Human Biological Aging: From Macromolecules To Organ Systems

دانلود کتاب Human Biological Aging: From Macromolecules To Organ Systems

32000 تومان موجود

کتاب پیری بیولوژیکی انسان: از درشت مولکول ها تا سیستم های اندام نسخه زبان اصلی

دانلود کتاب پیری بیولوژیکی انسان: از درشت مولکول ها تا سیستم های اندام بعد از پرداخت مقدور خواهد بود
توضیحات کتاب در بخش جزئیات آمده است و می توانید موارد را مشاهده فرمایید


این کتاب نسخه اصلی می باشد و به زبان فارسی نیست.


امتیاز شما به این کتاب (حداقل 1 و حداکثر 5):

امتیاز کاربران به این کتاب:        تعداد رای دهنده ها: 13


توضیحاتی در مورد کتاب Human Biological Aging: From Macromolecules To Organ Systems

نام کتاب : Human Biological Aging: From Macromolecules To Organ Systems
عنوان ترجمه شده به فارسی : پیری بیولوژیکی انسان: از درشت مولکول ها تا سیستم های اندام
سری :
نویسندگان :
ناشر : John Wiley & Sons
سال نشر : 2016
تعداد صفحات : 341
ISBN (شابک) : 9781118967027 , 111896702X
زبان کتاب : English
فرمت کتاب : pdf
حجم کتاب : 67 مگابایت



بعد از تکمیل فرایند پرداخت لینک دانلود کتاب ارائه خواهد شد. درصورت ثبت نام و ورود به حساب کاربری خود قادر خواهید بود لیست کتاب های خریداری شده را مشاهده فرمایید.


فهرست مطالب :


