Substance P : from pain to cancer /
Substance P: From Pain to Cancer, a volume in the Molecular Mediators in Health and Disease: How Cells Communicate series, provides a complete discussion of substance P biology, its role in normal physiology and a variety of diseases. The volume provides an introduction to substance P and its pharma...
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| Формат: | Електронний ресурс eКнига |
| Мова: | Англійська |
| Опубліковано: |
London, United Kingdom :
Academic Press,
[2025]
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| Серія: | Molecular Mediators in Health and Disease: How Cells Communicate
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| Предмети: | |
| Онлайн доступ: | ScienceDirect |
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| 245 | 0 | 0 | |a Substance P : |b from pain to cancer / |c volume editor: Robert Vink. |
| 264 | 1 | |a London, United Kingdom : |b Academic Press, |c [2025] | |
| 300 | |a 1 online resource. | ||
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| 338 | |a online resource |b cr |2 rdacarrier | ||
| 490 | 0 | |a Molecular Mediators in Health and Disease: How Cells Communicate | |
| 520 | |a Substance P: From Pain to Cancer, a volume in the Molecular Mediators in Health and Disease: How Cells Communicate series, provides a complete discussion of substance P biology, its role in normal physiology and a variety of diseases. The volume provides an introduction to substance P and its pharmacology, followed by exploring its role across the human body including cardiovascular function, micturition, learning and memory, emesis, respiration and sleep. It then discusses the critical role of substance P in several disease states including acute brain injury, neurodegeneration, seizures, depression and anxiety, cancer, musculoskeletal disorders, and viral infection, including COVID-19. The book closes with a look towards future perspectives for substance P. Substance P: From Pain to Cancer is an ideal reference for researchers across the life sciences interested in understanding the role of this multi-functioning mediator and its biological significance. | ||
| 500 | |a Includes index. | ||
| 588 | 0 | |a Online resource; title from PDF title page (ScienceDirect, viewed November 20, 2024). | |
| 505 | 0 | |a Intro -- Substance P: From Pain to Cancer -- Copyright -- Contents -- Contributors -- Preface -- Series preface -- Chapter 1: The synthesis, release, and binding of substance P -- 1. Introduction -- 2. Substance P synthesis -- 3. Substance P release -- 4. Substance P binds to neurokinin receptors -- 5. Substance P binding activates a variety of signaling pathways -- 6. Regulation of substance P/NK-1 receptor activity -- 7. Conclusion -- References -- Chapter 2: Distribution of substance P receptors in mammals -- 1. Introduction -- 2. NK1R -- 2.1. Biochemical and phylogenetic characteristics of NK1R -- 2.2. Tissue distribution of NK1R in mammals -- 2.2.1. NK1R in the nociceptive and neurogenic inflammation system -- 2.2.2. NK1R in the brain -- 2.2.3. NK1R in the gastrointestinal tract -- 2.2.4. NK1R in the cardiovascular system -- 2.2.5. NK1R in the respiratory system -- 2.2.6. NK1R in skin -- 2.2.7. NK1R in immune cells -- 2.2.8. NK1R in reproductive organs -- 3. MRGPRX2 (MRGX2) -- 3.1. Biochemical and phylogenetic characteristics of MRGPRX2 (MRGX2) -- 3.2. Tissue-distribution of MRGPRX2 in human and MrgprB2 in mice -- 4. Conclusion and perspectives -- References -- Chapter 3: Substance P in nonmammalian biology: Evolutionarily conserved tachykinin signaling -- 1. Introduction -- 2. Tachykinins and their receptors in mammals -- 3. Tachykinins and their receptors in deuterostome invertebrates and protochordates -- 4. Tachykinins and their receptors in nonmammalian vertebrates -- 4.1. TK signaling in cephalochordates and agnate chordates -- 4.2. TK signaling in elasmobranchs (sharks) -- 4.3. TK signaling in teleost fish -- 4.4. Tachykinin signaling in amphibians -- 4.4.1. Frog and toad tachykinins and receptors -- 4.4.2. Frog skin tachykinins -- 5. Tachykinins and their receptors in protostome invertebrates. | |
