The Experts below are selected from a list of 255 Experts worldwide ranked by ideXlab platform

Ronald H. Goldstein - One of the best experts on this subject based on the ideXlab platform.

  • Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice
    Laboratory Investigation, 2002
    Co-Authors: Edgar C. Lucey, Gordon L. Snider, Joseph Keane, Ping-ping Kuang, Ronald H. Goldstein
    Abstract:

    Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice

  • Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice
    Laboratory Investigation, 2002
    Co-Authors: Edgar C. Lucey, Gordon L. Snider, Joseph Keane, Ping-ping Kuang, Ronald H. Goldstein
    Abstract:

    A single intratracheal dose of porcine pancreatic elastase, which is cleared from the lung by 24 hours, was administered to wild-type, IL-1β type 1 receptor-deficient, double TNF-α (type 1 and type 2) receptor-deficient, and combined TNF-α (type 1 receptor) plus IL-1β receptor-deficient mice. The mean linear intercept (Lm) of saline-treated mice was 32(3) μm [mean(SE)]. For wild-type elastase-treated mice, Lm was 81(6) μm at 21 days versus 52(5) μm at 5 days after treatment, indicating that alveolar wall remodeling occurs long after the elastase injury. At 21 days, Lm values were 67(10), 62(3), and 39(5) μm in elastase-treated mice deficient in the IL-1β receptor, double TNF-α receptors, and combined receptors, respectively. The level of apoptosis assessed by a terminal deoxynucleotidyl transferase-catalyzed in situ nick end-labeling assay was increased at 5 days after elastase treatment and was markedly and similarly attenuated in the IL-1β, the double TNF-α, and the combined receptor-deficient mice. Our results indicate that inflammatory mediators exacerbate Elastase-Induced Emphysema. We estimate that in the combined TNF-α + IL-1β receptor-deficient mice, inflammation accounts for about 80% of the Emphysema that develops after elastase treatment; decreased apoptosis of lung cells likely contributes to decreased severity of Emphysema.

Edgar C. Lucey - One of the best experts on this subject based on the ideXlab platform.

  • The Moderation of Elastase-Induced Emphysema in the Hamster by Intratracheal Pretreatment or Post-treatment with Succinyl Alanyl Alanyl Prolyl Valine Chloromethyl Ketone1–4
    The American review of respiratory disease, 2015
    Co-Authors: Phillip J. Stone, James D. Calore, Gordon L. Snider, Carl Franzblau, Edgar C. Lucey, Mario J. Castillo, James C. Powers
    Abstract:

    The capacity of the synthetic elastase inhibitor, succinyl alanyl alanyl prolyl valine chloromethyl ketone (CMK), to moderate Elastase-Induced Emphysema in hamsters was examined using morphometric and physiologic measurements. When 0.5 mg of CMK in saline was injected intratracheally 1 h before the intratracheal injection of 0.1 mg of porcine pancreatic elastase, the hamsters did not develop Emphysema. When CMK was injected intratracheally 1 h after elastase, the severity of Emphysema was reduced by approximately 50% compared with control animals receiving saline 1 h after elastase. The CMK was ineffective when administered tntratracheally 4 h after elastase.

  • Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice
    Laboratory Investigation, 2002
    Co-Authors: Edgar C. Lucey, Gordon L. Snider, Joseph Keane, Ping-ping Kuang, Ronald H. Goldstein
    Abstract:

    Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice

  • Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice
    Laboratory Investigation, 2002
    Co-Authors: Edgar C. Lucey, Gordon L. Snider, Joseph Keane, Ping-ping Kuang, Ronald H. Goldstein
    Abstract:

    A single intratracheal dose of porcine pancreatic elastase, which is cleared from the lung by 24 hours, was administered to wild-type, IL-1β type 1 receptor-deficient, double TNF-α (type 1 and type 2) receptor-deficient, and combined TNF-α (type 1 receptor) plus IL-1β receptor-deficient mice. The mean linear intercept (Lm) of saline-treated mice was 32(3) μm [mean(SE)]. For wild-type elastase-treated mice, Lm was 81(6) μm at 21 days versus 52(5) μm at 5 days after treatment, indicating that alveolar wall remodeling occurs long after the elastase injury. At 21 days, Lm values were 67(10), 62(3), and 39(5) μm in elastase-treated mice deficient in the IL-1β receptor, double TNF-α receptors, and combined receptors, respectively. The level of apoptosis assessed by a terminal deoxynucleotidyl transferase-catalyzed in situ nick end-labeling assay was increased at 5 days after elastase treatment and was markedly and similarly attenuated in the IL-1β, the double TNF-α, and the combined receptor-deficient mice. Our results indicate that inflammatory mediators exacerbate Elastase-Induced Emphysema. We estimate that in the combined TNF-α + IL-1β receptor-deficient mice, inflammation accounts for about 80% of the Emphysema that develops after elastase treatment; decreased apoptosis of lung cells likely contributes to decreased severity of Emphysema.

