It is clear that lysosomal enzymes often play a role in the destruction of the cytoplasm, but very few authorities feel that they initiate the process (Chapters 1, 2, 3, 5 -8, 12, 13). The cells show many forms of damage, and sometimes even complete destruction, before Iysosomes become a dominant part of the environ ment. What initiates the process is still unclear, although in several instances it appears that the death of a cell may arise from anyone of several pathways (Chapters, 10, II). It is rather interesting that evolution has chosen to achieve the same goal by different means.…mehr
It is clear that lysosomal enzymes often play a role in the destruction of the cytoplasm, but very few authorities feel that they initiate the process (Chapters 1, 2, 3, 5 -8, 12, 13). The cells show many forms of damage, and sometimes even complete destruction, before Iysosomes become a dominant part of the environ ment. What initiates the process is still unclear, although in several instances it appears that the death of a cell may arise from anyone of several pathways (Chapters, 10, II). It is rather interesting that evolution has chosen to achieve the same goal by different means. Apparently no one point is exceptionally or pre ferentially vulnerable, though a common pathway, such as permeability of the plasma membrane to calcium (Chapter 7), might currently be too subtle for routine identification. Factors which affect membrane stability and which induce mem brane bending can lead to blebing, cell fragmentation and death. Thus, more work on the changing chemistry of the plasma membrane in relation to environmental fluctuations would be welcomed. Space requirements and the major orientation of the book forced the exclusion of several very interesting topics: an evolutionary treatment of the advantages of cell death as a means of eliminating vestigial organs or embryonic scaffolding; or consider ation of the merits of body sculpting by cell death rather than cell growth.Hinweis: Dieser Artikel kann nur an eine deutsche Lieferadresse ausgeliefert werden.
1 Cell death: a new classification separating apoptosis from necrosis.- 1.1 Introduction.- 1.2 Necrosis.- 1.3 Apoptosis.- 1.4 Validity of the classification.- 1.5 Summary and conclusions.- References.- 2 Cell death in embryogenesis.- 2.1 Introduction.- 2.2 Limb development and cell death.- 2.3 Development of the nervous system.- 2.4 Differentiation of the reproductive system.- 2.5 Epithelial cell death during fusion of the secondary palate in mammalian development.- 2.6 Lysosomes and the control of embryonic cell death at the cellular level.- References.- 3 Cell death in metamorphosis Richard.- 3.1 Introduction.- 3.2 Amphibian metamorphosis.- 3.3 Metamorphosis in invertebrates.- 3.4 A model of cell death in metamorphosis.- 3.5 Cell death in metamorphosis: the future.- References.- 4 Tissue homeostasis and cell death.- 4.1 Introduction.- 4.2 Growth patterns.- 4.3 Organ growth control.- 4.4 Model systems - the thymus.- 4.5 Homeostasis in malignant tissue.- 5 Cell senescence and death in plants.- 5.1 Introduction.- 5.2 Examination of senescent and dying cells.- 5.3 Biochemical and cytochemical consideration.- 5.4 Possibile interpretations of the biochemical, cytochemical and ultrastructural studies.