Promotional Information

Springer Book Archives

Table of Contents

I. Opposing Concepts in Cell Physiology: History and Background.- 1. The Early History of Cell Physiology.- 1.1. The Evolution of Physiology as the Physics and Chemistry of Living Phenomena.- 1.2. The Cell Theory.- 1.3. The Discovery of Protoplasm.- 1.4. Colloidal Chemistry and the Concept of Bound Water.- 1.5. Traube’s Semipermeable Copper Ferrocyanide Gel Membrane and the Introduction of the van’t Hoff Equation.- 1.6. Pfeffer’s Membrane Theory.- 1.7. Summary.- 2. Evolution of the Membrane and Bulk Phase Theories.- 2.1. Concepts of the Nature of the Plasma Membrane.- 2.1.1. The Lipoidal Theory of Overton.- 2.1.2. Mosaic Membranes with Pores.- 2.1.3. Membranes with Charged Pores and Selective Ionic Permeability.- 2.1.4. The Paucimolecular Membrane of Davson and Danielli.- 2.2. Cellular Electrical Potentials and Swelling in the Context of the Membrane Theory.- 2.2.1. Early History of Cellular Electrical Potentials.- 2.2.2. Bernstein’s Membrane Theory and the Diffusion Potential.- 2.2.3. The Cremer-Haber-Klemensiewicz Theory for Glass Electrodes.- 2.2.4. Phase Boundary Potentials and the Baur-Beutner Controversy.- 2.2.5. Michaelis’s Theory of the Cation-Permeable Collodion Membrane.- 2.2.6. The Donnan Theory of Membrane Equilibrium.- 2.3. Cellular Ionic Distribution in the Context of the Membrane Theory.- 2.3.1. Boyle and Conway’s Theory of Membrane Potentials, Ionic Distribution, and Swelling’.- 2.4 Early Criticisms of and Experimental Evidence against the Membrane Theory.- 2.5. Inquiries into the Nature of Protoplasm.- 2.5.1. Protoplasm as a Structural Substance.- 2.5.2. Fischer’s Theory of Protoplasm.- 2.5.3. Lepeschkin’s Vitaid Theory.- 2.5.4. Nasonov’s Phase Theory of Permeability and Bioelectric Potentials.- 2.5.5. Bungenberg de Jong’s Concept of Protoplasm as a Coacervate.- 2.6. Early Inquiries into the Physical State of Water and Ions in Living Cells.- 2.6.1. Bound Water.- 2.6.2. Bound K+.- 2.7. Rejection of the Bulk Phase Theories.- 2.7.1. Evidence against the Bulk Phase Theories.- 2.7.2. Evidence against the Concepts of Bound K+ and Bound Water.- 2.8. Summary.- 3. The Emergence of the Steady-State Membrane Pump Concept.- 3.1. Major Developments Providing the Background for the Acceptance of the Membrane Pump Theory.- 3.1.1. The Disproof of the Original Equilibrium Membrane Theory.- 3.1.2. The Concept That the Constituents of Living Beings Are in a State of Dynamic Equilibrium.- 3.1.3. The Hill-Embden Controversy and “A-lactic Acid” Muscle Contraction.- 3.1.4. The High-Energy Phosphate Bond as the Immediate Source of Energy for Biological Work Performance, Including Ionic Pumping.- 3.2. The Postulation of the Na+ Pump.- 3.3. Arguments and Evidence in Support of the Na+ Pump Theory.- 3.3.1. The Dependence of Ionic Distribution on Continued Metabolic Activities and Normal Temperature.- 3.3.2. The Energy Requirement of the Na+ Pump Appears to Be Adequately Met by Cell Metabolism.- 3.3.3. Active Solute Transport by Epithelial Tissues and Giant Algal Cells.- 3.4. The Further Development of the Membrane Theory of Cellular Electrical Potential in the Context of the Membrane Pump Theory: The Ionic Theory of Hodgkin, Katz, and Huxley.- 3.4.1. The Hodgkin-Katz-Goldman Equation.- 3.4.2. The Hodgkin-Huxley Theory of the Action Potential.- 3.4.3. The Hodgkin-Huxley Theory of Permeability Changes during the Action Potential.- 3.4.4. Experimental Confirmation of the Membrane Theory of the Resting and Action Potentials.- 3.5. Summary.- 4. The Reemergence of the Bulk Phase Theories.