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ویرایش:
نویسندگان: Carlos Guido Musso (editor). Adrian Covic (editor)
سری:
ISBN (شابک) : 303136788X, 9783031367885
ناشر: Springer
سال نشر: 2023
تعداد صفحات: 219
زبان: English
فرمت فایل : PDF (درصورت درخواست کاربر به PDF، EPUB یا AZW3 تبدیل می شود)
حجم فایل: 6 مگابایت
در صورت تبدیل فایل کتاب Organ Crosstalk in Acute Kidney Injury: Basic Concepts and Clinical Practices به فرمت های PDF، EPUB، AZW3، MOBI و یا DJVU می توانید به پشتیبان اطلاع دهید تا فایل مورد نظر را تبدیل نمایند.
توجه داشته باشید کتاب تداخل اعضای بدن در آسیب حاد کلیه: مفاهیم اساسی و اقدامات بالینی نسخه زبان اصلی می باشد و کتاب ترجمه شده به فارسی نمی باشد. وبسایت اینترنشنال لایبرری ارائه دهنده کتاب های زبان اصلی می باشد و هیچ گونه کتاب ترجمه شده یا نوشته شده به فارسی را ارائه نمی دهد.
Foreword Contents Chapter 1: Nosology and Semiotics 1.1 Introduction 1.2 A Brief Historiography of Semiotics and Health/Medicine 1.3 Semiotic Aspects of Nosology 1.4 Fundamental Elements of a Biosemiotic Perspective on Human Health 1.4.1 The Umwelt 1.4.2 Body and Environment 1.4.3 Physiology, Behaviour and Perception 1.4.4 Endosemiosis 1.5 Contributions to Biosemiotic Medicine 1.5.1 Process-Based Medicine in Light of the Ontogeny of the Human Being 1.5.2 Biosemiotic Medicine Within and Beyond Human Health Studies 1.5.3 The Human Being Conceived of as a System of Interrelated Sign Systems 1.5.4 The Human Microbiome: The Human Organism Conceived of as an Ecosystem 1.5.5 A Biosemiotic Understanding of Organ Crosstalk References Chapter 2: Acute Kidney Injury: Definition and Generalities 2.1 Introduction 2.2 Prerenal AKI 2.3 Renal or Intrinsic AKI 2.4 Obstructive AKI 2.5 AKI Implications 2.6 Conclusion References Chapter 3: Hormones 3.1 General Principles of the Endocrine System 3.1.1 Structure, Organization, and Function of the Endocrine System 3.2 Hormone Synthesis: Basic Concepts 3.2.1 Transport 3.3 Mechanisms of Hormone Action 3.3.1 Types of Receptors 3.3.2 Membrane Receptors 3.3.3 Intracellular Receptors 3.4 Regulation of Hormone Levels, Synthesis, and Secretion 3.5 Water and Electrolyte Balance 3.6 Antidiuretic Hormone and Extracellular Fluid (ECF) Osmolality 3.7 Endocrine Regulation of Water Balance 3.8 Sodium and Potassium Balance and the Renin-Angiotensin-Aldosterone System (RAAS) 3.9 The RAAS and the Regulation of Sodium and Potassium Homeostasis 3.10 Natriuretic Factors 3.11 Conclusion References Chapter 4: Neurotransmitters and Autonomous Nervous System 4.1 Introduction 4.1.1 Autonomic Nervous System (ANS) 4.1.2 Anatomy of ANS 4.2 Mechanism of Action 4.2.1 Chemical Synapse 4.2.2 Neurotransmitters 4.2.3 Catecholamines 4.2.4 Acetylcholine (ACh) 4.2.5 Nitric Oxide (NO) 4.3 Sympathetic Nervous System and Kidneys 4.4 Central Nervous System Control of Renal Function 4.5 Acute Kidney Injury and Special Conditions 4.6 Septic Acute Renal Injury 4.7 Conclusions References Chapter 5: Cytokines, Chemokines, Inflammasomes, Myokines and Complement-Related Factors in Acute Kidney Injury 5.1 Cytokines in Acute Kidney Injury (AKI) 5.1.1 Tumor Necrosis Factor-Alpha (TNF-α) 5.1.2 Interferon Gamma (IFNγ) 5.1.3 Transforming Growth Factor-Beta (TGF-β) 5.1.4 Interleukin 1-Beta (IL-1β) 5.1.5 Interleukin 2 (IL-2) 5.1.6 Interleukin 6 (IL-6) 5.1.7 Interleukin 18 (IL-18) 5.1.8 Interleukin 20 (IL-20) 5.2 Immunoregulation by Cytokines in AKI 5.2.1 Chemokines in AKI 5.2.2 Inflammasome 5.2.3 Canonical Inflammasome 5.2.4 NLRP3 5.2.5 Non-Canonical Inflammasomes 5.2.6 Inflammasomes in AKI 5.3 Complement-Related Factors in AKI References Chapter 6: Genetic, Epigenetics, and Cell Adhesion in Acute Kidney Injury 6.1 Introduction 6.2 Epigenetics of Cell Adhesion and Migration in AKI 6.2.1 Why Polymorphic Variants Might Better Explain the Interplay Between Acute Kidney Disease and Its Effect on Patients 6.2.2 Some Genes and Polymorphic Variants That Could Exacerbate Acute Kidney Injury 6.2.3 Polymorphism Associated with Inflammatory Responses 6.2.3.1 Tumor Necrosis Factor-α (TNF-α) 6.2.3.2 Interleukin 6 (IL6) and Interleukin 10 (IL10) 6.2.3.3 Human Leukocyte Antigen–Major Histocompatibility Complex (HLA-DR) 6.2.4 Polymorphisms Associated with Vascular