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Book Details
Abstract
This invaluable book presents a concise discussion on the most important topics of ophthalmology — mechanism of ophthalmic diseases, imaging techniques used for diagnosis, novel therapies and drug delivery systems. It also covers current knowledge about anti-VEGF therapies that revolutionized neovascular AMD treatment, anti-inflammatory and dry eye treatment, as well as nanoparticles use of drug delivery.Written by experts in ophthalmology, this unique volume provides a comprehensive overview of the latest research in the field. This is an essential reading that will provide up-to-date reference to practicing physicians and current knowledge to residents and students.
Table of Contents
| Section Title | Page | Action | Price |
|---|---|---|---|
| Contents | v | ||
| Introduction | 1 | ||
| Chapter 1: Pathology and Mechanism of Eye Diseases | 3 | ||
| 1. Introduction | 3 | ||
| 2. The Eye | 3 | ||
| 2.1. Anterior eye | 4 | ||
| 2.2. Posterior eye | 4 | ||
| 2.2.1. The retina | 5 | ||
| 2.2.2. The photoreceptor cells | 5 | ||
| 3. The Phototranduction Cascade | 7 | ||
| 3.1. Activation of the phototransduction cascade | 8 | ||
| 3.2. Deactivation of the phototransduction cascade | 8 | ||
| 3.3. Adaptation of the phototransduction cascade | 9 | ||
| 4. The Visual Cycle | 10 | ||
| 5. Pathology of Eye Diseases | 10 | ||
| 5.1. Leber congenital amaurosis | 11 | ||
| 5.2. Retinitis pigmentosa | 11 | ||
| 6. Mechanisms of Eye Diseases | 12 | ||
| 6.1. Rod photoreceptor cell metabolism | 13 | ||
| 6.2. The complement pathway and the alternative pathway | 14 | ||
| 6.3. Lipofuscin accumulation | 15 | ||
| 6.4. Non-autonomous cone cell death | 16 | ||
| 6.5. Calcium-dependent apoptosis | 16 | ||
| 6.6. The unfolded protein response | 17 | ||
| 6.7. Ciliary defects | 19 | ||
| 6.8. Intracellular trafficking defects | 20 | ||
| 6.9. Structural defects | 21 | ||
| 6.10. Processing of messenger RNA and transcriptional defects | 22 | ||
| 7. Summary | 22 | ||
| 8. References | 23 | ||
| Chapter 2: Ophthalmic Imaging | 33 | ||
| 1. Introduction | 33 | ||
| 2. Fluorescein Angiography | 34 | ||
| 2.1. Principles of fluorescein angiography | 34 | ||
| 2.2. Interpretation of fluorescein angiography | 35 | ||
| 2.2.1. Age-related macular degeneration (AMD) | 39 | ||
| 3. Indocyanine Green Angiography | 41 | ||
| 3.1. Principles of indocyanine green angiography | 41 | ||
| 3.2. Interpretation of indocyanine green angiography | 42 | ||
| 3.2.1. Polypoidal choroidal vasculopathy (PCV) | 43 | ||
| 3.2.2. Retinal angiomatous proliferation (RAP) | 43 | ||
| 3.2.3. Central serous chorioretinopathy | 44 | ||
| 3.2.4. Inflammatory eye diseases | 44 | ||
| 4. Optical Coherence Tomography | 45 | ||
| 4.1. Principles of optical coherence tomography | 45 | ||
| 4.2. Choroidal imaging using OCT | 48 | ||
| 5. Fundus Autofluorescence | 49 | ||
| 6. Widefield Imaging | 52 | ||
| 6.1. Pseudocolor fundus images | 53 | ||
| 6.2. Widefield fluorescein angiography | 54 | ||
| 6.3. Widefield fundus autofluorescence | 55 | ||
| 7. Conclusion | 56 | ||