  • The specific treatment of Emphysema.
    The European respiratory journal. Supplement, 1990
    Co-Authors: Gordon L. Snider, Phillip J. Stone, Edgar C. Lucey
    Abstract:

    : Cigarette smoking is the major risk factor for development of Emphysema. Many people are unable to stop smoking despite skilled support. The elastase-antielastase imbalance hypothesis for the pathogenesis of Emphysema suggests that treatment with a supplemental elastase inhibitor might prevent development of Emphysema in susceptible people. Many elastase inhibitors have been developed. Poorly soluble inhibitors do not prevent Emphysema when tested in an animal model of Elastase-Induced Emphysema. Irreversible inhibitors are effective in a dose-response manner. Reversible but tight-binding large molecular weight inhibitors, which clear slowly from the lungs, are effective in vivo. Small molecular weight, reversible inhibitors prevent haemorrhage after human neutrophil elastase instillation into the lungs but may potentiate Emphysema. Only 15% of long-term smokers are susceptible to the development of Emphysema. Susceptible smokers can be identified by the development of airflow obstruction. An outcome study of efficacy of elastase inhibitor therapy would be prohibitively expensive. However, a study of the process of development of Elastase-Induced Emphysema is feasible. Measurement of alterations in elastase load of the lungs, elastase derived fibrinopeptides, circulating elastin peptides and urinary desmosines could be used for this purpose.

Gordon L. Snider - One of the best experts on this subject based on the ideXlab platform.

  • The Moderation of Elastase-Induced Emphysema in the Hamster by Intratracheal Pretreatment or Post-treatment with Succinyl Alanyl Alanyl Prolyl Valine Chloromethyl Ketone1–4
    The American review of respiratory disease, 2015
    Co-Authors: Phillip J. Stone, James D. Calore, Gordon L. Snider, Carl Franzblau, Edgar C. Lucey, Mario J. Castillo, James C. Powers
    Abstract:

    The capacity of the synthetic elastase inhibitor, succinyl alanyl alanyl prolyl valine chloromethyl ketone (CMK), to moderate Elastase-Induced Emphysema in hamsters was examined using morphometric and physiologic measurements. When 0.5 mg of CMK in saline was injected intratracheally 1 h before the intratracheal injection of 0.1 mg of porcine pancreatic elastase, the hamsters did not develop Emphysema. When CMK was injected intratracheally 1 h after elastase, the severity of Emphysema was reduced by approximately 50% compared with control animals receiving saline 1 h after elastase. The CMK was ineffective when administered tntratracheally 4 h after elastase.

  • Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice
    Laboratory Investigation, 2002
    Co-Authors: Edgar C. Lucey, Gordon L. Snider, Joseph Keane, Ping-ping Kuang, Ronald H. Goldstein
    Abstract:

    Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice

  • Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice
    Laboratory Investigation, 2002
    Co-Authors: Edgar C. Lucey, Gordon L. Snider, Joseph Keane, Ping-ping Kuang, Ronald H. Goldstein
    Abstract:

    A single intratracheal dose of porcine pancreatic elastase, which is cleared from the lung by 24 hours, was administered to wild-type, IL-1β type 1 receptor-deficient, double TNF-α (type 1 and type 2) receptor-deficient, and combined TNF-α (type 1 receptor) plus IL-1β receptor-deficient mice. The mean linear intercept (Lm) of saline-treated mice was 32(3) μm [mean(SE)]. For wild-type elastase-treated mice, Lm was 81(6) μm at 21 days versus 52(5) μm at 5 days after treatment, indicating that alveolar wall remodeling occurs long after the elastase injury. At 21 days, Lm values were 67(10), 62(3), and 39(5) μm in elastase-treated mice deficient in the IL-1β receptor, double TNF-α receptors, and combined receptors, respectively. The level of apoptosis assessed by a terminal deoxynucleotidyl transferase-catalyzed in situ nick end-labeling assay was increased at 5 days after elastase treatment and was markedly and similarly attenuated in the IL-1β, the double TNF-α, and the combined receptor-deficient mice. Our results indicate that inflammatory mediators exacerbate Elastase-Induced Emphysema. We estimate that in the combined TNF-α + IL-1β receptor-deficient mice, inflammation accounts for about 80% of the Emphysema that develops after elastase treatment; decreased apoptosis of lung cells likely contributes to decreased severity of Emphysema.