- 4.1. Kamnev’s Study of Sugar Distribution in Frog Muscle.- 4.2. Troshin’s Sorption Theory.- 4.2.1. Osmotic Behavior of Living Cells.- 4.2.2. Cells as Colloidal Coacervates.- 4.2.3. Solute Exclusion and Accumulation.- 4.3. Rekindled Doubts about the Revised Membrane Pump Theory.- 4.3.1. Discovery of the Non-Donnan Distribution of Many Permeant Substances.- 4.3.2. Reinvestigation of the Question of Whether or Not Cells Have Enough Energy to Operate the Postulated Na+ Pump.- 4.4. Ling’s Fixed-Charge Hypothesis.- 4.4.1. A New Molecular Mechanism for the Selective Accumulation of K+ over Na+ in Living Cells.- 4.4.2. Some Distinctive Features of Ling’s Fixed-Charge Hypothesis.- 4.5. Molecular Mechanisms of Selective Ionic Permeability.- 4.5.1. The Membrane Carrier Model.- 4.5.2. Ling’s Fixed-Charge Hypothesis.- 4.6. The Surface Adsorption Theory of the Cellular Resting Potential.- 4.6.1. Three Historical Models: Glass, Oil, and Collodion.- 4.6.2. The Surface Adsorption Theory of Cellular Electrical Potentials.- 4.7. Summary.- 5. Experimental Tests of the Alternative Theories.- 5.1. Evidence Supporting the Membrane Pump Theory.- 5.1.1. Full Ionic Dissociation of K+ Salts in Water at Ionic Strengths Similar to Those in Living Cells.- 5.1.2. High Mobility of K+ in Living Cells.- 5.1.3. High K+ Activity in Living Cells.- 5.1.4. Genetic Control of Permeases or Sugar Pumps.- 5.1.5. Na+,K+-Activated ATPase as the Na+ Pump.- 5.1.6. “High Energy” Contained in the Phosphate Bonds of ATP Provides the Immediate Source of Energy for Na+ Pumping..- 5.2. Evidence against the Pump Hypothesis.- 5.2.1. There Is Not Enough Energy to Operate the Na+ Pump.- 5.2.2. Reassessment of the High Energy of the “High-Energy Phosphate Bond”.- 5.2.3. Failure to Demonstrate Selective K+ Accumulation and Na+ Exclusion by a Cytoplasm-Free Squid Axon Membrane Sac.- 5.2.4. Failure to Prove Selective Ion Pumping in Membrane Vesicles.- 5.2.5. Studies of the Red Cell Ghost.- 5.2.6. Ouabain-Sensitive Selective Accumulation of K+ over Na+ in an Effectively Membrane (Pump)-less Open-Ended Muscle Cell (EMOC) Preparation.- 5.3. Summary.- II. The Association-Induction Hypothesis.- 6. The Association-Induction Hypothesis I. Association of Ions and Water with Macromolecules.- 6.1. The Living State.- 6.1.1. The General Concept of a High-Energy Resting State.- 6.1.2. The Major Components of Living Systems.- 6.1.3. Protoplasm and the Living State.- 6.2. Association of Ions.- 6.2.1. Enhanced Counterion Association in a Fixed-Charge System.- 6.2.2. The Theory of Selective Ionic Adsorption and Its Variation with the Electron Density or c- Value of the Fixed Anionic Sites.- 6.2.3. Reversal of Ionic Selectivity Ratios: Comparison of Theory with Experiment in Ion Exchange Resins.- 6.2.4. Generalized Relations between c-Value and Adsorption Constants.- 6.2.5. Salt Linkages, c-Value, and the in Vitro Demonstration of Selective Na+ and K+ Adsorption on Isolated Proteins.- 6.3. Association of Water.- 6.3.1. Historical Background.- 6.3.2. The Polarized Multilayer Theory of Cell Water.- 6.3.3. Theory of Solute Exclusion from Water Existing in the State of Polarized Multilayers.- 6.3.4. in Vitro Experimental Testing of the Polarized Multilayer Theory of Cell Water in Model Systems.- 6.4. Summary.- 7. The Association-Induction Hypothesis II. The Inductive Effect and the Control of Physiological Activities.- 7.1. The Inductive Effect.- 7.1.1. Early Theories of the Molecular Inductive Effect.- 7.1.2. Chiang and Tai’s Theory: A Quantitative Relation between Molecular Structure and Chemical Reactivity.- 7.1.3. Functional Groups Affected by the Inductive Effect.