| 505 | 8 | |a 5.1. Identification of invertebrate tachykinin precursors and receptors -- 5.2. Distribution and functions of tachykinins in invertebrates -- 5.2.1. Early studies of distribution and functional diversity of tachykinins in invertebrates -- 5.2.2. Distribution and functions of TKs in insects -- 5.2.3. TK signaling in crustaceans -- 5.2.4. Mollusks -- 5.2.5. Nematode worms -- 5.3. Functional roles of TK signaling in Drosophila -- 5.4. Invertebrate gland tachykinins as secreted toxins or vasodilatory factors -- 5.5. A case of novel ligands for an insect TK receptor and a case of promiscuity -- 5.6. Natalisins, a sister group of tachykinins in arthropods -- 6. Conserved roles of tachykinin signaling in the animal kingdom -- 7. Notes on the evolution of tachykinin signaling -- 8. Conclusions and perspectives -- 9. Summary -- Acknowledgments -- References -- Chapter 4: Methodological foundations of substance P detection -- 1. Introduction -- 2. SP measurement: Handling of blood sample -- 3. SP measurements from tissues -- 3.1. Sample obtaining -- 3.2. Sample preparation -- 3.3. Solid-phase extraction (SPE) -- 4. Detection by radioimmunoassay (RIA) and enzyme immunoassay (EIA) -- 5. Effects of protease inhibitor cocktail in EIA -- 6. Differentiation of neuronal and nonneuronal SP levels -- 7. Immunohistochemical detection -- 8. Measurement of SP in tears -- 9. SP levels in other body secretions -- 10. Conclusion -- References -- Chapter 5: Substance P receptor antagonists -- 1. Introduction -- 2. Ligands of the neurokinin-1 receptor -- 2.1. Neurokinin-1 receptor is the high-affinity receptor for substance P -- 2.2. The design and synthesis of peptide and nonpeptide neurokinin-1 receptor antagonists -- 2.3. The neurokinin-1 receptor antagonists binding sites -- 3. Current medical use of neurokinin-1 receptor antagonists. | |
| 505 | 8 | |a 3.1. Neurokinin-1 receptor antagonists as antiemetics -- 3.2. Studies in other pathologies -- 3.3. Features of neurokinin-1 receptor antagonists worth considering for broader clinical use -- 4. Concluding remarks -- References -- Chapter 6: Substance P in the cardiovascular system -- 1. Introduction -- 2. Substance P in the heart -- 2.1. Localization of SP in the heart -- 2.2. SP receptors -- 2.3. Function of SP in the heart -- 2.3.1. Effect throughout intracardiac nervous system -- 2.3.2. Effect of SP on coronary circulation -- 2.3.3. Direct effect of SP on cardiomyocytes and fibroblasts -- 3. Substance P in the vascular system -- 3.1. Localization of members of the SP signaling system in the vessels -- 3.2. Effects of SP on the vessels of the bloodstream -- 4. Effect of SP on the control of cardiovascular system functions -- 5. Conclusion -- References -- Chapter 7: Substance P in lower urinary tract function and dysfunction -- 1. Introduction -- 1.1. Overview -- 1.2. Neural circuits in control of urinary continence and micturition -- 2. Effects of capsaicin on substance P in micturition -- 3. Bladder function in neonates and preprotachykinin A gene deletion -- 3.1. Bladder function in neonates -- 3.2. Preprotachykinin A gene deletion -- 4. Components of the urinary system that control lower urinary tract function -- 4.1. Bladder -- 4.2. Urethra -- 4.3. Ganglionic neurons -- 4.4. Spinal cord -- 4.5. Supraspinal regions -- 5. Effects of systemic administration of NK1 antagonist in animals -- 6. Pathophysiological changes in the lower urinary tract -- 6.1. Animal models of lower urinary tract dysfunction -- 6.1.1. Chemically induced cystitis -- 6.1.2. Bladder outlet obstruction -- 6.1.3. Hyperreflexia after spinal cord injury -- 6.2. Lower urinary tract dysfunction in humans -- 6.2.1. Interstitial cystitis -- 6.2.2. Bladder outflow obstruction. | |
