Human biological aging : from macromolecules to organ-systems /

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Hlavní autor: Bilder, Glenda (Autor)
Typ dokumentu: Kniha
Jazyk:Angličtina
Vydáno: Hoboken, New Jersey : Wiley-Blackwell, [2016]
Témata:
On-line přístup:Elektronická verze přístupná pouze pro studenty a pracovníky MU
Příbuzné jednotky:Tištěná verze:: Human biological aging : from macromolecules to organ-systems.
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505 0 |a Human Biological Aging: From Macromolecules to Organ Systems -- Contents -- Preface -- About the Companion Website -- Section 1: The Foundation -- Essential Preparatory Material -- Chapter 1: Orientation -- Beginnings of Biogerontology -- Multiple Disciplines Come Together to Study Biological Aging -- Population Aging -- Dramatic Increase in Life Expectancy Due to Public Health Advancements: Sanitation, Clean Water, Vaccines, and Antibiotics -- Does Living Longer Assure Living Healthier? -- Characteristics of Aging -- The Fundamentals of Physics Describe Aging as the Loss of "Molecular Fidelity" That Exceeds Repair and Replacement -- The Commencement of Aging Is Debated -- Rates of Aging Among Different Species May Be Rapid, Gradual, or Negligible -- The Senescence Phenotype Is Highly Variable -- Components of Longevity -- Longevity Is in Part Heritable Through Expression of Longevity Determinants: Mechanisms of Maintenance, Repair, and Replacement -- Longevity of the Centenarians and Supercentenarians Reveals Few Common Threads -- Stochastic Events Exert Major Impact on Lifespan -- Theories of Aging Overview -- Summary -- Critical Thinking -- Key Terms -- Bibliography -- Chapter 2: Measurements and Models -- The Scientific Method -- Types of Data -- Not All Data are of Equal Value -- Issues with Aging Studies in Man -- Studies of Human Aging Encounter Difficulties: Heterogeneity, Organizational Level, and Others -- Aging Assessed from Demographic or Individual Perspective -- Measurement of the Aging Process -- Study Designs Are Mainly Cross-Sectional and Longitudinal -- Cross-Sectional Study Design Infers Aging -- Longitudinal Study Design Measures Aging Directly -- Randomized Controlled Trials and Meta-Analysis are Additional Formats for the Study of Aging in Man -- Caloric Restriction: Life Extension Experiment. 
505 8 |a Physiological Changes with Caloric Restriction -- CR in Man is Underway -- Mechanisms of Caloric Restriction -- CR is Analogous to Food Shortage in the "Wild" -- Caloric Restriction as an Example of Hormesis -- Laboratory Animal Models -- Animal Models Are Useful Adjuncts to the Study of the Aging Process -- Yeast: Saccharomyces cerevisiae -- Roundworm: Caenorhabditis elegans -- Fruit fly: Drosophila melanogaster -- Mouse: Mus musculus -- Nonhuman Primate: Macaca mulatta -- Man As Model: Baltimore Longitudinal Study -- Progeroid Syndromes as Premature Aging -- Summary -- Critical Thinking -- Key Terms -- Bibliography -- Chapter 3: Evolutionary Theories of Aging -- Historical Views and Insights -- Unsupportable Programmed Aging Is Replaced by Evolutionary Tenets -- Darwin's Evolutionary Tenets -- Natural Selection Favors Survival Traits -- Genes and Evolution -- Genes (DNA Sequences) Possess the Hereditary Information That Is Passed from Generation to Generation through the Germline (Gametes) -- Evolved Traits Arise through Genetic Variations -- Contemporary Evolutionary Theories: Disposable Soma Theory (Dst), Antagonistic Pleiotropy Theory (Apt), and Mutation Accumulation Theory (Mat) -- Aging Is a Side Effect of Evolution -- Antagonistic Pleiotropy Theory -- Genes that Benefit Fitness in the Young Become Deleterious in the Aged -- Mutation Accumulation -- Genes Expressed Late in Life Remain in the Gene Pool and May Be Deleterious -- Disposable Soma Theory -- Evolutionary Life History of a Species Determines Degree of Investment in Germline (Reproductive Success) and in Soma Maintenance (Longevity) -- DST Predictions: Relation of Fecundity and Longevity -- Relation of Longevity and Maintenance Mechanisms -- DST Explains the Lifespan Extension Effects of Caloric Restriction as an Evolutionary Conserved Adaptation to Food Shortage. 