- 7.2. The Direct F-Effect and the Molecular Mechanisms of Physiological Control.- 7.2.1. Association of Protons and Adsorption of Cations.- 7.2.2. Changes in H-Bonding.- 7.3. Modulation and Control of Physiological Activities.- 7.3.1. The One-Receptor-Site System as a Model for Competitive Interaction.- 7.3.2. The Two-Receptor-Site System as a Model for Noncompetitive Facilitation and Inhibition.- 7.4. Cooperativity: Molecular Basis for Controlled and Coordinated Physiological Activities.- 7.4.1. The Indirect F-Effect: The Propagated Inductive Effect.- 7.4.2. The Yang-Ling Cooperative Adsorption Isotherm.- 7.4.3. The Control of Shifts between Discrete Cooperative States by the Adsorption and Desorption of Cardinal Adsorbents.- 7.4.4. An Analysis of the Theoretical Model of Controlled Cooperative Interaction.- 7.5. Summary.- 8. The Physical State of K+ and Na+ in Living Cells.- 8.1. A Reassessment of the Critical Experiments of Hill and Kupalov…..- 8.2. Experimental Proof That the Bulk of Muscle K+ Is in an Adsorbed State.- 8.2.1. Early Work on Localization of K+.- 8.2.2. Electron Microscopic Demonstration of Localization of K+.- 8.2.3. Autoradiographic Demonstration of Localization of K+.- 8.2.4. Energy-Dispersive X-Ray Microanalysis.- 8.2.5. Laser Microprobe Mass Spectrometric Analysis.- 8.2.6. Implications of the Adsorbed State of K+ in Muscle Cells….- 8.3. X-Ray Absorption Edge Fine Structure of K+ in Frog Erythrocytes.- 8.4. Secondary Evidence for K+ Adsorption in Living Cells.- 8.4.1. K+ Mobility in Living Cells.- 8.4.2. K+ Activity in Living Cells Measured with an Ion-Specific Microelectrode.- 8.4.3. NMR Relaxation Times of 23Na+ and 39K+ in Living Cells.- 8.5. Summary.- 9. The Physical State of Water in Living Cells.- 9.1. Introduction.- 9.2. Solvent Properties.- 9.2.1. Inanimate Models.- 9.2.2. Biopolymers and Viruses.- 9.2.3. Living Cells.- 9.3. Freezing Points.- 9.3.1. Theoretical Expectations.- 9.3.2. Behavior of Models.- 9.3.3. Freezing Pattern of Living Cells.- 9.4. Vapor Sorption Isotherms.- 9.5. Infrared and Raman Spectra.- 9.6. Dielectric Dispersion.- 9.6.1. Model Systems.- 9.6.2. Living Cells.- 9.7. NMR Relaxation Times of Water Protons and Other Nuclei.- 9.7.1. NMR Theories.- 9.7.2. NMR Studies of Water in Solutions of Native Globular Proteins.- 9.7.3. NMR Studies of Water in Living Cells.- 9.7.4. Concluding Remarks on the Current Status of NMR Studies.- 9.8. Quasielastic Neutron Scattering.- 9.9. Summary.- 10. ATP and the Source of Energy for Biological Work Performance.- 10.1. The General Question of the Energization of Biological Work.- 10.2. The Heat Engine Theory.- 10.3. The High-Energy Phosphate Bond Concept.- 10.4. The Energy Source for Biological Work Performance According to the AI Hypothesis.- 10.4.1. The Immediate Source of Energy for Biological Work Performance.- 10.4.2. The Source of Energy for Cyclic Work Performance.- 10.5. Summary.- III. Applications of the Association-Induction Hypothesis to Traditional Problems in Cell Physiology.- 11. Selective Distribution of Ions, Sugars, and Free Amino Acids.- 11.1. The General Theory of Solute Distribution.- 11.1.1. Equation Describing Solute Distribution.- 11.1.2. Control of Solute Distribution by Cardinal Adsorbents.- 11.1.3. The Effect of Temperature on Solute Distribution.- 11.2. Experimental Testing of the Theory.- 11.2.1. Basic Patterns of Solute Distribution: Free and Adsorbed Fractions.- 11.2.2. Cooperativity in Solute Adsorption.- 11.2.3. Effect of Temperature on Solute Distribution.- 11.2.4. Control of Solute Distribution by Cardinal Adsorbents.