| 505 | 8 | |a 6.2.3. Detrusor overactivity -- 6.2.4. Genitourinary prolapse -- 7. Clinical trials -- 7.1. Serlopitant -- 7.2. Aprepitant -- 7.3. Cizolirtine -- 8. Concluding remarks -- References -- Chapter 8: Role of the substance P in learning and memory -- 1. Introduction -- 2. Nonassociative learning-Habituation and sensitization -- 3. Simple associative learning-Classical conditioning -- 4. Simple associative learning-Operant conditioning -- 5. Memory for innate behavioral sequences -- 6. Memory for learned behavioral sequences -- 7. Summary and conclusion -- References -- Chapter 9: Substance P in nausea and vomiting -- 1. Introduction -- 1.1. Nausea and vomiting in health, disease and therapy -- 1.1.1. Definitions and terminology -- 1.1.2. Nausea and vomiting in biological and clinical contexts -- 1.1.3. The need for drugs to block nausea and vomiting -- 1.2. A brief overview of nausea and vomiting physiology and pharmacology -- 1.2.1. Induction of vomiting -- Abdominal vagal afferents -- Area postrema -- Vestibular system -- Descending cerebral pathways -- 1.2.2. Induction of nausea -- 2. Links between substance P, nausea and vomiting -- 2.1. Induction of vomiting by exogenous SP and related tachykinins in preclinical models -- 2.1.1. Systemic administration -- 2.1.2. Central nervous system administration -- 2.1.3. SP secreting tumors and tachykinin administration in humans -- 2.2. Actions of tachykinins on the digestive tract potentially contributing to the induction of nausea and vomiting and a ... -- 2.2.1. Exogenous tachykinins -- 2.2.2. Effects of receptor antagonists on GI functions -- 2.2.3. Effects of receptor antagonists on GI functions associated with nausea and vomiting -- Upper GI vagal functions -- Gastric ICCs -- 2.3. Presence of SP and NK1 receptors in neural pathways implicated in nausea and vomiting -- 2.3.1. Abdominal vagal afferents. | |
| 505 | 8 | |a 2.3.2. Brainstem -- Area postrema -- Nucleus tractus solitarius -- Ventrolateral brainstem -- 2.3.3. Mid-brain and cerebral structures -- 2.3.4. Digestive tract -- 2.4. Release of SP by emetic stimuli in humans and animals -- 3. Vomit-blocking effects of NK1 receptor antagonists and studies with antagonists at other tachykinin receptors -- 3.1. Preclinical studies of NK1RAs in species with a vomiting reflex -- 3.2. Are NK2 and NK3 receptors involved in vomiting? -- 3.3. Some challenges of species differences in studying the antivomiting effects of NK1RAs -- 3.3.1. Species and receptor selectivity -- 3.3.2. Anomalies -- 3.3.3. Studies in the least shrew (Cryptotis parva) -- 4. Clinical efficacy of NK1 receptor antagonists -- 4.1. Spectrum of efficacy -- 4.1.1. Chemotherapy-induced nausea and vomiting -- 4.1.2. Postoperative nausea and vomiting -- 4.1.3. Gastroparesis -- 4.1.4. Other clinical indications -- 4.1.5. Motion sickness -- 5. Site(s) of action -- 6. Concluding comments -- Acknowledgments -- References -- Chapter 10: Substance P in the central control of respiration -- 1. Introduction -- 2. Substance P in the control of breathing -- 3. Localization of substance P and neurokinin receptors -- 4. Cellular actions within central respiratory sites -- 5. Physiological role(s) of substance P in the control of breathing -- 6. Chemosensitivity -- 7. The broader role of neuromodulation in the orchestration of behavioral functions -- References -- Chapter 11: Substance P in bone metabolism -- 1. Introduction -- 1.1. Bone structure -- 1.2. Bone metabolism -- 2. Substance P and bone cells -- 2.1. Substance P and osteoclasts -- 2.2. Substance P and osteoblasts -- 2.3. Substance P and osteocytes -- 3. Substance P and bone metabolism -- 3.1. Health -- 3.2. Trauma -- 3.3. Disease-Osteoporosis -- 4. Conclusion -- References. | |
| 532 | 8 | |a Trusted Intermediary contact: t.narup@elsevier.com | |
| 532 | 8 | |a Publisher contact for further accessibility information: t.narup@elsevier.com | |
| 650 | 0 | |a Substance P |x Physiological effect. | |
| 650 | 6 | |a Substance P |0 (CaQQLa)201-0038700 |x Effets physiologiques. |0 (CaQQLa)201-0374337 | |
| 650 | 7 | |a Substance P |x Physiological effect |2 fast |0 (OCoLC)fst01136766 | |
| 700 | 1 | |a Vink, Robert, |d 1958- |e editor. |1 https://id.oclc.org/worldcat/entity/E39PCjx66GCFFccdjhjKfXCqQq | |
| 856 | 4 | 0 | |3 ScienceDirect |u https://www.sciencedirect.com/science/book/9780443221941 |