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Oxidative stress and the critically ill patient [E-Book]

Contributor(s): Series: Cell biology research progress | Public health in the 21st century seriesPublisher: New York : Nova Biomedical, [2012]Description: 1 online resourceContent type:
  • text
Media type:
  • computer
Carrier type:
  • online resource
ISBN:
  • 9781620815762
  • 1620815761
  • 1620815834
  • 9781620815830
Subject(s): Online resources:
Contents:
4.5. Nitric Oxide Synthase4.6. Mieloperoxidase; 4.7. Cytochrome P450; 5. In Vivo Effects of Free Radicals; 5.1. Physiological Functions; 5.2. Pathophysiological Effects; Oxidative Damage; 6. Antioxidant Defense Systems; and Oxidative Stress; 7. Biomarkers of Oxidative Stress; 8. Oxidative Stress and Diseases; 8.1. Cardiovascular Diseases; 8.2. Hypertension; 8.3. Atherosclerosis; 8.4. Metabolic Syndrome and Diabetes; 8.5. Neurodegenerative Diseases; 8.6. Cancer; 8.7. Rheumatoid Arthritis; 8.8. Aging; Conclusion; References; Chapter II: Pathophysiology of Sepsis and Septic Shock; Abstract.
Abbreviations2. Introduction; 3. Pathophysiology of Sepsis; 3.1. Basic Molecular Mechanisms of Inflammation in Sepsis; 3.1.1. Pathogen-Host Interaction; 3.1.2. Neutrophils; 3.1.3. Cytokines; 3.1.4. Coagulation Disorders in Sepsis; 3.1.5. Endothelial Cells; 3.1.6. Complement Activation; 3.2. Immunoparalysis; 4. Pathophysiology of Septic Shock; Conclusions and Future Goals; References; Chapter III: Inflammation; Abstract; Abbreviations; 2. Introduction; 3. Current Concepts of the Inflammatory Response; 3.1. Cellular Mediators; 3.1.1. Neutrophils; 3.1.2. Macrophages; 3.1.3. Other Cells.
3.2. Cytokines, Chemokines and Lipid Mediators3.2.1. Lipid Mediators; 3.2.1.1. Resolvins Improve the Course of Inflammation; 3.2.2. Novel Cytokines; 3.3. The Role of Toll-Like Receptors; 3.3.1. Clinical Aspects; 3.4.1. Nuclear Factor kappaB; 3.4.1.1 Nuclear Factor kappaB and Oxidative Stress; 3.4.1.2. Nuclear Factor kappaB and SIRS/Sepsis; 3.4.2. STAT-3; 4. The Relationship between Ros Production; and the Inflammatory Response; in Critical Patients; 4.1. Gene Expression; 4.2. Paracrine Effects of ROS; 5. Biomarkers of the Inflammatory Response; in Critically Ill Patients.
5.1. Clinical Trials that Support the Prognostic Values of Procalcitonin5.2. Others Proposed Biomarkers in Critical Ill Patients; Conclusions and Perspectives; References; Chapter IV: Mitochondrial Dysfunction; Abstract; Abbreviations; 1. Introduction; 2. Mitochondrial Physiology; and Pathophysiology; Oxidative Phosphorylation; Sources of Reactive Species in Mitochondria; Mitochondria as an Oxygen Sensor; Role of Mitochondria in Apoptosis; 3. Mitochondrial Dysfunction; 3.1. Evidence Supporting the Occurrence of Mitochondrial Dysfunction; in Sepsis.
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Includes bibliographical references and index.

Description based on print version record and provided by publisher.

4.5. Nitric Oxide Synthase4.6. Mieloperoxidase; 4.7. Cytochrome P450; 5. In Vivo Effects of Free Radicals; 5.1. Physiological Functions; 5.2. Pathophysiological Effects; Oxidative Damage; 6. Antioxidant Defense Systems; and Oxidative Stress; 7. Biomarkers of Oxidative Stress; 8. Oxidative Stress and Diseases; 8.1. Cardiovascular Diseases; 8.2. Hypertension; 8.3. Atherosclerosis; 8.4. Metabolic Syndrome and Diabetes; 8.5. Neurodegenerative Diseases; 8.6. Cancer; 8.7. Rheumatoid Arthritis; 8.8. Aging; Conclusion; References; Chapter II: Pathophysiology of Sepsis and Septic Shock; Abstract.

Abbreviations2. Introduction; 3. Pathophysiology of Sepsis; 3.1. Basic Molecular Mechanisms of Inflammation in Sepsis; 3.1.1. Pathogen-Host Interaction; 3.1.2. Neutrophils; 3.1.3. Cytokines; 3.1.4. Coagulation Disorders in Sepsis; 3.1.5. Endothelial Cells; 3.1.6. Complement Activation; 3.2. Immunoparalysis; 4. Pathophysiology of Septic Shock; Conclusions and Future Goals; References; Chapter III: Inflammation; Abstract; Abbreviations; 2. Introduction; 3. Current Concepts of the Inflammatory Response; 3.1. Cellular Mediators; 3.1.1. Neutrophils; 3.1.2. Macrophages; 3.1.3. Other Cells.

3.2. Cytokines, Chemokines and Lipid Mediators3.2.1. Lipid Mediators; 3.2.1.1. Resolvins Improve the Course of Inflammation; 3.2.2. Novel Cytokines; 3.3. The Role of Toll-Like Receptors; 3.3.1. Clinical Aspects; 3.4.1. Nuclear Factor kappaB; 3.4.1.1 Nuclear Factor kappaB and Oxidative Stress; 3.4.1.2. Nuclear Factor kappaB and SIRS/Sepsis; 3.4.2. STAT-3; 4. The Relationship between Ros Production; and the Inflammatory Response; in Critical Patients; 4.1. Gene Expression; 4.2. Paracrine Effects of ROS; 5. Biomarkers of the Inflammatory Response; in Critically Ill Patients.

5.1. Clinical Trials that Support the Prognostic Values of Procalcitonin5.2. Others Proposed Biomarkers in Critical Ill Patients; Conclusions and Perspectives; References; Chapter IV: Mitochondrial Dysfunction; Abstract; Abbreviations; 1. Introduction; 2. Mitochondrial Physiology; and Pathophysiology; Oxidative Phosphorylation; Sources of Reactive Species in Mitochondria; Mitochondria as an Oxygen Sensor; Role of Mitochondria in Apoptosis; 3. Mitochondrial Dysfunction; 3.1. Evidence Supporting the Occurrence of Mitochondrial Dysfunction; in Sepsis.

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