- 11.3. Summary.- 12. Permeability.- 12.1. Evidence against the Conventional Lipoidal Membrane Theory.- 12.1.1. K+-Specific Ionophores Do Not Increase the Permeability of Living Cell Membranes to K+.- 12.1.2. There Is Not Enough Lipid in Many Membranes to Provide a Continuous Bilayer.- 12.1.3. Removal of Membrane Lipids from the Liver Mitochondrion Inner Membrane Does Not Alter the Trilayer Structure.- 12.2. What Is the Rate-Limiting Step for the Entry of Water into Living Cells?.- 12.3. Polarized Water as the Semipermeable, Selective Permeability Barrier.- 12.4. Permeability of Cells to Ions.- 12.4.1. Influx of Ions.- 12.4.2. Efflux of Ions.- 12.5. Sugar Permeation and Its Control by Insulin.- 12.6. Amino Acid Permeation and Its Dependence on External Na+.- 12.6.1. The Saturable and Nonsaturable Fractions in the Uptake and Exodus of Amino Acids.- 12.6.2. Permeation of Glycine and Other Neutral Amino Acids into Ehrlich Ascites Cells.- 12.6.3. The Saturable Fraction.- 12.7. Surface Protein Adsorption Sites as the Seat of the Selective Adsorption-Desorption Route for Entry of Amino Acids.- 12.8. Summary.- 13. Swelling, Shrinkage, and Volume Control of Living Cells.- 13.1. The Refutation of the Membrane Theory of Cell Volume Regulation.- 13.2. Polarized Water in Lieu of Free Intracellular K+ in the Maintenance of Osmotic Pressure of Living Cells.- 13.3. What Does the Vapor Sorption Isotherm Tell Us about the Osmotic Behavior of Living Cells?.- 13.4. Swelling of Living Cells in Isotonic KC1 and Other Salt Solutions.- 13.5. The Variable Number of K+, Rb+, and Cs+ Adsorption Sites: The Role of Salt Linkages.- 13.6. The Mechanism of Cell Swelling Caused by the Depletion of ATP and the Role of NaCl in the Medium.- 13.7. Classification of Cell and Tissue Swelling.- 13.8. Summary 461.- 14. Electrical Potentials.- 14.1. Evidence against the Membrane Theory of Cellular Electrical Potentials.- 14.1.1. The Indifference of Resting Potential in Frog Muscle to External Cl- Concentration.- 14.1.2. Do the Resting and Action Potentials Depend on the Intracellular Concentrations of K+ and Na+?.- 14.1.3. The Electrogenic Na+ Pump Hypothesis.- 14.1.4. All-or-None Opening and Closing of Na+ and K+ Gates.- 14.1.5. The Independence Principle.- 14.1.6. The Significance of the Demonstration of the Localization of the Bulk of Intracellular K+ in Frog Muscle.- 14.2. Evidence for the Surface Adsorption Theory of Cellular Resting Potentials.- 14.2.1. Collodion-Coated Glass Electrode.- 14.2.2. Colacicco’s Experiment on Oil Membranes.- 14.2.3. Edelmann’s Experiment on Guinea Pig Heart Trabecular Muscle.- 14.3. Experimental Observations Not Explicable by the Membrane Theory but in Harmony with the Surface Adsorption Theory.- 14.3.1. The Adsorbed State of Cell K+.- 14.3.2. The Lack of a Relation between External Cl- and ?.- 14.3.3. The Contradictory Reports on the Relation between ? and Intracellular K+.- 14.4. The Molecular Mechanism of the Resting and Action Potentials 477.- 14.4.1. The New Equation for the Cellular Resting Potential.- 14.4.2. The Control of the Resting Potential by Cardinal Adsorbents According to the AI Hypothesis.- 14.4.3. Changes of the Resting Potential of Toad Oocytes during the Maturation Process.- 14.4.4. Effect of Mechanical Puncturing of the Cell Surface on Oocyte Activation 488.- 14.5. Molecular Events Underlying Excitation.- 14.5.1. Basic Molecular Structure and Properties of the Cell Surface of Muscle and Nerve According to the AI Hypothesis.- 14.5.2. The Molecular Basis of the Sudden, Transient Permeability Increase during Excitation.- 14.6. Summary.