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Biophysics and cancer

Author: Claudio A Nicolini
Publisher: New York : Plenum Press, ©1986.
Edition/Format:   Print book : EnglishView all editions and formats
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Additional Physical Format: Online version:
Nicolini, Claudio A.
Biophysics and cancer.
New York : Plenum Press, ©1986
(OCoLC)564786142
Document Type: Book
All Authors / Contributors: Claudio A Nicolini
ISBN: 0306421224 9780306421228
OCLC Number: 13327320
Description: xv, 463 pages : illustrations ; 24 cm
Contents: 1. Normal Cells and Cancer Cells: Macromolecular Structures and Cellular Functions.- 1.1. Background.- 1.2. Native Chromatin-DNA Structure.- 1.2.1. What Is Chromatin?.- 1.2.2. Secondary Structure.- 1.2.3. Tertiary Structure.- 1.2.4. Quaternary Structure.- 1.2.5. Quinternary Structure.- 1.3. Nuclear Structure.- 1.3.1. Nuclear Pore Membrane and Chromosome Scaffold.- 1.3.2. Nuclear Matrix and Control of Nuclear Volume.- 1.3.3. Levels of DNA Organization in Situ.- 1.3.4. Active versus Inactive Genes: Euchromatin versus Heterochromatin.- 1.3.5. Structural Models.- 1.4. What Is a Gene?.- 1.5. Ribosomes.- 1.5.1. Protein Synthesis.- 1.5.2. Genetic Code.- 1.6. Modification in the Control of Cell Proliferation.- 1.6.1. Continuously Dividing Cells.- 1.6.2. DNA Synthesis Initiation.- 1.6.3. Induced Proliferation of Quiescent Cells.- 1.6.4. Water and Ions.- 1.6.5. Chromosomal Protein Modifications.- 1.7. Modifications in the Control of Cell Differentiation.- 1.8. Modifications in the Control of Cell Transformation.- 1.8.1. Cancer Genes.- 1.8.2. Virus and Spontaneous Neoplastic Transformation.- 1.8.3. Chemically Induced Neoplastic Transformation.- 1.8.4. Water.- 1.8.5. Negative Superhelical Turns and Z-DNA.- 1.9. Modifications in the Control of Cellular Aging.- 1.10. Membranes.- 1.10.1. Membrane Structure.- 1.10.2. Membrane Transport.- 1.10.3. Membrane and Neoplastic Transformation.- 1.11. Cytoskeleton.- 1.12. Control Mechanisms for Normal versus Abnormal Cell Growth.- 1.13. Molecular Mechanisms and Models for Gene Expression.- 1.14. Conclusions and Future Trends.- 2. Cancer Cause and Prevention.- 2.1. Background.- 2.2. Possible Causes of Cancer.- 2.2.1. Environment.- 2.2.2. Drugs.- 2.2.3. Viruses.- 2.2.4. Heredity and Spontaneous Induction.- 2.3. Cancer Prevention.- 2.3.1. Long-Term Tests.- 2.3.2. Short-Term Tests.- 3. Cancer Detection and Treatment.- 3.1. Background.- 3.2. Present Status of Human Cancer Detection and Treatment.- 3.2.1. Survival Data.- 3.2.2. Combination Chemotherapy and Radiotherapy.- 3.2.3. Immunotherapy.- 3.2.4. Phototherapy.- 3.3. Alternative Analytical Approaches.- 3.3.1. Pharmaco-Cell Kinetics.- 3.3.2. Pharmaco-Enzyme Kinetics.- 3.3.3. Pharmaco-Tissue Kinetics.- 3.4. New Observables.- 3.4.1. Cell Growth and Differentiation Parameters: G0-Q Cells and Metastatic Variants.- 3.4.2. Cell Heterogeneity, Reverse Transformation, and Macrophage Activation.- 3.4.3. Drug Sensitivity.- 3.4.4. Real-Time Response Monitoring.- 3.4.5. Biochemical Determination of Enzymatic Constants.- 3.5. Theoretical Simulation at the Cellular Level: Optimized Drug Metabolism Parameters in Animals.