- 5.5 Mechanisms of cell senescence and death revisited.- 6 The tissue kinetics of cell loss.- 6.1 Introduction.- 6.2 The cell cycle.- 6.3 The organization of cell populations.- 6.4 The measurement of the kinetics of cell loss.- 6.5 Some examples involving the measurement of cell loss kinetics in normal tissues.- 6.6 The kinetics of cell loss in tumours.- 6.7 Tissue responses.- 6.8 Conclusions.- References.- 7 Cell death and the disease process. The role of calcium.- 7.1 Introduction.- 7.2 Stages of cell injury 209 7.2.1 Comments on the stages.- 7.3 Mechanisms of progression.-7.4 The role of ion shifts in cell injury.- 7.5 Calcium and cell injury.- 7.6 Hypothesis.- 7.7 Summary 234 References.- 8 Cell death in vitro.- 8.1 Introduction.- 8.2 Cell aging and death in vitro.- 8.3 Donor age versus cell doubling potential.- 8.4 Species lifespan versus cell doubling potential.- 8.5 The finite lifetime of normal cells transplanted in vivo.- 8.6 Population doublings in vivo.- 8.7 Organ clocks.- 8.8 Clonal variation.- 8.9 Irradiation, DNA repair and effects of visible light.- 8.10 Cytogenetic studies.- 8.11 Error accumulation.- 8.12 The proliferating pool.- 8.13 Efforts to increase population doubling potential.- 8.14 Phase III in cultured mouse fibroblasts.- 8.15 Phase III theories.- 8.16 Can cell death be normal?.- 8.17 Dividing, slowly dividing and non-dividing cells.- 8.18 Aging or differentiation?.- 8.19 Functional and biochemical changes that occur in cultured normal human cells.- 8.20 Immortal cells.- References.- 9 Nucleic acids in cell death.- 9.1 The basic problem.- 9.2 Protein synthesis in eukaryotic cells.- 9.3 Nucleic acids in silk glands.- 9.4 Limitations of present data.- 9.5 Future developments 290 References.- 10 Mechanism(s) of action of nerve growth factor in intact and lethally injured sympathetic nerve cell in neonatal rodents.- 10.1 Introduction.- 10.2 Historical survey.- 10.3 The salivary NGF: morphological and biochemical effects induced in its target cells.- 10.4 Dual access and mechanisms of action of NGF in its target cells.- 10.5 Destruction of immature sympathetic nerve cells by immunochemical, pharmacological and surgical procedures.- 10.6 Surgical axotomy.- 10.7 Protective effects of NGF against 6-OHDA, guanethidine, vinblastine, AS-NGF and surgical axotomy.- 10.8 Some considerations and concluding remarks.- References.-11 Glucocorticoid-induced lymphocyte death.- 11.1 Introduction.- 11.2 Glucocorticoid receptors and metabolic effects in lymphocytes.- 11.3 Lethal effects of glucocorticoids on lymphocytes.- 11.4 Genetic analysis of glucocorticoid-induced cell death.- 11.5 Mechanisms of glucocorticoid-induced cell death.- 11.6 Conclusions.- References.- 12 The role of the LT system in cell destruction in vitro.- 12.1 Introduction.- 12.2 Molecular characteristics of the LT systems of cytotoxic effector molecules.- 12.3 Cellular processes involved in LT release by unstimulated (primary) and stimulated (secondary) human lymphocytes.- 12.4 Types of lytic reactions induced by lytic molecules of various weights in vitro.- 12.5 Conclusions.- References.- 13 Techniques for demonstrating cell death.- 13.1 Introduction.- 13.2 Microscopical.- 13.3 Cytochemical and biochemical.- References.- Author index.