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
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
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
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
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
Extrinsic Aging Markedly Changes Epidermal Structure
Intrinsic Aging of the Epidermis
Intrinsic Aging Slows Epidermal Activity
Aging of the Hair Follicles Leads to Graying
Aging of the Dermis
The Dermis Is Thicker Than the Epidermis and Loosely Configured
Extrinsic Aging of the Dermis
Deep Wrinkles Result from Extrinsically Induced Changes
Intrinsic Aging in the Dermis
Modest Dermal Changes Occur with Intrinsic Aging
Dermal Glands Are Affected with Intrinsic Aging: Controversial Findings
Aging of the Hypodermis
The Hypodermis Is One of Several Fat Depots
The Hypodermis Fat Decreases with Age
Menopause and Skin
Menopause Adds to Intrinsic Aging
Consequences of Aging Skin
Many Functions of Skin Are in Danger of Decline
Barrier Function of Skin Is Reduced with Age
Dry Skin Is One Cause of Pruritus
Temperature Regulation Diminishes with Age
Vitamin D Production Declines with Age
Wound Healing Declines with Age
Increased Prevalence of Benign and Malignant Skin Cancers Result from Aged Skin
Aging Face Syndrome
Broad-Spectrum Sunscreens Reduce UVR Exposure
Retinoids as Antiaging Compounds
Oral and Topical Estrogen Reverse Aging of Skin After Menopause
Summary
Critical Thinking
Key Terms
Bibliography
Chapter 7: Aging of the Skeletal Muscle System
Orientation to Skeletal Muscle
Skeletal Muscles Provide Mobility, Strength, Independence, Metabolism, and Thermoregulation
Skeletal Muscles Consist of Bundles of Myocytes Innervated with a Motoneuron
Skeletal Muscle Senescent Phenotype
Sarcopenia Is the Age-related Loss of Muscle Mass
Rate of Loss of Muscle Mass with Age Is Highly Variable
Myocytes (Type II) Decrease in Number and Size; Fat Content Increases
Dynapenia Is an Age-Associated Loss of Muscle Strength
Rate of Loss of Muscle Strength Is Highly Variable
Molecular/Cellular Myocyte Changes with Age
Role of mt, Contractile Proteins, and Motoneurons
Aged Myocytes Show Reduced Protein Synthesis, Dysfunctional Mitochondria, and Alterations in Excitation-Contraction Coupling
Causative Factors
Many Factors Influence the Senescent Muscle Phenotype, Especially Physical Inactivity
Physical Inactivity
Inadequate Consumption of High-Quality Protein
Balance between Protein Anabolism and Catabolism Preserves Muscle Mass
Other Contributing Factors: Neurological, Hormonal, Stem Cell
Postulated Decline in Motoneuron Function
Reduced Levels of Hormones Impede Maintenance
Pluripotent Cells Fail to Differentiate
Consequences of Sarcopenia/Dynapenia
Dynapenia Contributes to Reduced Mobility, Falls, Hospitalization, and Frailty Syndrome
Frailty Syndrome Predicts Increased Risk of Morbidity and Death
Other Consequences: Metabolic, Endocrine, and Thermoregulation
Basal Metabolic Rate Declines Due in Part to Sarcopenia
Insulin Resistance
Thermoregulation Declines with Sarcopenia
Interventions
Exercises
Resistance Exercises Minimize Sarcopenia/Dynapenia
Effect of Exercise on Myocyte Biology
Chronic Aerobic Exercise Produces Muscle Efficiency, Muscle Endurance, and Many Other Benefits
Aerobic Exercise Effects on the Myocyte
Consumption of Adequate Amounts of Protein
Four-Pronged Exercise Program
Summary
Critical Thinking
Key Terms
Bibliography
Chapter 8: Aging of the Skeletal System
Overview
Bone Structure
Bone Is a Mix of Porous and Compact Bone
Modeling and Remodeling Processes
Bone Senses and Responds to Mechanical Strain
Modeling and Remodeling Establish Bone Strength
Bone Cells (Osteoblasts, Osteoclasts, and Osteocytes) with Different Functions Create the Density and Geometry of Bone (Figure 8.2)
Inevitable Loss of Bone
Changes in Mechanical Strain
With Age, Modeling Nearly Stops and Remodeling Is Stimulated by Strains Below the CSS
Bone Cell Functions Deteriorate with Age