| 8. References | 56 | ||
| Chapter 3: Pharmacogenomics of Response to Anti-VEGF Therapy in Exudative Age-Related Macular Degeneration | 63 | ||
| 1. Introduction | 63 | ||
| 2. Results | 65 | ||
| 2.1. Pharmacogenetics for genes associated with AMD in the comparison of AMD treatments trials (CATT) | 65 | ||
| 2.1.1 Conclusions | 73 | ||
| 2.2. Pharmacogenetics of complement factor H (Y402H) and treatment of exudative AMD with ranibizumab | 73 | ||
| 2.2.1. Conclusions | 74 | ||
| 2.3. Complement factor H Y402H gene polymorphism and response to intravitreal bevacizumab in exudative AMD | 74 | ||
| 2.3.1. Conclusions | 75 | ||
| 2.4. Association of complement factor H and LOC387715 genotypes with response of exudative AMD to intravitreal bevacizumab | 75 | ||
| 2.4.1. Conclusions | 75 | ||
| 2.5. Involvement of genetic factors in the response to a variable-dosing ranibizumab treatment regimen for AMD | 76 | ||
| 2.5.1. Conclusions | 76 | ||
| 2.6. Association between high-risk disease loci and response to anti-vascular endothelial growth factor treatment for wet AMD | 77 | ||
| 2.6.1. Conclusions | 77 | ||
| 2.7. CFH, VEGF and HTRA1 promoter genotype may influence the response to intravitreal ranibizumab for neovascular AMD | 78 | ||
| 2.7.1. Conclusions | 78 | ||
| 2.8. Association of genetic polymorphisms with response to bevacizumab for neovascular AMD in the Chinese population | 78 | ||
| 2.8.1. Conclusion | 79 | ||
| 2.9. VEGF-A polymorphisms predict short-term functional response to intravitreal ranibizumab in exudative AMD | 79 | ||
| 2.9.1. Conclusion | 80 | ||
| 2.10. The influence of genetics on response to treatment with ranibizumab (Lucentis) for AMD: the Lucentis genotype study | 80 | ||
| 2.10.1. Conclusion | 81 | ||
| 2.11. Genetic influences on the outcome of anti-vascular endothelial growth factor treatment in neovascular AMD | 81 | ||
| 2.11.1. Conclusion | 82 | ||
| 2.12. Genetic association with response to intravitreal ranibizumab in patients with neovascular AMD | 82 | ||
| 2.12.1. Conclusion | 83 | ||
| 2.13. Variants in the VEGF-A gene and treatment outcome after anti-VEGF treatment for neovascular AMD | 83 | ||
| 2.13.1. Conclusion | 84 | ||
| 2.14. Common variant in VEGFA and response to anti-VEFF therapy for neovascular AMD | 84 | ||
| 2.14.1. Conclusion | 85 | ||
| 2.15. Variants in the APOE gene are associated with improved outcome after anti-VEGF treatment for neovascular AMD | 85 | ||
| 2.15.1. Conclusion | 85 | ||
| 2.16. Cumulative effect of risk alleles in CFH, ARMS2, and VEGF-A on the response to ranibizumab treatment in AMD | 86 | ||
| 2.16.1. Conclusion | 86 | ||
| 3. Discussion | 86 | ||
| 4. References | 91 | ||
| Chapter 4: Dry Eye Therapy | 97 | ||
| 1. Introduction | 97 | ||
| 2. Background of DED | 98 | ||
| 2.1. Definition of DED | 98 | ||
| 2.2. Types of DED | 99 | ||
| 2.3. Pathophysiology of DED | 100 | ||
| 3. Potential Targets for DED | 102 | ||
| 3.1. Tear deficiency or increased evaporation | 102 | ||
| 3.2. Inflammation | 103 | ||
| 3.3. Mucin secretion | 104 | ||
| 3.4. Autologous serum tears | 104 | ||