- 3.5.1. DRUGFIT Model.- 3.5.2. Mathematical Techniques for Fitting the DRUGFIT Model to Experimental Data.- 3.5.3. Animal Model.- 3.5.4. B-16 Tumors.- 3.5.5. Small Intestinal Crypt Cells.- 3.5.6. Differential Response.- 3.5.7. Regression Equations.- 3.6. Treatment Optimization in Animals.- 3.6.1. Synchronization versus Recruitment.- 3.6.2. SIVFIT and Optimal Control Theory.- 3.6.3. Suggested Strategies: Time Scale and Dosage.- 3.6.4. Actual Results: Survival and Selected Killing of Metastases.- 3.7. Drug Interaction and Molecular Perturbation in Animals.- 3.7.1. Experimental versus Theoretical Isobols.- 3.7.2. Time-Dependent Changes in Nucleotide Pools.- 3.8. Extrapolation to Human Cancer.- 3.8.1. Early Cancer Detection.- 3.8.2. Flow and Scanning Cytometry.- 3.8.3. Monoclonal Antibody Testing.- 3.8.4. DNA Probes.- 3.8.5. X Rays-1. Normal Cells and Cancer Cells: Macromolecular Structures and Cellular Functions.- 1.1. Background.- 1.2. Native Chromatin-DNA Structure.- 1.2.1. What Is Chromatin?.- 1.2.2. Secondary Structure.- 1.2.3. Tertiary Structure.- 1.2.4. Quaternary Structure.- 1.2.5. Quinternary Structure.- 1.3. Nuclear Structure.- 1.3.1. Nuclear Pore Membrane and Chromosome Scaffold.- 1.3.2. Nuclear Matrix and Control of Nuclear Volume.- 1.3.3. Levels of DNA Organization in Situ.- 1.3.4. Active versus Inactive Genes: Euchromatin versus Heterochromatin.- 1.3.5. Structural Models.- 1.4. What Is a Gene?.- 1.5. Ribosomes.- 1.5.1. Protein Synthesis.- 1.5.2. Genetic Code.- 1.6. Modification in the Control of Cell Proliferation.- 1.6.1. Continuously Dividing Cells.- 1.6.2. DNA Synthesis Initiation.- 1.6.3. Induced Proliferation of Quiescent Cells.- 1.6.4. Water and Ions.- 1.6.5. Chromosomal Protein Modifications.- 1.7. Modifications in the Control of Cell Differentiation.- 1.8. Modifications in the Control of Cell Transformation.- 1.8.1. Cancer Genes.- 1.8.2. Virus and Spontaneous Neoplastic Transformation.- 1.8.3. Chemically Induced Neoplastic Transformation.- 1.8.4. Water.- 1.8.5. Negative Superhelical Turns and Z-DNA.- 1.9. Modifications in the Control of Cellular Aging.- 1.10. Membranes.- 1.10.1. Membrane Structure.- 1.10.2. Membrane Transport.- 1.10.3. Membrane and Neoplastic Transformation.- 1.11. Cytoskeleton.- 1.12. Control Mechanisms for Normal versus Abnormal Cell Growth.- 1.13. Molecular Mechanisms and Models for Gene Expression.- 1.14. Conclusions and Future Trends.- 2. Cancer Cause and Prevention.- 2.1. Background.- 2.2. Possible Causes of Cancer.- 2.2.1. Environment.- 2.2.2. Drugs.- 2.2.3. Viruses.- 2.2.4. Heredity and Spontaneous Induction.- 2.3. Cancer Prevention.- 2.3.1. Long-Term Tests.- 2.3.2. Short-Term Tests.- 3. Cancer Detection and Treatment.- 3.1. Background.- 3.2. Present Status of Human Cancer Detection and Treatment.- 3.2.1. Survival Data.- 3.2.2. Combination Chemotherapy and Radiotherapy.- 3.2.3. Immunotherapy.- 3.2.4. Phototherapy.- 3.3. Alternative Analytical Approaches.- 3.3.1. Pharmaco-Cell Kinetics.- 3.3.2. Pharmaco-Enzyme Kinetics.- 3.3.3. Pharmaco-Tissue Kinetics.- 3.4. New Observables.- 3.4.1. Cell Growth and Differentiation Parameters: G0-Q Cells and Metastatic Variants.