1 Cell death: a new classification separating apoptosis from necrosis.- 1.1 Introduction.- 1.2 Necrosis.- 1.3 Apoptosis.- 1.4 Validity of the classification.- 1.5 Summary and conclusions.- References.- 2 Cell death in embryogenesis.- 2.1 Introduction.- 2.2 Limb development and cell death.- 2.3 Development of the nervous system.- 2.4 Differentiation of the reproductive system.- 2.5 Epithelial cell death during fusion of the secondary palate in mammalian development.- 2.6 Lysosomes and the control of embryonic cell death at the cellular level.- References.- 3 Cell death in metamorphosis Richard.- 3.1 Introduction.- 3.2 Amphibian metamorphosis.- 3.3 Metamorphosis in invertebrates.- 3.4 A model of cell death in metamorphosis.- 3.5 Cell death in metamorphosis: the future.- References.- 4 Tissue homeostasis and cell death.- 4.1 Introduction.- 4.2 Growth patterns.- 4.3 Organ growth control.- 4.4 Model systems - the thymus.- 4.5 Homeostasis in malignant tissue.- 5 Cell senescence and death in plants.- 5.1 Introduction.- 5.2 Examination of senescent and dying cells.- 5.3 Biochemical and cytochemical consideration.- 5.4 Possibile interpretations of the biochemical, cytochemical and ultrastructural studies.- 5.5 Mechanisms of cell senescence and death revisited.- 6 The tissue kinetics of cell loss.- 6.1 Introduction.- 6.2 The cell cycle.- 6.3 The organization of cell populations.- 6.4 The measurement of the kinetics of cell loss.- 6.5 Some examples involving the measurement of cell loss kinetics in normal tissues.- 6.6 The kinetics of cell loss in tumours.- 6.7 Tissue responses.- 6.8 Conclusions.- References.- 7 Cell death and the disease process. The role of calcium.- 7.1 Introduction.- 7.2 Stages of cell injury 209 7.2.1 Comments on the stages.- 7.3 Mechanisms of progression.-7.4 The role of ion shifts in cell injury.- 7.5 Calcium and cell injury.- 7.6 Hypothesis.- 7.7 Summary 234 References.- 8 Cell death in vitro.- 8.1 Introduction.- 8.2 Cell aging and death in vitro.- 8.3 Donor age versus cell doubling potential.- 8.4 Species lifespan versus cell doubling potential.- 8.5 The finite lifetime of normal cells transplanted in vivo.- 8.6 Population doublings in vivo.- 8.7 Organ clocks.- 8.8 Clonal variation.- 8.9 Irradiation, DNA repair and effects of visible light.- 8.10 Cytogenetic studies.- 8.11 Error accumulation.- 8.12 The proliferating pool.- 8.13 Efforts to increase population doubling potential.- 8.14 Phase III in cultured mouse fibroblasts.- 8.15 Phase III theories.- 8.16 Can cell death be normal?.- 8.17 Dividing, slowly dividing and non-dividing cells.- 8.18 Aging or differentiation?.- 8.19 Functional and biochemical changes that occur in cultured normal human cells.- 8.20 Immortal cells.- References.- 9 Nucleic acids in cell death.- 9.1 The basic problem.- 9.2 Protein synthesis in eukaryotic cells.- 9.3 Nucleic acids in silk glands.- 9.4 Limitations of present data.- 9.5 Future developments 290 References.- 10 Mechanism(s) of action of nerve growth factor in intact and lethally injured sympathetic nerve cell in neonatal rodents.- 10.1 Introduction.- 10.2 Historical survey.- 10.3 The salivary NGF: morphological and biochemical effects induced in its target cells.- 10.4 Dual access and mechanisms of action of NGF in its target cells.- 10.5 Destruction of immature sympathetic nerve cells by immunochemical, pharmacological and surgical procedures.- 10.6 Surgical axotomy.- 10.7 Protective effects of NGF against 6-OHDA, guanethidine, vinblastine, AS-NGF and surgical axotomy.- 10.8 Some considerations and concluding remarks.- References.-11 Glucocorticoid-induced lymphocyte death.- 11.1 Introduction.- 11.2 Glucocorticoid receptors and metabolic effects in lymphocytes.- 11.3 Lethal effects of glucocorticoids on lymphocytes.- 11.4 Genetic analysis of glucocorticoid-induced cell death.- 11.5 Mechanisms of glucocorticoid-induced cell death.- 11.6 Conclusions.- References.- 12 The role of the LT system in cell destruction in vitro.- 12.1 Introduction.- 12.2 Molecular characteristics of the LT systems of cytotoxic effector molecules.- 12.3 Cellular processes involved in LT release by unstimulated (primary) and stimulated (secondary) human lymphocytes.- 12.4 Types of lytic reactions induced by lytic molecules of various weights in vitro.- 12.5 Conclusions.- References.- 13 Techniques for demonstrating cell death.- 13.1 Introduction.- 13.2 Microscopical.- 13.3 Cytochemical and biochemical.- References.- Author index.
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