| 3.5. Hormonal mechanisms | 105 | ||
| 4. Current Status of Ocular Drugs and Therapies | 105 | ||
| 4.1. Stepwise approach from dry eye workshop report | 106 | ||
| 4.2. Ocular lubricants | 106 | ||
| 4.3. Anti-inflammatory drugs | 108 | ||
| 4.3.1. Cyclosporine A ( Restasis®) | 108 | ||
| 4.3.2. Corticosteroids | 110 | ||
| 4.4. Dietary supplementation | 111 | ||
| 4.5. Other ocular drugs and therapies for dry eye disease | 112 | ||
| 5. Ongoing Clinical Trials and Potential Future Therapies (Table 4) | 113 | ||
| 5.1. Mucin secretagogues | 113 | ||
| 5.1.1. Rebamipide | 113 | ||
| 5.1.2 Diquafosol tetrasodium | 113 | ||
| 5.2. Ocular lubricants | 116 | ||
| 5.2.1 Sodium hyaluronate | 116 | ||
| 5.3. Anti-inflammatory antibiotics | 116 | ||
| 5.4. Autologous | 117 | ||
| 5.4.1. Serum tears | 117 | ||
| 5.4.2. Autologous plasma | 118 | ||
| 5.5. Hormonal therapy | 119 | ||
| 5.6. Anti-inflammatory drugs and immunomodulators | 120 | ||
| 5.6.1. Cyclokat (Nova22007) | 120 | ||
| 5.6.2 Resolvin E1 (RvE1) | 121 | ||
| 5.6.3. Lifitegrast (SAR 1118) | 121 | ||
| 5.6.4. EGP-437 | 122 | ||
| 5.6.5. CF101 | 123 | ||
| 5.6.6. Topical tofacitinib (CP-690,550) | 124 | ||
| 5.6.7. Thymosin β4 (RGN-259) | 124 | ||
| 5.6.8. Topical tacrolimus | 125 | ||
| 5.7. Biologics | 125 | ||
| 5.7.1. Topical infliximab | 125 | ||
| 5.7.2. IL-1 Receptor antagonist | 126 | ||
| 5.8. MIM-D3 | 126 | ||
| 6. Conclusions | 127 | ||
| 7. References | 127 | ||
| Chapter 5: Ocular Inflammation Therapy | 145 | ||
| 1. Introduction | 145 | ||
| 2. Ocular Inflammatory Diseases | 146 | ||
| 3. Inflammatory Casacade Overview | 148 | ||
| 4. Ocular Drugs and Delivery Systems in Ocular Inflammation | 148 | ||
| 4.1. Nonsteroidal anti-inflammatory drugs | 148 | ||
| 4.1.1. Topical non-steroidal anti-inflammatory drugs | 149 | ||
| 4.1.2. Systemic non-steroidal anti-inflammatory drugs | 150 | ||
| 4.2. Glucocorticosteroids | 150 | ||
| 4.2.1. Topical corticosteroids | 152 | ||
| 4.2.2. Systemic corticosteroids | 154 | ||
| 4.2.3. Periocular corticosteroids | 155 | ||
| 4.2.4. Intravitreal injections of corticosteroids | 156 | ||
| 4.2.5. Intravitreal implants | 157 | ||
| 4.2.5.1. Retisert® implant | 157 | ||
| 4.2.5.2. Ozurdex® | 158 | ||
| 4.2.5.3. Other implants | 160 | ||
| 4.3. Immunomodulatory therapy | 160 | ||
| 4.3.1. Chemotherapeutic agents | 162 | ||
| 4.3.1.1. Antimetabolites | 162 | ||
| 4.3.1.2. Alkylating agents | 164 | ||
| 4.3.1.3. Signal transduction inhibitors | 166 | ||
| 4.3.2. Biologic response modifiers | 169 | ||
| 4.3.2.1. TNF-a inhibitors | 169 | ||
| 4.3.2.2. IL-2 receptor inhibitors | 173 | ||
| 4.3.2.3. Rituximab | 173 | ||
| 4.3.2.4. Abatacept | 173 | ||
| 4.3.2.5. IFN | 174 | ||
| 5. Ongoing Clinical Trials and Potential Future Therapeutic Approaches | 177 | ||
| 6. Conclusion | 182 | ||
| 7. References | 182 | ||
| Chapter 6: Nanoparticles for Ocular Drug Delivery | 197 | ||
| 1. Introduction | 197 | ||
| 2. Liposomes | 200 | ||
| 3. Polymeric Nanoparticles | 204 | ||
| 4. Dendrimers | 207 | ||
| 5. Inorganic Nanoparticles | 212 | ||
| 6. Outlook | 216 | ||
| 7. References | 216 | ||
| Index | 225 |