- IV. A Reevaluation of Current Concepts in Physiology and Biochemistry.- 15. Oxidative Phosphorylation, ATP Synthesis, and Other Aspects of Mitochondrial Physiology.- 15.1. The Central Role of ATP in Biological Work Performance.- 15.2. The Sources of ATP.- 15.2.1. Creatine Phosphate and Arginine Phosphate.- 15.2.2. Glycolysis or Fermentation.- 15.2.3. Respiratory Chain.- 15.3. Theories of the Mechanism of Oxidative Phosphorylation and Their Critiques.- 15.3.1. The Chemical Coupling Hypothesis.- 15.3.2. The Conformation Coupling Hypothesis.- 15.3.3. The Chemiosmotic Hypothesis.- 15.4. A Tentative Model of the Inductive-Associative Coupling Mechanism for Electron Transport and Oxidative Phosphorylation.- 15.4.1. The Coupling Mechanism.- 12.4.2. Comparison with Model Systems.- 15.5. New Interpretations of Observations in Mitochondrial Physiology.- 15.5.1. Swelling and Shrinkage.- 15.5.2. “Transport” of ATP.- 15.5.3. Uncouplers, Ionophores, Ca2+, Mg2+, ATP, and Other Cardinal Adsorbents.- 15.5.4. Synchronous Oscillatory Changes in Properties of Mitochondria.- 15.6. Summary.- 16. Muscle Contraction and Related Phenomena.- 16.1. Early Theories of Muscle Contraction.- 16.1.1. Engelmann’s Heat Engine Theory.- 16.1.2. The Osmotic Theories of McDougall and MacDonald.- 16.1.3. The Lactic Acid Theory.- 16.1.4. The Engelhardt-Ljubimova Theory.- 16.1.5. The Actin-Myosin Association Theory of Szent-Gyorgyi.- 16.1.6. The Active Relaxation Theory.- 16.1.7. The Electrostatic Extension-Entropic Contraction Theory.- 16.1.8. The Earlier Association-Induction Model.- 16.2. Current Views of the Mechanism of Muscle Contraction.- 16.2.1. The Sliding Filament Theories.- 16.2.2. The Kinetics of the Unregulated Actin-Myosin-ATP System.- 16.2.3. The Control Mechanism.- 16.2.4. Other Recent Theories of Muscle Contraction.- 16.3. Critique of the Sliding Filament Model.- 16.3.1. The Energy Problem.- 16.3.2. The Number, Duration, and Synchronization of Cycles of Cross-Bridge Formation and Breakage.- 16.3.3. What Keeps the Filaments from Tangling Up?.- 16.3.4. Why Should the Bulk of Water in the I Bands Move with the Telescoping Thin Filaments?.- 16.4. A Tentative Model of Muscle (and Nonmuscle Cell) Contraction: An Updated Theory According to the AI Hypothesis.- 16.4.1. The Resting, Relaxed Muscle.- 16.4.2. Contraction.- 16.4.3. Relaxation.- 16.5. Agreements and Disagreements with Relevant Existing Knowledge.- 16.5.1. Electron Microscopic and X-Ray Diffraction Evidence of the Continuing Existence of Thin Filaments.- 16.5.2. A Key Role of Cell Water in Muscle Contraction.- 16.5.3. A Mechanism That Prevents the Filaments from Tangling Up.- 16.5.4. A Key Role of K+ Adsorption and Desorption in Muscle Contraction.- 16.5.5. The Source of Energy and Force in Muscle Contraction.- 16.6. Summary.- 17. Active Transport across Intestinal Epithelia and Other Bifacial Cell Systems.- 17.1. Unifacial and Bifacial Cells.- 17.2. Concepts of Active Solute Transport Based on the Membrane Pump Theory.- 17.2.1. The “Two-Membrane Theory” of Koefoed-Johnson and Ussing.- 17.2.2. The Standing Osmotic Gradient Theory of Diamond and Bossert.- 17.2.3. The Pericellular Pump Theory of Cereijido and Rotunno.- 17.2.4. The Na+ Gradient Hypothesis of Sugar and Amino Acid Transport.- 17.3. Cooperative Adsorption-Desorption Model of Active Transport across Epithelia and other Bifacial Cell Systems.- 17.4. Application of the Model to Experimental Findings.- 17.4.1. Cyclic Changes of Adsorption-Desorption as the Basis for Active Transport.- 17.4.2. Location of the Pumping Mechanism.- 17.4.3. The Source of Energy for Active Transport.