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Basic biology and clinical aspects of inflammation / edited by Robert F. Diegelmann & Charles E. Chalfant, Department of Biochemistry and Molecular Biology, Virginia Commonwealth University Medical Center, 1101 East Marshall Street, Sanger Hall, Room 2-007, Richmond Virginia, 23298-0614, USA.
- Format:
- Book
- Series:
- Frontiers in Inflammation
- Frontiers in inflammation ; volume 1
- Language:
- English
- Subjects (All):
- Inflammation.
- Biology.
- Physical Description:
- 1 online resource (494 p.)
- Edition:
- 1st ed.
- Place of Publication:
- Sharjah, United Arab Emirates : Bentham Science, [2016]
- Summary:
- Basic Biology and Clinical Aspects of Inflammation provides information about the critical cells and biochemical mediators involved in the complex process of inflammation. Readers are introduced to the basic scientific background on the subject, after which the book progresses towards translational research in clinical settings. Topics covered in this volume include, the modulation of inflammation during normal and chronic wound healing, altered metabolism during inflammation processes, the effect of ageing on inflammatory processes, as well as details about the underlying molecular processes behind specific clinical pathologies that are driven by excessive inflammation in the body (allergic reactions, type 2 diabetes, cardiac and vascular disease, arthritis, periodontal disease, inflammatory bowel disease and neuroinflammation). The volume also provides the latest information on pharmacotherapy for inflammation and interesting contributions towards the mathematical modeling and network analysis of inflammation. Basic Biology and Clinical Aspects of Inflammation features contributions from by a distinguished group of international researchers and clinicians highly recognized for their specific expertise in the field of inflammation. The information presented in this reference is useful to academics, medical professionals, health care regulators and pharmaceutical scientists.
- Contents:
- Intro
- Contents
- Foreword
- Preface
- List Of Contributors
- Introduction To Basic Biology And Clinical Aspects Of Inflammation
- Introduction
- Chapter 2
- Chapter 3
- Chapter 4
- Chapter 5
- Chapter 6
- Chapter 7
- Chapter 8
- Chapter 9
- Chapter 10
- Chapter 11
- Chapter 12
- Chapter 13
- Chapter 14
- Chapter 15
- Chapter 16
- Conflict Of Interest
- Acknowledgements
- References
- Cell Mediators Of Acute Inflammation
- Toll-Like Receptors
- Mast Cells
- Triggers Of Mast Cell Degranulation
- Mediators Released By Mast Cells
- Neutrophils
- Macrophages
- Macrophage Function And Phenotypes
- Adaptive Immune Cells In Acute Inflammation
- Gamma Delta T Cells
- Th17 T Lymphocytes
- Summary
- Biochemical Mediators Of Inflammation And Resolution
- Biosynthesis Of Lipid Mediators
- Phospholipase A2
- Group Iva Cytosolic Phospholipase A2 (Cpla2α)
- Secretory Phospholipase A2 (Spla2)
- Group Via Phospholipase A2 (Ipla2β)
- Eicosanoid Production Pathways
- Cyclooxygenase (Cox) Pathway
- Lipoxygenase Pathway
- Cytochrome P450 Pathway
- Pro-Inflammatory Lipid Mediators
- Pro-Resolution Lipid Mediators
- Biosyntheis Of Cytokines And Chemokines
- Pro-Inflammatory Cytokines And Chemokines
- Pro-Resolution Cytokines And Chemokines
- Conclusion
- Wound Healing And Dermatologic Aspects Of Inflammation
- Normal Dermatological Response In Wound Healing
- The Inflammatory Phase Of Wound Healing
- Monocytes And Macrophages
- T Lymphocytes
- The Proliferative Phase
- The Remodeling Or Maturation Phase
- Why Don'T Chronic Wounds Heal?
- Common Wound Healing Problems And Inflammation
- Diabetes
- Venous Insufficiency.