Hemodynamic Response and Cellular Metabolic Homeostasis 6.3 Conclusion References Chapter 7: Organs Crosstalk Perspective 7.1 Introduction 7.2 Biosemiotics: Life as a Dialogue 7.3 Biosemiotics: Health and Disease as a Process 7.4 Organic Intercommunication: The Crosstalk Perspective 7.5 Conclusion References Chapter 8: Kidney–Brain Crosstalk in Acute Kidney Injury 8.1 Introduction 8.2 Pathological Crosstalk 8.2.1 Inflammation 8.3 Blood–Brain Barrier 8.4 Oxidative Stress 8.5 Uremia 8.6 Metabolic Acidosis and Drug Toxicity 8.7 Pathological Activation of Neurohormonal Systems 8.8 Protective Responses During Injury 8.9 Conclusion References Chapter 9: Kidney–Lung Crosstalk in Acute Kidney Injury 9.1 Introduction 9.2 Pathophysiology 9.3 Renal-Induced Lung Damage 9.3.1 Cytokine Induced Damage 9.3.2 Immune Cells 9.3.3 Ischemia Induced Damage 9.3.4 Pulmonary Edema 9.4 Lung-Induced Renal Damage 9.4.1 Systemic Inflammation 9.4.2 Ventilator-Induced Lung Injury 9.4.3 Hypoxia and Hypercapnia 9.5 Conclusion References Chapter 10: Kidney–Heart Crosstalk in Acute Kidney Injury 10.1 Introduction 10.2 Cardiorenal Syndrome 10.3 Acute Cardiorenal Syndrome 10.3.1 Hemodynamic and Neurohumoral Response 10.3.2 Inflammatory Response 10.4 Acute Renal-Cardiac Syndrome 10.5 Acute HF Treatment and Its Relationship with Renal Function 10.6 Conclusion References Chapter 11: Kidney–Gut Crosstalk in Acute Kidney Injury 11.1 Introduction 11.1.1 Gut Barrier 11.1.2 Metabolites Derived from Microbiota 11.1.3 Microbiota and Immunity 11.1.4 Microbiome and Uremic Toxins 11.2 Kidney–Gut Crosstalk in AKI 11.2.1 AKI and Dysbiosis 11.2.2 AKI and Barrier Integrity 11.2.3 AKI and Altered Immunity 11.2.4 Crosstalk in Septic AKI 11.3 Therapeutic Targets 11.3.1 Selective Decontamination of the Digestive Tract (SDD) 11.3.2 Probiotics 11.3.3 Short-Chain Fatty Acids (SCFAs) 11.4 Conclusions References Chapter 12: Kidney–Liver Crosstalk in Acute Kidney Injury 12.1 Introduction 12.2 Definitions 12.3 Pathogenesis of Hepatorenal Syndrome 12.3.1 Circulatory Dysfunction 12.3.2 Systemic Inflammation 12.3.3 Cirrhotic Cardiomyopathy 12.3.4 Cytokines 12.4 Clinical Application of Kidney Biomarkers 12.5 Prevention of Hepatorenal Syndrome 12.5.1 Prevention of Circulatory Dysfunction 12.5.2 Antibiotic Prophylaxis 12.6 Management and Treatment of Hepatorenal Syndrome 12.7 Conclusion References Chapter 13: Kidney–Muscle Crosstalk in Acute Kidney Injury 13.1 Acute Kidney Injury Definition Based on Creatinine and Creatinine Metabolism 13.2 Rhabdomyolysis 13.3 AKI and Muscular Damage 13.4 Conclusion References Chapter 14: Kidney–Placenta Crosstalk in Acute Kidney Injury 14.1 Introduction 14.2 Placenta-Kidney Perspective 14.3 Physiological Adaptation to Pregnancy 14.4 Pathogenesis of Pregnancy-Related Diseases and its Impact on Healthy Kidneys 14.5 Pregnancy Effects on Kidney Disease 14.6 Renal Damage: Kidney-Placenta Perspective 14.7 AKI in CKD Pregnant Woman 14.8 Post-Renal Pregnancy-Related Acute Kidney Injury (Pr-AKI) 14.9 Conclusion References Chapter 15: Renal Replacement Treatment, Blood Purification, and Crosstalk in Acute Kidney Injury 15.1 Introduction 15.2 High-Flow Kidney Replacement Therapy and Sepsis 15.3 Kidney Replacement Therapy in Acute Neurological Injury (ANI) and AKI 15.4 Kidney Replacement Therapy in Acute Heart Failure (AHF) and AKI 15.4.1 Cardiorenal Syndrome 15.4.2 Clinical Evidence 15.5 Kidney Replacement Therapy in Acute Liver Injury (ALI) and AKI 15.5.1 Artificial Extracorporeal Hepatic Assistance Systems 15.5.2 Plasmapheresis 15.5.3 Dialysis with Albumin 15.5.4 Hemoperfusion in Sepsis and AKI 15.5.5 Hemoperfusion in AKI Associated with COVID-19 15.5.6 Hemoperfusion in Cardiovascular Surgery 15.6 Conclusion References Chapter 16: Acute Kidney Injury and Organ Crosstalk in COVID-19 16.1 Acute Kidney Injury in COVID-19 (AKI-COVID-19) 16.2 Crosstalk in AKI COVID-19 16.2.1 Cytokine Storm 16.2.2 Chemokines 16.2.3 Immune Cells Response 16.2.3.1 Innate Immune Response 16.2.3.2 Acquired Immune Response 16.2.4 Other Organ Compromise in COVID-19 16.2.4.1 Lung 16.2.4.2 Heart 16.2.4.3 Muscles 16.2.4.4 Coagulation 16.2.4.5 Vessels 16.2.4.6 Colon 16.3 Conclusion References Index