505 8 |a The DST Applies Only to Species that Age and Reproduce Sexually -- Summary -- Critical Thinking -- Key Terms -- Bibliography -- Section 2: Basic Components -- Introduction to Macromolecules and Cells -- Loss of Molecular Fidelity Is the Essence of Aging -- Biological Organization of the Organism Begins with Atoms That Combine to Form Molecules and More Complex Structures: Macromolecules, Cells, Tissues, Organs, and Organ Systems -- Biologically Important Atoms -- Key Molecules Are Amino Acids, Fatty Acids, Sugars, Bases, Water, and Phosphates -- Major Macromolecules Are Proteins, Lipids, Polysaccharides, and Nucleic Acids -- Macromolecules Are Constantly Formed (Biosynthesized) and Broken Down (Degraded) -- The Three-Dimensional Structure of Macromolecules Determines Function -- Altered Structure Produces Reduced or Absent Function -- The Cell Is the Smallest Enclosed Unit of Living Matter -- Chapter 4: Aging of Macromolecules -- Introduction to Oxidative Stress Hypotheses -- Oxidation/Reduction Principles -- Transfer of One or More Electrons between Molecules is Essential for Oxidation and Reduction Reactions -- Free Radicals Initiate Damage Because They are Highly Reactive Particles with an Unpaired Electron -- Non-Radical Oxidants are Strong Oxidants with Paired Electrons -- They May Act as Signal Molecules and as Mediators of the Oxidative State of the Cell -- Oxidative Stress -- Oxidative Stress Represents the Measureable Increase in Radical and Non-Radical Oxidants in an Organism -- Sources of Oxidative Stress -- Oxidative Stress Arises from External and Internal Sources under Controlled and Uncontrolled Conditions -- Targets of Oxidative Stress: Nucleic Acids, Proteins, and Lipids -- Nucleic Acids as Oxidative Targets -- Oxidation of Nucleic Acids Cause Major Detrimental Effects on Gene Expression and Cell Division. 
505 8 |a Oxidative Target: Proteins -- Protein Activity is Diverse, Essential to Normal Cell Function, and Tightly Regulated -- Protein Glycation Produces Cross-Linkage -- Oxidation Disrupts Enzyme Activity -- Direct Damage or Loss of Cell Signaling Deprives the Cell of Important Protein-Dependent Activities -- Lipids as Oxidative Targets -- Spontaneous Oxidation of Membrane Unsaturated Fatty Acids Produces a Variety of Toxic Compounds -- Enzymatically Controlled Oxidations Yield Important Signaling Molecules -- Saccharides as Oxidative Initiators -- Elevated Levels of Sugars Pose Serious Oxidation Threat -- Countermeasures -- Maintenance Mechanisms that Suppress Oxidative Stress: Antioxidant Enzymes -- Redox Pairs -- NER/BER System -- Msr System -- Cell Organelles -- SOD/Catalase/Glutathione Peroxidase are Antioxidant Enzymes that Convert Oxidants to Less Reactive Species -- Glutathione and Thioredoxin are Redox Pairs that Shuttle Two Electrons to Prevent Persistent Oxidation of Thiol and Similar Groups -- Msr System is a Selective System that Prevents Oxidation of Thiol Groups on the Amino Acid Methionine -- NER and BER Systems Protect Nucleic Acids from Oxidation -- The Composition of the Macromolecule is Important -- Strengths and Weaknesses of Oxidative Stress Theories -- Oxidative Stress Hypothesis -- Redox Stress Hypothesis -- Summary -- Critical Thinking -- Key Terms -- Bibliography -- Chapter 5: Aging of Cells -- Role of Organelle -- Organelles Separately and Together Maintain the Cell -- How Organelles Age -- Mt Contain Their Own DNA -- Mt Biosynthesize ATP to Power the Cell -- Mt Determine the Fate of the Cell -- Mt Regulate the Level of ROS -- Mt Dysfunction Is Present in Tissues from Aged Humans -- The mt Free Radical Theory of Aging Proposes mt ROS as a Cause of Aging -- Mt are Mobile with Changing Morphology. 
505 8 |a Altered mt Dynamics as Effecter of Cell Aging -- Lysosomes Recycle Defective Substructures, Oxidized Macromolecules, and Other Cell Components -- Autophagy Occurs by Three Different Pathways -- Autophagy Declines with Age Possibly Due to Loss of the Receptor-Transporter (LAMP-2A) and/or Defective mt -- Peroxisomes Perform Oxidations and Biosynthesize Compounds -- Peroxisomes Lose the Ability to Import Catalase to Degrade Hydrogen Peroxide -- Nucleus Is the Locus of the Genetic Blueprint for the Cell -- DNA Experiences Telomere Shortening and Epigenetic Modifications -- Proposed Deficiency of Nuclear Lamins -- Cellular Aging: Observations and Hypotheses -- The Cell Cycle Is a Tightly Regulated Process of Checklists and Checkpoints -- Permanent Cell Cycle Arrest (Replicative Senescence) Occurs with Age -- Mitotic Cells Express the Senescence-Associated Secretory Phenotype (SASP) -- Stem Cells Are Pluripotent and Replenish Missing Cells -- Aging Postmitotic Cells May Activate Apoptosis: Cause of Tissue Atrophy -- Organelle Dysfunction Is the Main Reason Postmitotic Cells Undergo Apoptosis -- Cell Death Occurs By Autophagy, Apoptosis, or Necrosis -- Relation of Cellular Aging to Disease -- Summary -- Critical Thinking -- Key Terms -- Bibliography -- Section 3: Organ Systems: Outer Covering and Movement: Integumentary, Skeletal Muscles, and Skeletal Systems -- Chapter 6: Aging of the Integumentary System -- Overview -- Unique Aspects of the Integument (Skin) -- Skin Aging Results from Extrinsic and Intrinsic Effects -- Skin Layers -- Epidermis, Dermis, and Hypodermis Define the Skin -- Keratinocytes of the Epidermis Are Continually Renewed from the Basal Layer -- Melanocytes and Langerhans Cells Provide Protection -- Aging of the Epidermis -- Extrinsic Aging of the Epidermis -- UVR Is the Main Cause of Extrinsic Aging -- Pollution Also Contributes. 
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