- 17.4.4. Coupling of Ion and Water Transport.- 17.4.5. The Relation between “Homocellular” Regulation of Cell K+ and Na+ Composition and “Homoepithelial” Na+ Transport.- 17.4.6. Coupling of Na+ Transport with Sugar and Amino Acid Transport.- 17.5. Summary.- V. A Tentative Approach to Some Unsolved Problems in Biology and Medicine.- 18. The Control of Protein Synthesis.- 18.1. Transcription and Translation in Prokaryotes.- 18.1.1. The lac Operon and the Control of Gene Transcription.- 18.1.2. The Role of K+, Na+, Glycerol, and DMSO in DNA Transcription.- 18.1.3. The Role of K+ in mRNA Translation.- 18.2. The Control of Gene Function in Eukaryotes.- 18.2.1. Gene Transcription.- 18.2.2. mRNA Translation and Protein Synthesis.- 18.3. Summary.- 19. Growth and Differentiation.- 19.1. Mosaic and Regulative Eggs.- 19.2. Maturation of Amphibian Eggs.- 19.2.1. Ca2+ and the Depolarization of the Electrical Potential.- 19.2.2. Maturation-Promoting Factor.- 19.2.3. A Key Role of Adsorbed Na+ in the Control of Maturation.- 19.2.4. An Attempt to Provide a Consistent Theoretical Framework for Future Investigation.- 19.2.5. Other Cytoplasmic Factors in Maturing Oocytes: Cytostatic Factor and Chromosome-Condensing Activity.- 19.3. Fertilization (or Activation) of Sea Urchin Eggs.- 19.3.1. Alteration of Surface Proteins Accompanying Activation.- 19.3.2. Electrical Potential Changes Accompanying Activation.- 19.3.3. Ca2+ Release Accompanying Activation.- 19.3.4. Requirement of External Na+ in Egg Fertilization.- 19.4. Differentiation.- 19.4.1. Brief Historical Sketch.- 19.4.2. Classical Transplantation Experiments of Spemann and Mangold.- 19.4.3. In Search of the Evocator.- 19.4.4. Barth and Barth’s Experiments and Theory of Differentiation.- 19.4.5. Landstrom and Lavtrup’s Work on Differentiation.- 19.4.6. Concluding Remarks on Differentiation.- 19.5. The Cell Cycle.- 19.5.1. The Transition Probability Model.- 19.5.2. The Control of Entry into the C Phase.- 19.5.3. Control of Chromosome Condensation.- 19.5.4. The Promotion of Differentiation of Enucleated Eggs by Nuclear Transplantation.- 19.6. The Stem Cells: “Immortal” Queen Bees of the Society of Renewing Cells.- 19.7. Some Molecular Mechanisms According to the AI Hypothesis.- 19.7.1. Migration of Proteins (and RNA) between the Nucleus and the Cytoplasm.- 19.7.2. Nuclear Swelling during DNA Replication.- 19.8. Amphibian Metamorphosis.- 19.8.1. Thyroid Hormones.- 19.8.2. Prolactin.- 19.9. Summary.- 20. Cancer.- 20.1. General Theories of Cancer.- 20.1.1. The Somatic Mutation Theory: Historical Background.- 20.1.2. Dramatic Recent Confirmation of the Somatic Mutation Theory.- 20.1.3. The Maldifferentiation Theory.- 20.2. Physiological Theories of Cancer.- 20.2.1. Szent-Gyorgyi’s Theory of Cancer.- 20.2.2. Cone’s Theory of Cancer.- 20.3. What Distinguishes Cancer from Normal Tissues?.- 20.3.1. The Morphological Generalization.- 20.3.2. The Warburg Generalization.- 20.3.3. The Greenstein Generalization.- 20.3.4. The Roberts-Frankel Generalization.- 20.3.5. The Damadian Generalization.- 20.3.6. The Ling-Murphy Generalization.- 20.4. Another Apparent Paradox and the Bright Future of Cancer Research.- Appendixes.- A. Nuclear Magnetic Resonance Spectroscopy.- A.1. NMR Relaxation Time, Tx.- A.2. Proton Resonance Spectrum, Linewidth, and T2.- A.2.1. Chemical Shift.- A.2.2. Linewidth and T2.- A.3. The Relation of Tx and T2 to the Rotational Correlation Time, Tc.- A.4. Orientation-Dependent Doublet Structure on NMR Spectral Line Shape.- B. Infrared and Raman Spectra.- References.- Abbreviations.- Notation List.