- 3.4.2. Cell Heterogeneity, Reverse Transformation, and Macrophage Activation.- 3.4.3. Drug Sensitivity.- 3.4.4. Real-Time Response Monitoring.- 3.4.5. Biochemical Determination of Enzymatic Constants.- 3.5. Theoretical Simulation at the Cellular Level: Optimized Drug Metabolism Parameters in Animals.- 3.5.1. DRUGFIT Model.- 3.5.2. Mathematical Techniques for Fitting the DRUGFIT Model to Experimental Data.- 3.5.3. Animal Model.- 3.5.4. B-16 Tumors.- 3.5.5. Small Intestinal Crypt Cells.- 3.5.6. Differential Response.- 3.5.7. Regression Equations.- 3.6. Treatment Optimization in Animals.- 3.6.1. Synchronization versus Recruitment.- 3.6.2. SIVFIT and Optimal Control Theory.- 3.6.3. Suggested Strategies: Time Scale and Dosage.- 3.6.4. Actual Results: Survival and Selected Killing of Metastases.- 3.7. Drug Interaction and Molecular Perturbation in Animals.- 3.7.1. Experimental versus Theoretical Isobols.- 3.7.2. Time-Dependent Changes in Nucleotide Pools.- 3.8. Extrapolation to Human Cancer.- 3.8.1. Early Cancer Detection.- 3.8.2. Flow and Scanning Cytometry.- 3.8.3. Monoclonal Antibody Testing.- 3.8.4. DNA Probes.- 3.8.5. X Rays-Computerized Axial Tomography.- 3.8.6. NMR Imaging.- 3.8.7. Diagnostic Ultrasound.- 3.8.8. Modeling as a Useful Adjunct in Cancer Chemotherapy.- 3.8.9. Treatment Strategies Based on Cancer Cell Biology and on Analytical Modeling.- 3.8.10. Medical Artificial Intelligence.- 4. Experimental Probes.- 4.1. Background.- 4.2. Preparative Tools.- 4.2.1. Tissue Culture.- 4.2.2. Radioactive Labeling.- 4.2.3. Macromolecule Isolation, Size, and Shape.- 4.2.4. Chromophore Identification: Absorbance and Emission Photometry.- 4.2.5. Activation Analysis.- 4.3. Probes for Lower-Order Structures.- 4.3.1. Template Activity and Restriction Enzymes.- 4.3.2. Genetic Engineering and Protein Engineering.- 4.3.3. Circular Dichroism and Optical Rotatory Dispersion.- 4.3.4. Scattering of Unpolarized and Polarized Light.- 4.3.5. Dye Binding Studies.- 4.3.6. Thermal Denaturation.- 4.3.7. Linear Dichroism and Flow Birefringence.- 4.3.8. Scattering and Diffraction by Neutrons and X Rays.- 4.3.9. Nuclear Magnetic Resonance.- 4.4. Probes for Higher-Order Structures in Situ.- 4.4.1. Electron Microscopy.- 4.4.2. Premature Chromosome Condensation and Cell Fusion.- 4.4.3. Computer-Enhanced Image Analysis.- 4.4.4. Immunocytology.- 4.4.5. Microviscoelastometry.- 4.4.6. Microcalorimetry.- 4.4.7. Microfluorimetry.- 4.4.8. Fluorescence Staining of Macromolecules.- 4.4.9. Complex Dielectric Constants.- 4.4.10. Laser Spectroscopy.- 4.4.11. Biophysical Instrumentation for Electrical Phenomena.- 5. Theoretical Probes.- 5.1. Background.- 5.2. Enzyme Kinetics.- 5.2.1. Michaelis-Menten Equation.- 5.2.2. Lineweaver-1. Normal Cells and Cancer Cells: Macromolecular Structures and Cellular Functions.- 1.1. Background.- 1.2. Native Chromatin-DNA Structure.- 1.2.1. What Is Chromatin?.- 1.2.2. Secondary Structure.- 1.2.3. Tertiary Structure.- 1.2.4. Quaternary Structure.- 1.2.5. Quinternary Structure.- 1.3. Nuclear Structure.- 1.3.1. Nuclear Pore Membrane and Chromosome Scaffold.- 1.3.2. Nuclear Matrix and Control of Nuclear Volume.- 1.3.3. Levels of DNA Organization in Situ.