  • The specific treatment of Emphysema.
    The European respiratory journal. Supplement, 1990
    Co-Authors: Gordon L. Snider, Phillip J. Stone, Edgar C. Lucey
    Abstract:

    : Cigarette smoking is the major risk factor for development of Emphysema. Many people are unable to stop smoking despite skilled support. The elastase-antielastase imbalance hypothesis for the pathogenesis of Emphysema suggests that treatment with a supplemental elastase inhibitor might prevent development of Emphysema in susceptible people. Many elastase inhibitors have been developed. Poorly soluble inhibitors do not prevent Emphysema when tested in an animal model of Elastase-Induced Emphysema. Irreversible inhibitors are effective in a dose-response manner. Reversible but tight-binding large molecular weight inhibitors, which clear slowly from the lungs, are effective in vivo. Small molecular weight, reversible inhibitors prevent haemorrhage after human neutrophil elastase instillation into the lungs but may potentiate Emphysema. Only 15% of long-term smokers are susceptible to the development of Emphysema. Susceptible smokers can be identified by the development of airflow obstruction. An outcome study of efficacy of elastase inhibitor therapy would be prohibitively expensive. However, a study of the process of development of Elastase-Induced Emphysema is feasible. Measurement of alterations in elastase load of the lungs, elastase derived fibrinopeptides, circulating elastin peptides and urinary desmosines could be used for this purpose.

Joseph Keane - One of the best experts on this subject based on the ideXlab platform.

  • Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice
    Laboratory Investigation, 2002
    Co-Authors: Edgar C. Lucey, Gordon L. Snider, Joseph Keane, Ping-ping Kuang, Ronald H. Goldstein
    Abstract:

    Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice

  • Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice
    Laboratory Investigation, 2002
    Co-Authors: Edgar C. Lucey, Gordon L. Snider, Joseph Keane, Ping-ping Kuang, Ronald H. Goldstein
    Abstract:

    A single intratracheal dose of porcine pancreatic elastase, which is cleared from the lung by 24 hours, was administered to wild-type, IL-1β type 1 receptor-deficient, double TNF-α (type 1 and type 2) receptor-deficient, and combined TNF-α (type 1 receptor) plus IL-1β receptor-deficient mice. The mean linear intercept (Lm) of saline-treated mice was 32(3) μm [mean(SE)]. For wild-type elastase-treated mice, Lm was 81(6) μm at 21 days versus 52(5) μm at 5 days after treatment, indicating that alveolar wall remodeling occurs long after the elastase injury. At 21 days, Lm values were 67(10), 62(3), and 39(5) μm in elastase-treated mice deficient in the IL-1β receptor, double TNF-α receptors, and combined receptors, respectively. The level of apoptosis assessed by a terminal deoxynucleotidyl transferase-catalyzed in situ nick end-labeling assay was increased at 5 days after elastase treatment and was markedly and similarly attenuated in the IL-1β, the double TNF-α, and the combined receptor-deficient mice. Our results indicate that inflammatory mediators exacerbate Elastase-Induced Emphysema. We estimate that in the combined TNF-α + IL-1β receptor-deficient mice, inflammation accounts for about 80% of the Emphysema that develops after elastase treatment; decreased apoptosis of lung cells likely contributes to decreased severity of Emphysema.

Ping-ping Kuang - One of the best experts on this subject based on the ideXlab platform.

  • Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice
    Laboratory Investigation, 2002
    Co-Authors: Edgar C. Lucey, Gordon L. Snider, Joseph Keane, Ping-ping Kuang, Ronald H. Goldstein
    Abstract:

    Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice

  • Severity of Elastase-Induced Emphysema Is Decreased in Tumor Necrosis Factor-α and Interleukin-1β Receptor-Deficient Mice
    Laboratory Investigation, 2002
    Co-Authors: Edgar C. Lucey, Gordon L. Snider, Joseph Keane, Ping-ping Kuang, Ronald H. Goldstein
    Abstract:

    A single intratracheal dose of porcine pancreatic elastase, which is cleared from the lung by 24 hours, was administered to wild-type, IL-1β type 1 receptor-deficient, double TNF-α (type 1 and type 2) receptor-deficient, and combined TNF-α (type 1 receptor) plus IL-1β receptor-deficient mice. The mean linear intercept (Lm) of saline-treated mice was 32(3) μm [mean(SE)]. For wild-type elastase-treated mice, Lm was 81(6) μm at 21 days versus 52(5) μm at 5 days after treatment, indicating that alveolar wall remodeling occurs long after the elastase injury. At 21 days, Lm values were 67(10), 62(3), and 39(5) μm in elastase-treated mice deficient in the IL-1β receptor, double TNF-α receptors, and combined receptors, respectively. The level of apoptosis assessed by a terminal deoxynucleotidyl transferase-catalyzed in situ nick end-labeling assay was increased at 5 days after elastase treatment and was markedly and similarly attenuated in the IL-1β, the double TNF-α, and the combined receptor-deficient mice. Our results indicate that inflammatory mediators exacerbate Elastase-Induced Emphysema. We estimate that in the combined TNF-α + IL-1β receptor-deficient mice, inflammation accounts for about 80% of the Emphysema that develops after elastase treatment; decreased apoptosis of lung cells likely contributes to decreased severity of Emphysema.