Trabecular Structure Disappears and Cortical Structure Becomes More Like Trabecular Bone; Gender Differences
Large Epidemiological Studies Show Bone Loss in Men and Women, but Greater Loss in Women
Nonmechanical Factors: Hormones, Vitamin D, and Calcium
Loss of Estrogen Contributes Significantly to Bone Loss in Both Elderly Women and Men
Vitamin D and Calcium Deficiency Activate Parathyroid Hormone-Directed Bone Resorption
Growth Hormone Levels Decline with Age: A Change that May Influence Bone Function
Insulin Resistance May Exacerbate Bone Loss
Elevated Levels of Adrenal Steroids Enhance Bone Loss
Smoking Exerts Numerous Effects to Augment Bone Loss
Osteopenia; Osteoporosis
Extent of Bone Loss Defined by DXA and FRAX
Pharmacotherapy for Osteoporosis Reduces Fracture Risk
Nonpharmacological Interventions
Most Fractures Result from Falls: Ways to Prevent
Value of Exercise for Bone Loss Prevention Is Debated
Aging in Joints: Osteoarthritis
Osteoarthritis, an Inflammatory, Destructive, Painful Joint Disorder, Has Many Causes
Summary
Critical Thinking
Key Terms
Bibliography
Section 4: Internal Organ Systems: Cardiovascular, Pulmonary, Gastrointestinal, and Urinary Systems
Introduction
Chapter 9: Aging of the Cardiovascular System
Overview
Heart
Structure: Matrix, Cells, Valves
The Fibroblast is the Most Abundant Cell Type: Role in Matrix Turnover
Collagen Fibrosis Due to Aberrant Fibroblasts; Cross-Linkage Stiffens the Ventricles
Left Ventricular Hypertrophy Is Debated; Heart Appears to Remodel Its Shape
CMs Are Muscle Cells that Contract and Relax to Pump the Blood
Renewal of CMs Declines with Age; Senescent CMs Increase
Aging of Aortic and Mitral Valves May Progress to Valve Disease
Function: Diastolic Relaxation, Maximal Heart Rate in Exercise
Cardiac Cycle Includes Contraction (Systole) and Relaxation (Diastole)
Myocardial Relaxation Slows with Age: Problem with the Twist
Cardiac Response to Exercise Declines with Age, Primarily Due to Reduced Augmentation of HR
Control of Heart Rate
Preconditioning Benefit Lessens with Age
Vasculature
Wall Remodeling
Three Layers to the Vasculature
Matrix Deterioration Leads to Arterial Stiffness
Intimal-Medial Thickness Increases with Age
Vasculature Dysfunction
Endothelial Cell Becomes Dysfunctional; Loss of Vasodilator
Smooth Muscle Cells Regulate TSVR and Fill the Media
Medial Smooth Muscle Cells Migrate and Modulate
Baroreflex Sensitivity Decreases with Age
Age As Risk Factor for Cv Disease
Present and Future Interventions: Aerobic Exercise, Pharmacotherapy, and Caloric Restriction
Chronic Aerobic Exercise Minimizes the Effect of Age on CV Structure and Function
Pharmacological Therapy That Blocks Angiotensin Provides Some Benefits
Caloric Restriction in Animal Models Retards CV Aging
Summary
Critical Thinking
Key Terms
Bibliography
Chapter 10: Aging of the Pulmonary System
Overview
Impact of the Environment
Pulmonary Structure/Function
Essential Components are Thoracic Cavity, Airways, and Lung Tissue
Respiration Requires Mechanical Effort from Skeletal Muscles and Regulation from Nerves
External Respiration Allows Exchange of Oxygen and Carbon Dioxide
Age Changes in the Thoracic Cavity
Thoracic Cavity Remodels with Hyperkyphosis and Becomes Stiffer
Role of Cartilage Calcification in Loss of Chest Compliance
Dynapenia of Respiratory Muscles Reduces Pulmonary Function
Age Changes in the Airways
Bronchodilators Are Less Effective in Elderly
Airway Clearance Declines with Age
Age Changes in Lung Tissue
Dilated Alveolar Sacs and Decreased Number of Pulmonary Capillaries Limit Gas Diffusion
Carotid Body Chemoreceptors Deteriorate with Age but the Significance Is Unclear
Mechanics of Breathing: Rest and During Exercise
Pulmonary Function Tests Measure Physical Fitness
Forced Expiration/Inspiratory Volumes and Forced Vital Capacity Decrease with Age
Maximal Oxygen Consumption (VO2max) Wanes with Age
Consequences
Severe Stresses Challenge Reduced Pulmonary Function Reserve of the Elderly
Interventions for Healthy Aging
Exercise Training Improves Pulmonary Function