- Aging And Wound Repair
- Pyoderma Gangrenosum
- Metabolic Regulation Of Inflammation
- Inflammation As A Link Between Obesity And Metabolic Syndrome
- Classic Inflammation Vs. Metabolic Inflammation
- Molecular Pathways That Link Inflammation And Insulin Resistance
- Resident And Infiltrated Immune Cells In Adipose Tissue
- Lymphocytes
- Mast Cells And Eosinophils
- Therapeutic Opportunities For Metabolic Diseases
- Anti-Inflammation Therapeutics
- Reverse The Imbalance Of Excess Caloric Intake And Energy Expenditure: A Second Thought
- Aging And Inflammation
- Immunosenescence
- Inflammaging
- Biological And Molecular Basis For Aging-Associated Chronic Inflammation
- Changes In The Basal Levels Of Systemic Inflammatory Mediators In Human And Rodents During Aging
- Molecular And Cellular Mechanisms For Aging-Associated Induction Of Cytokine Production In The Absence Of Infection
- Aging-Associated Changes In The Homeostasis Of Bioactive Lipid Metabolites
- The Concept Of Cellular Hyperresponsiveness To Pro-Inflammatory Agonists
- Dietary And Pharmacological Interventions That Suppress Aging-Associated Rise In Inflammatory Markers
- Caloric Restriction
- Other Dietary Approaches That Attenuate Inflammaging
- Exercise
- Concluding Remarks
- Allergic Inflammation
- Cells Involved In Allergic Inflammation
- B Lymphocytes
- Eosinophils
- Basophils
- Innate Lymphoid Type 2 Cells
- Innate Cytokines Involved In Th2 Immune Bias
- Interleukin-25
- Interleukin-33
- Thymic Stromal Lymphopoietin.
- Pharmacologic Modulation Of Innate Cytokines Important In Th2 Immunity
- Adaptive Cytokines Involved In Th2 Immune Bias
- Interleukin-4
- Interleukin-13
- Interleukin-5
- Interleukin-9
- Interleukin-3
- Granulocyte-Monocyte Colony Stimulating Factor
- Interleukin-10
- Pharmacologic Modulation Of Adaptive Cytokines Important In Th2 Immunity
- Inflammation In Type 2 Diabetes
- Inflammatory Mechanisms In The Pathogenesis Of Diabetes
- Inflammatory Mechanisms Of Beta Cell Dysfunction/Failure In Diabetes
- Inflammation In Adipose Tissue And Insulin Resistance
- Tissue Hypoxia
- Adipocyte Cell Death
- Nf-Kb And Jnk Pathways
- M2 Vs M1 Macrophages Phenotype
- Inflammation In The Development Of Diabetes Complications
- Age/Rage Signalling And Inflammation In Diabetes
- Oxidative Stress And Inflammation
- Inflammation In Specific Diabetes Complications
- Diabetic Nephropathy
- Diabetic Neuropathy
- Diabetic Foot/Charcot
- The Vascular Tree And Heart With Relationship To Inflammation
- Endothelial Cell Biology (The Link Between Blood And Tissue)
- Coagulation/Inflammation Interface
- Microvascular Architecture
- Hemoglobin/Inflammation
- Platelet Ec Interactions
- Chemokines
- Atherosclerosis- Chronic Vascular Inflammation
- Vasculitis
- Rheumatoid And Degenerative Arthritis-Associated Inflammation
- Anatomical And Physiological Background
- Defining The Joint
- Joint Capsule, Synovium And Synovial Fluid
- Articular Cartilage
- Terminological Notes On Inflammation And Arthritis Reflecting Elusive Pathogenesis
- Clinical Presentations
- Epidemiology.
