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Biography; Contents; Chapter 1: Introduction; References; Chapter 2: The Physiology and Pharmacology of Nausea and Vomiting Induced by Anticancer Chemotherapy in Humans; 2.1 Introduction; 2.2 Why Should Anticancer Therapies Induce Nausea and Vomiting? An Evolutionary Perspective; 2.3 Animal Models vs. the Clinic and the Problems of Studying Nausea in Humans; 2.3.1 Cancer Patients and Animal Models: Limitations; 2.3.2 The Problems of Studying Nausea in Humans; 2.3.2.1 Definition; 2.3.2.2 Biomarkers; 2.3.2.3 Investigating Nausea in Patients and Healthy Volunteers.
2.3.2.4 Assessing Efficacy of Anti-emetics Against Nausea2.3.2.5 Can Nausea Be Studied in Animals?; 2.4 The Physiology of Nausea; 2.4.1 Hormones; 2.4.2 The Autonomic Nervous System and the Stomach; 2.4.3 The Brain; 2.5 The Physiology of Retching and Vomiting; 2.5.1 Pre-expulsion; 2.5.1.1 Skin; 2.5.1.2 Cardiovascular System; 2.5.1.3 Digestive Tract; 2.5.2 Expulsion; 2.5.3 Between Emetic Episodes; 2.6 Inputs: How Are Nausea and Vomiting Induced?; 2.6.1 The Tongue and Pharynx; 2.6.2 The Gastrointestinal Tract and Visceral Afferents; 2.6.2.1 Abdominal Vagal Afferents; Mechanoreceptors.
Mucosal Afferents2.6.2.2 Splanchnic Afferents; 2.6.3 The Area Postrema; 2.6.4 The Vestibular System and Vestibulo-Visual Conflicts; 2.6.5 Cortical Inputs; 2.7 Central Integration; 2.8 Endogenous Anti-emetic Mechanisms; 2.8.1 Pulmonary Vagal Afferents; 2.8.2 Brain Mechanisms; 2.9 Acute and Delayed CINV: Mechanism, Pathways and Aspects of Anti-emetic Pharmacology; 2.9.1 Before Chemotherapy; 2.9.2 Acute Phase of Emesis Induced by Chemotherapy; 2.9.2.1 The Latent Period and the Enterochromaffin Cell-Vagal Afferent Unit; 2.9.2.2 Sustaining and Stopping the Acute Emetic Response.
2.9.3 Delayed Phase Induced by Chemotherapy2.9.3.1 Subsequent Cycles; 2.10 Concluding Comments; References; Chapter 3: First-Generation 5-HT3 Receptor Antagonists; 3.1 Introduction; 3.2 Physiology of CINV; 3.3 Development of First-Generation 5-HT3 Antagonists; 3.3.1 Ondansetron; 3.3.2 Dolasetron; 3.3.3 Tropisetron; 3.3.4 Granisetron; 3.4 Development of Palonosetron; 3.5 Clinical Studies; 3.5.1 Initial Studies; 3.5.1.1 Placebo-Controlled Studies; 3.5.1.2 Dose-Finding Studies; 3.5.1.3 Comparison Studies with Older Agents; 3.5.2 The Role of Corticosteroids.
3.5.3 First-Generation 5-HT3 Antagonists Compared3.5.4 Intravenous Compared to Oral Therapy; 3.5.5 Summary of Characteristics of First-Generation 5-HT3 Receptor Antagonists; 3.6 Palonosetron: A Second-Generation 5-HT3 Antagonist; 3.7 Novel Delivery Methods; 3.7.1 Transdermal Granisetron; 3.7.2 Sustained-Release Subcutaneous Granisetron; 3.8 Conclusion; References; Chapter 4: Palonosetron; 4.1 Development of Palonosetron; 4.2 Safety; 4.3 Clinical Development of Palonosetron; 4.4 Alternative Formulations; 4.5 Multiple-Day Chemotherapy.
2.3.2.4 Assessing Efficacy of Anti-emetics Against Nausea2.3.2.5 Can Nausea Be Studied in Animals?; 2.4 The Physiology of Nausea; 2.4.1 Hormones; 2.4.2 The Autonomic Nervous System and the Stomach; 2.4.3 The Brain; 2.5 The Physiology of Retching and Vomiting; 2.5.1 Pre-expulsion; 2.5.1.1 Skin; 2.5.1.2 Cardiovascular System; 2.5.1.3 Digestive Tract; 2.5.2 Expulsion; 2.5.3 Between Emetic Episodes; 2.6 Inputs: How Are Nausea and Vomiting Induced?; 2.6.1 The Tongue and Pharynx; 2.6.2 The Gastrointestinal Tract and Visceral Afferents; 2.6.2.1 Abdominal Vagal Afferents; Mechanoreceptors.
Mucosal Afferents2.6.2.2 Splanchnic Afferents; 2.6.3 The Area Postrema; 2.6.4 The Vestibular System and Vestibulo-Visual Conflicts; 2.6.5 Cortical Inputs; 2.7 Central Integration; 2.8 Endogenous Anti-emetic Mechanisms; 2.8.1 Pulmonary Vagal Afferents; 2.8.2 Brain Mechanisms; 2.9 Acute and Delayed CINV: Mechanism, Pathways and Aspects of Anti-emetic Pharmacology; 2.9.1 Before Chemotherapy; 2.9.2 Acute Phase of Emesis Induced by Chemotherapy; 2.9.2.1 The Latent Period and the Enterochromaffin Cell-Vagal Afferent Unit; 2.9.2.2 Sustaining and Stopping the Acute Emetic Response.
2.9.3 Delayed Phase Induced by Chemotherapy2.9.3.1 Subsequent Cycles; 2.10 Concluding Comments; References; Chapter 3: First-Generation 5-HT3 Receptor Antagonists; 3.1 Introduction; 3.2 Physiology of CINV; 3.3 Development of First-Generation 5-HT3 Antagonists; 3.3.1 Ondansetron; 3.3.2 Dolasetron; 3.3.3 Tropisetron; 3.3.4 Granisetron; 3.4 Development of Palonosetron; 3.5 Clinical Studies; 3.5.1 Initial Studies; 3.5.1.1 Placebo-Controlled Studies; 3.5.1.2 Dose-Finding Studies; 3.5.1.3 Comparison Studies with Older Agents; 3.5.2 The Role of Corticosteroids.
3.5.3 First-Generation 5-HT3 Antagonists Compared3.5.4 Intravenous Compared to Oral Therapy; 3.5.5 Summary of Characteristics of First-Generation 5-HT3 Receptor Antagonists; 3.6 Palonosetron: A Second-Generation 5-HT3 Antagonist; 3.7 Novel Delivery Methods; 3.7.1 Transdermal Granisetron; 3.7.2 Sustained-Release Subcutaneous Granisetron; 3.8 Conclusion; References; Chapter 4: Palonosetron; 4.1 Development of Palonosetron; 4.2 Safety; 4.3 Clinical Development of Palonosetron; 4.4 Alternative Formulations; 4.5 Multiple-Day Chemotherapy.