- 1.3.4. Active versus Inactive Genes: Euchromatin versus Heterochromatin.- 1.3.5. Structural Models.- 1.4. What Is a Gene?.- 1.5. Ribosomes.- 1.5.1. Protein Synthesis.- 1.5.2. Genetic Code.- 1.6. Modification in the Control of Cell Proliferation.- 1.6.1. Continuously Dividing Cells.- 1.6.2. DNA Synthesis Initiation.- 1.6.3. Induced Proliferation of Quiescent Cells.- 1.6.4. Water and Ions.- 1.6.5. Chromosomal Protein Modifications.- 1.7. Modifications in the Control of Cell Differentiation.- 1.8. Modifications in the Control of Cell Transformation.- 1.8.1. Cancer Genes.- 1.8.2. Virus and Spontaneous Neoplastic Transformation.- 1.8.3. Chemically Induced Neoplastic Transformation.- 1.8.4. Water.- 1.8.5. Negative Superhelical Turns and Z-DNA.- 1.9. Modifications in the Control of Cellular Aging.- 1.10. Membranes.- 1.10.1. Membrane Structure.- 1.10.2. Membrane Transport.- 1.10.3. Membrane and Neoplastic Transformation.- 1.11. Cytoskeleton.- 1.12. Control Mechanisms for Normal versus Abnormal Cell Growth.- 1.13. Molecular Mechanisms and Models for Gene Expression.- 1.14. Conclusions and Future Trends.- 2. Cancer Cause and Prevention.- 2.1. Background.- 2.2. Possible Causes of Cancer.- 2.2.1. Environment.- 2.2.2. Drugs.- 2.2.3. Viruses.- 2.2.4. Heredity and Spontaneous Induction.- 2.3. Cancer Prevention.- 2.3.1. Long-Term Tests.- 2.3.2. Short-Term Tests.- 3. Cancer Detection and Treatment.- 3.1. Background.- 3.2. Present Status of Human Cancer Detection and Treatment.- 3.2.1. Survival Data.- 3.2.2. Combination Chemotherapy and Radiotherapy.- 3.2.3. Immunotherapy.- 3.2.4. Phototherapy.- 3.3. Alternative Analytical Approaches.- 3.3.1. Pharmaco-Cell Kinetics.- 3.3.2. Pharmaco-Enzyme Kinetics.- 3.3.3. Pharmaco-Tissue Kinetics.- 3.4. New Observables.- 3.4.1. Cell Growth and Differentiation Parameters: G0-Q Cells and Metastatic Variants.- 3.4.2. Cell Heterogeneity, Reverse Transformation, and Macrophage Activation.- 3.4.3. Drug Sensitivity.- 3.4.4. Real-Time Response Monitoring.- 3.4.5. Biochemical Determination of Enzymatic Constants.- 3.5. Theoretical Simulation at the Cellular Level: Optimized Drug Metabolism Parameters in Animals.- 3.5.1. DRUGFIT Model.- 3.5.2. Mathematical Techniques for Fitting the DRUGFIT Model to Experimental Data.- 3.5.3. Animal Model.- 3.5.4. B-16 Tumors.- 3.5.5. Small Intestinal Crypt Cells.- 3.5.6. Differential Response.- 3.5.7. Regression Equations.- 3.6. Treatment Optimization in Animals.- 3.6.1. Synchronization versus Recruitment.- 3.6.2. SIVFIT and Optimal Control Theory.- 3.6.3. Suggested Strategies: Time Scale and Dosage.- 3.6.4. Actual Results: Survival and Selected Killing of Metastases.- 3.7. Drug Interaction and Molecular Perturbation in Animals.- 3.7.1. Experimental versus Theoretical Isobols.- 3.7.2. Time-Dependent Changes in Nucleotide Pools.- 3.8. Extrapolation to Human Cancer.- 3.8.1. Early Cancer Detection.- 3.8.2. Flow and Scanning Cytometry.- 3.8.3. Monoclonal Antibody Testing.- 3.8.4. DNA Probes.- 3.8.5. X Rays-Computerized Axial Tomography.- 3.8.6. NMR Imaging.- 3.8.7. Diagnostic Ultrasound.- 3.8.8. Modeling as a Useful Adjunct in Cancer Chemotherapy.- 3.8.9. Treatment Strategies Based on Cancer Cell Biology and on Analytical Modeling.