- Etiopathogenesis Of Rheumatoid And Degenerative Arthritis
- Overall Pathophysiology
- Contribution Of The Genetic Background
- Influence Of Epigenetic Modifications
- Features Predominant To Rheumatoid Arthritis Pathology
- Adaptive Immunological Events
- B-Lymphocytes And Autoantibody Production
- T-Cell Activation
- Activation Of Synovial Fibroblasts
- Effects Deriving From Innate Immunity
- Intracellular Signaling Via Toll-Like Receptors
- Complement Activation
- Important Common Pro-Inflammatory Mediators Of Arthritic Inflammation
- Diagnostic Paths In Clinical Disease Management
- Current Therapeutic Procedures, Actual Limitations And Potential Future Options
- Concluding Remarks And Future Perspectives
- Inflammation In Oral Diseases
- A. The Unique Niche Of The Oral Cavity
- B. Microbial Environment
- C. Oral Mucosal Inflammation And Immune Responses
- D. Sublingual Immunotherapy
- E. Mediators Of Oral Inflammation
- Inflammation In Oral Health And Diseases
- A. Wound Healing
- B. Autoimmune Mucosal Diseases
- C. Dental Caries
- D. Periodontal Diseases
- E. Reactive Oral Lesions
- F. Infectious Diseases
- G. Malignancies
- Anti-Inflammatory Strategies In Oral Diseases
- A. Mechanical
- B. Biochemical
- C. Innovative New Therapies
- Intestinal Inflammation And Inflammatory Bowel Disease
- Lessons Learned From Linkage Analysis And Gwas
- Alterations In The Gut Microbiome In Ibd
- Dysbiosis Contributes To Intestinal Inflammation
- Altered Immune Responses To Microbial Products
- Altered Intestinal Barrier Function And Permeability
- Alterations In The Adaptive Immune Response
- References.
- Neuroinflammation
- Central Nervous System Innate Immune Response
- Microglia
- Surveying (Resting) Microglia
- Activated Microglia
- Astrocyte
- Activating Signals
- Toll-Like Receptors (Tlr)
- Retinoic Acid-Inducible Gene 1 (Rig-I) And Rig-I-Like Receptors
- Inflammasome Sensors: Nod-Like Receptors
- Purinergic Receptors
- Inhibitory Signals
- Cx3Cl1/Cx3Cr1
- Cd200/Cd200R
- Effector Mechanisms
- Nicotinamide Adenine Dinucleotide Phosphate (Nadph) Oxidase Complex
- Nitric Oxide Synthase 2
- Inflammasome/Interleukin-1β
- Interleukin-6
- Tnf
- Central Nervous System Adaptive Immune Response/Autoimmunity
- Cns Immune Privilege
- Cns Trafficking/Cell Recruitment
- Integrins
- Cell-Mediated Cns Inflammation
- Encephalitogenic Cd4+ T Lymphocyte: Th1 Versus Th17
- Humoral Mediated Cns Inflammation
- Auto-Reactive Antibodies Against Cns Antigens
- Perspectives
- Pharmacotherapy For Inflammatory Processes
- Introduction And Scope Of The Chapter
- The Spectrum Of Currently Used Anti-Inflammatory Drugs: Their Utility In Identifying The 'Power Brokers' Of Inflammatory Disease
- Drugs Targeting The Release And Effects Of Histamine
- The Eicosanoids: Non-Steroidal Anti-Inflammatory Drugs (Nsaids) And Other Approaches To Control Their Activity
- Prostanoids And Their Regulation
- Therapeutic Exploitation Of Prostanoids And Their Receptors
- Leukotrienes And Their Regulation
- Platelet-Activating Factor (Paf): A Potent Lipid-Derived Mediator That Has So Far Failed To Deliver As A Drug Target
- Non-Steroidal Anti-Inflammatory Drugs (Nsaids)
- Conventional Nsaids
- Cox-2 Selective Nsaids (Coxibs)
- Glucocorticosteroids
- Dose And Indication Limiting Adverse Effects Of Glucocorticoids.
- Disease-Modifying Anti-Rheumatic Drugs (Dmards)- An Effective 'Hodgepodge' Of Compounds.
- Notes:
- Description based upon print version of record.
- Description based on online resource; title from PDF title page (ebrary, viewed May 2, 2017).
- ISBN:
- 9781681082271
- 1681082276
- OCLC:
- 948924410
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