Summary
Critical Thinking
Key Terms
Bibliography
Chapter 11: Aging of the Gastrointestinal and Urinary Systems
Overview
Gastrointestinal Tract and Associated Organs: Role in Nutrient Absorption and Microbiota Regulation
GI Age Changes
Age Changes: Generally Minor with Exception of Reduced Colonic Transit Time
Gut Microbiota Exhibits Loss of Diversity
Diversity of the Microbiota Decreases with Age and Diet
Liver, Salivary Glands, and Pancreas Exhibit Modest Decline with Age
Age-Associated Disorders
A Common Anorectal Disorder Is Chronic Constipation
Malnutrition
Urinary System
Components: Kidneys, Ureters, Bladder, and Urethra
Age Changes in the Kidney
Structural Changes in Nephrons May Lead to Some Loss of Kidney Function
Inhibition of RAS Promotes Longevity
Age-Related Conditions/Issues: Dehydration, Medication Toxicity, Nocturia, and Urinary Incontinence
Dehydration is Common in the Elderly
Nocturia Affects Sleep but is Manageable
Potential for Drug Toxicity
Urinary Incontinence Has Many Causes
Summary
Critical Thinking
Key Terms
Bibliography
Section 5: Regulatory Organ Systems: Central Nervous System, Sensory, Endocrine, and Immune Systems
Introduction
Chapter 12: Aging of the Central Nervous System
Overview
The Central Nervous System (CNS), Responsible for Cognitive Behaviors, Motor Coordination, and Regulatory Activities, Consists of the Brain and the Spinal Cord
Many Issues Hamper Progress in Understanding CNS Aging
Neuroimaging Technology Stirs Debate on the Aging Brain
Aging of the Brain
The CNS Is Comprised of Billions of Neurons and Assisted by Several Other Cell Types
Structural Changes
The Major Anatomical Divisions of the Brain Are the Cerebrum, Cerebellum, and the Brain Stem
Age-Associated Brain Shrinkage Remains Controversial
Serotonin and Dopamine Pathways Experience Reduced Activity
Connectivity between Neurons May Decrease with Age
Auxiliary Cells Senesce and Fail to Maintain Homeostasis
Functional Changes
Cognitive tests seek to define the loss of brain function
Cognitive Behavior Exhibits Selective Decline with Age
There Is No Consensus On Time of Onset of Cognitive Decline
Brain Patterns from Neuroimaging Reveal Differences in Elderly Compared to Young Subjects
Cognitive Reserve/Maintenance Is Improved by Physical, Social, and Mental Enrichment
Epidemiological/Cohort Studies Show Cognitive Stimulation Associated with Higher Cognitive Test Scores
Mental Training through Brain Exercises Improves Some Aspects of Cognitive Behavior
Physical Exercise Is Associated with Improved Cognitive Function
Neuroplasticity
Summary
Critical Thinking
Key Terms
Bibliography
Chapter 13: Aging of the Sensory System
General Principles
Age Increases Threshold, Decreases Discrimination, and Slows Reaction Time
Sensory Organs: Age Changes in Structure/Function
Sense of Vision
Reception of Light Waves Modified by Age at Multiple Loci: Cornea, Iris, Lens, Retinal Receptors, Optic Nerve, and Visual Cortex
Presbyopia Is the Loss of Accommodation: Near Vision
Reduced Diameter of the Iris Causes Senile Miosis
Photoreceptors and Neuronal Tissue Degenerate Over Time
The Cornea Thickens and Changes Curvature, Resulting in Decreased Refraction
Audition: Hearing Function
Sound Waves Travel through the Three Chambers of the Ear
Presbycusis Is Age-Related Hearing Loss
Olfaction: The Sense of Smell
An Abundance of Olfactory Receptors Reside in the Mucosa of the Upper Nasal Cavity
Olfaction Atrophy Diminishes Sense of Smell and Depresses Sense of Taste
Gustation: Sense of Taste
Decreased Taste Perception by the Elderly May Relate to Changes Other than Aging of Taste Buds
Somatosensory Afferents: Multiple Modalities of Touch, Vibration, Pressure, Temperature, Pain, and Proprioception
Proprioception Decreases with Age; Elevates Risk of Falls
Cutaneous Mechanoreceptors: Sense of Touch, Vibration, and Pressure
Nociceptors Sense Pain from Chemical, Mechanical, and Temperature Modalities; Role in Aging Unknown
Thermoreceptors
Consequences and Compensation