- 3.8.10. Medical Artificial Intelligence.- 4. Experimental Probes.- 4.1. Background.- 4.2. Preparative Tools.- 4.2.1. Tissue Culture.- 4.2.2. Radioactive Labeling.- 4.2.3. Macromolecule Isolation, Size, and Shape.- 4.2.4. Chromophore Identification: Absorbance and Emission Photometry.- 4.2.5. Activation Analysis.- 4.3. Probes for Lower-Order Structures.- 4.3.1. Template Activity and Restriction Enzymes.- 4.3.2. Genetic Engineering and Protein Engineering.- 4.3.3. Circular Dichroism and Optical Rotatory Dispersion.- 4.3.4. Scattering of Unpolarized and Polarized Light.- 4.3.5. Dye Binding Studies.- 4.3.6. Thermal Denaturation.- 4.3.7. Linear Dichroism and Flow Birefringence.- 4.3.8. Scattering and Diffraction by Neutrons and X Rays.- 4.3.9. Nuclear Magnetic Resonance.- 4.4. Probes for Higher-Order Structures in Situ.- 4.4.1. Electron Microscopy.- 4.4.2. Premature Chromosome Condensation and Cell Fusion.- 4.4.3. Computer-Enhanced Image Analysis.- 4.4.4. Immunocytology.- 4.4.5. Microviscoelastometry.- 4.4.6. Microcalorimetry.- 4.4.7. Microfluorimetry.- 4.4.8. Fluorescence Staining of Macromolecules.- 4.4.9. Complex Dielectric Constants.- 4.4.10. Laser Spectroscopy.- 4.4.11. Biophysical Instrumentation for Electrical Phenomena.- 5. Theoretical Probes.- 5.1. Background.- 5.2. Enzyme Kinetics.- 5.2.1. Michaelis-Menten Equation.- 5.2.2. Lineweaver-Burk Plot.- 5.2.3. Competitive Inhibition.- 5.2.4. Noncompetitive Inhibition.- 5.2.5. Feedback Inhibition and Activation.- 5.3. Signal Processing and Analysis.- 5.3.1. Correlation Function and Fourier Transform.- 5.3.2. Application of Fourier Techniques to Discrete Measurements.- 5.3.3. The Fast Fourier Transform.- 5.3.4. Algorithm for Cross-Correlation Computation.- 5.3.5. Search for Periodicities of Macromolecular Distribution within an Intact Cell.- 5.4. Statistical Mechanics and Thermodynamics of Cell Structures.- 5.4.1. Entropy, Free Energy, and Enthalpy.- 5.4.2. Statistical Mechanics.- 5.4.3. Multiple Equilibria.- 5.4.4. Biopolymer Conformation at Equilibrium.- 5.5. Polyelectrolyte Theory of Interactions among Biopolymers.- 5.5.1. Counterion Condensation and Molecular Theory.- 5.5.2. Persistence Length.- 5.5.3. Model for Chromatin Structure, as Influenced by Ionic Strength and H1 Modification.- 5.5.4. Comparison with Experimental Findings.- 5.6. Physicochemical Model for Dye-Nucleic Acid Interaction in Situ.- 5.6.1. Experimental Evidence from Studies in Solution.- 5.6.2. Description of the Model for in Situ Staining.- 5.7. Electromagnetic Theory of Polarized Light Scattering by Large Biopolymers.- 5.7.1. Multiple Scattering of Dipoles.- 5.7.2. Dielectric Ellipsoids within the Born Approximation.- 5.7.3. Specific Possible Interpretations and Experimental Predictions.- 5.8. Random Walk Model of Biopolymers.- 5.8.1. Basic Structure of the Model.- 5.8.2. Solution of the Elution Integral.- 5.8.3. DNA Chain Flexibility and Superpacking from Alkaline Elution Data.- 5.8.4. Differential Role of DNA Chain Length and Flexibility.- 5.9. Mean Field Theory of Gel Biopolymers.- Epilogue: A Final Comment.- Problems.- References.
Responsibility: Claudio Nicolini.

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