel gene expression patterns.

Carlos Flores – One of the best experts on this subject based on the ideXlab platform.

  • Genetic susceptibility to Acute Lung Injury.
    Critical Care Medicine, 2003
    Co-Authors: Jesús Villar, Carlos Flores, Sebastián Méndez-Álvarez
    Abstract:

    Objective: To review the complex interactions of markers of genetic susceptibility for critical illness and Acute Lung Injury. These may affect the responses of critically ill patients to Acute Lung Injury and Acute respiratory distress syndrome and may affect outcome. Data Sources and Study Selection: Published research and review articles related to genetic factors associated with susceptibility to critical illnesses and pulmonary disease. Data Extraction and Synthesis: Critical illness in adults often is followed by Acute Lung Injury, a phenomenon of Acute diffuse Lung inflammation. Physicians have long known that each patient responds differently to drugs and has a different risk for a particular event or outcome. Now, there is some evidence that cellular and humoral immune responses are subject to polymorphic genetic control, which explains the well-known diversity of clinical manifestations and outcomes in critically ill patients with the same disease. By revealing altered expression of relatively few genes involved in the responses to Lung Injury and repair, some investigators have found that these responses, and susceptibility to Acute Lung Injury, are heritable. In the last 5 yrs, we have discovered that an individual’s risks and cellular responses can be related to his or her own unique DNA. Conclusions: The search for an association between functional variants of a gene and clinical phenotype may help to identify key pathophysiological processes of disease. In the future, we will know much about which therapy is best for each individual patient in the intensive care unit.

  • Genetic susceptibility to Acute Lung Injury.
    Critical Care Medicine, 2003
    Co-Authors: Jesús Villar, Carlos Flores, Sebastián Méndez-Álvarez
    Abstract:

    Objective: To review the complex interactions of markers of genetic susceptibility for critical illness and Acute Lung Injury. These may affect the responses of critically ill patients to Acute Lung Injury and Acute respiratory distress syndrome and may affect outcome. Data Sources and Study Selection: Published research and review articles related to genetic factors associated with susceptibility to critical illnesses and pulmonary disease. Data Extraction and Synthesis: Critical illness in adults often is followed by Acute Lung Injury, a phenomenon of Acute diffuse Lung inflammation. Physicians have long known that each patient responds differently to drugs and has a different risk for a particular event or outcome. Now, there is some evidence that cellular and humoral immune responses are subject to polymorphic genetic control, which explains the well-known diversity of clinical manifestations and outcomes in critically ill patients with the same disease. By revealing altered expression of relatively few genes involved in the responses to Lung Injury and repair, some investigators have found that these responses, and susceptibility to Acute Lung Injury, are heritable. In the last 5 yrs, we have discovered that an individual’s risks and cellular responses can be related to his or her own unique DNA. Conclusions: The search for an association between functional variants of a gene and clinical phenotype may help to identify key pathophysiological processes of disease. In the future, we will know much about which therapy is best for each individual patient in the intensive care unit.

  • Genetic susceptibility to Acute Lung Injury.
    Critical care medicine, 2003
    Co-Authors: Jesús Villar, Carlos Flores, Sebastián Méndez-Álvarez
    Abstract:

    To review the complex interactions of markers of genetic susceptibility for critical illness and Acute Lung Injury. These may affect the responses of critically ill patients to Acute Lung Injury and Acute respiratory distress syndrome and may affect outcome. Published research and review articles related to genetic factors associated with susceptibility to critical illnesses and pulmonary disease. Critical illness in adults often is followed by Acute Lung Injury, a phenomenon of Acute diffuse Lung inflammation. Physicians have long known that each patient responds differently to drugs and has a different risk for a particular event or outcome. Now, there is some evidence that cellular and humoral immune responses are subject to polymorphic genetic control, which explains the well-known diversity of clinical manifestations and outcomes in critically ill patients with the same disease. By revealing altered expression of relatively few genes involved in the responses to Lung Injury and repair, some investigators have found that these responses, and susceptibility to Acute Lung Injury, are heritable. In the last 5 yrs, we have discovered that an individual’s risks and cellular responses can be related to his or her own unique DNA. The search for an association between functional variants of a gene and clinical phenotype may help to identify key pathophysiological processes of disease. In the future, we will know much about which therapy is best for each individual patient in the intensive care unit.