Visual Deficits Minimized with Refractive Extra/Intraocular Lens, Common Sense Practices, and Possible Exercises
ARHL Receives Partial Compensation from Hearing Devices but the Best Treatment Is Prevention of Noise Abuse
Proprioception Acuity Improves with Training
Somatosensory Receptors Preserved with Toxic Chemical Avoidance
Summary
Critical Thinking
Key Terms
Bibliography
Chapter 14: Aging of the Endocrine System
Neuroendocrine System
Overview
Glands, Hormones, and Regulation
Components of the Neuroendocrine System: Hypothalamus, Pituitary, and Peripheral Glands
Hormone Levels Are Controlled by a Negative Feedback Inhibition Mechanism
Neuroendocrine Age Changes
Menstrual Cycle Is Regulated by the Hypothalamus-Pituitary-Ovarian Axis
Estrogen Stimulates Specific Intracellular and Membrane Receptors to Produce Diverse Effects
Menopause
Menopause is Unique to Humans
Dramatic Loss of Reproductive Function Due to Ovarian Failure
Effects of Menopause Include New Profile of Estrogens, Vasomotor Reactivity (Hot Flushes), and Atrophy of E-Dependent Tissues
Menopause Facilitates Bone Loss
Menopause Accelerates Aging of the Skin
Controversial Use of HT to Prevent Cardiovascular Disease, Cognitive Decline, and Sexual Dysfunction
Risk/Benefits of Hormone Therapy
Andropause
Male Reproduction Is Regulated by the Hypothalamic-Pituitary-Testes Axis
Modest Age-Related Changes in the Hypothalamic-Pituitary-Testis Axis
T Therapy Remains Controversial for Late-Onset Hypogonadism
Dysregulation of the Hypothalamic-Pituitary-Testicular Axis Is One of Many Reasons for Benign Prostatic Hypertrophy
Hypothalamic-Pituitary-Adrenal Axis
Dysregulation of the Adrenal Glands Yields an Altered Response to Stress with Detrimental Consequences
Circulating Levels of DHEAS and Androgens Decline with Age
Effects of Aging on Aldosterone Are Unknown
Hypothalamic-Pituitary-Thyroid Axis
Hypothalamic-Pituitary-Liver Axis
Effects of GH Weaken with Age Due to Less Circulating GH and Reduced Tissue Sensitivity
Endocrine Glands: Separate From Neuroendocrine Axis
Melatonin Levels Decline with Age in Large Part Due to Changes in the Eye
Parathyroid Gland Senses Changes in Ionized Calcium
Basal and Stimulated Parathyroid Hormone Levels Change with Age
Pancreas: Nutrient Regulator
Insulin Facilitates Uptake and Utilization of Sugar by Muscle/Fat Tissues and Enhances Storage in Liver
Prevalence of T2D Increases with Age
Age and Lifestyle Choices Influence Insulin Sensitivity
Neuroendocrine Theory of Aging
Summary
Critical Thinking
Key Terms
Bibliography
Chapter 15: Aging of the Immune System
Overview
Barriers and Related Mechanisms
Components
Effects of Age
Reduced Barrier Quality Permits Pathogen Entry
Innate Immune System
Components; Role in Immunity
Innate Immune System Provides the First Line of Cellular and Humoral Defense Against Pathogens
Pattern Recognition Receptors/Phagocytosis Are Essential for Host Defense
Effects of Age
Signaling and Phagocytosis Decline with Age
Adaptive Immunity
T Cell; B Cell; Role in Immunity
Two Adaptive Immune Cell Types Are the T Cell and the B Cell
T Cells Perform Cell-Mediated Immunity: Helper, Cytotoxic, and Regulatory
B Cells Mediate Humoral Immunity by Production of Antibodies
Numerous Cytokines Facilitate Immunity
Immunosenescence
Thymus Gland Is One Determinant of T Cell Behavior
Immunosenescence Is the Gradual Dysregulation of Immune Function with Age
Consequences of Immunosenescence
Increased Prevalence of Infectious Diseases Due in Part to Immunosenescence
Incidence of Most Cancers Increases with Age
Response of the Elderly to Vaccines Is Suboptimal
Delayed Hypersensitivity Response Is Diminished
Presence of Autoantibodies Increases with Age
Reemergence of Latent Virus Is Common in the Elderly
Immunosenescence Is Associated with Chronic Inflammation
Preservation Strategies
Modification of Immunosenescence Is Possible in Animal Models
Immunological Theory of Aging
Summary
Critical Thinking
Key Terms
Bibliography
Index
End User License Agreement




پست ها تصادفی