Download e-book for iPad: Anti-Inflammatory Drugs by R. J. Gryglewski (auth.), Dr. John R. Vane, Dr. Sergio H.

By R. J. Gryglewski (auth.), Dr. John R. Vane, Dr. Sergio H. Ferreira (eds.)

ISBN-10: 3642668917

ISBN-13: 9783642668913

ISBN-10: 3642668933

ISBN-13: 9783642668937

Screening and Toxicity of anti inflammatory Drugs.- 19 Screening and review of the efficiency of anti inflammatory medications in vitro.- A. Introduction.- B. interplay With Non-Enzymic Proteins.- I. Binding to Plasma Proteins.- 1. Displacement Reactions.- 2. Disulphide Interchange Reactions.- three. defense opposed to Protein Denaturation.- four. Fibrinolytic Activity.- II. interplay With organic Membranes.- 1. results on Erythrocyte Membrane.- 2. results on Lysosomal Membrane.- three. Cytotoxic Properties.- four. results on Leucocyte Migration.- C. interplay With Enzymic Proteins.- I. normal Considerations.- II. interplay With Enzymes fascinated about Carbohydrate, Protein, and Nucleic Acid Metabolism.- 1. Carbohydrate, Protein, and Amino Acid Metabolism.- 2. Nucleic Acid and Nucleotide Metabolism.- III. Inhibition of Prostaglandin Synthetase.- 1. Prostaglandin Synthetase System.- 2. Assay of Prostaglandin Synthetase Activity.- three. Prostaglandin Synthetase Inhibitors.- four. Inhibition of Platelet Aggregation.- five. results on tender Muscle.- D. Conclusions.- References.- 20 Inhibition of Erythema and native Hyperthermia.- A. Introduction.- B. Ultraviolet (UV) mild and the Erythematous Response.- C. Instrumentation.- I. mild resources for Induction of Erythema.- II. dimension of Erythema and native Hyperthermia.- 1. Erythema.- 2. dermis Temperature.- D. Procedures.- I. Erythema.- 1. UV-Induced.- 2. Thurfyl Nicotinate-Induced.- three. Miscellaneous techniques for generating Erythema.- II. neighborhood Hyperthermia.- 1. neighborhood Hyperthermia in Paws of Rats Injected With Irritants.- 2. neighborhood Hyperthermia in UV-Irradiated Skin.- E. Inhibition of Erythema and native Hyperthermia.- I. UV-Induced Erythema.- 1. Systemic management of Drugs.- 2. Topically or Intradermally.- II. Tetrahydrofurfuryl Nicotinate (THFN) Erythema.- III. different Erythemas.- IV. neighborhood Hyperthermia.- F. Conclusion.- References.- 21 Oedema and elevated Vascular Permeability.- A. common rules of Assays.- I. Statistical concerns in Assay Work.- 1. dating of Dose to Effect.- 2. Definition of ED50.- three. self belief Limits.- four. Coefficent of Variation.- five. The g Value.- 6. The Lambda price, ?.- 7. blunders of varieties I and II.- B. tools for generating and Measuring Oedema and elevated Vascular Permeability.- I. Oedemas of the Rat’s Paw.- 1. Measurement.- 2. brokers inflicting Paw Oedema; features of Oedemas because of numerous Agents.- II. elevated Vascular Permeability.- III. Oedema within the Pleural Space.- C. Conclusion.- References.- 22 temporary Drug keep an eye on of Crystal-Induced Inflammation.- A. historic Aspects.- B. Mechanism of Crystal-Induced Inflammation.- I. Phagocytosis.- II. Membranolysis.- III. Inflammatory Mediators.- IV. Chemotactic Factors.- C. Experimental Models.- I. Animal.- II. Man.- D. treatment of Acute assaults of Gout and Pseudogout.- I. Gout.- II. Pseudogout.- E. Summary.- References.- 23 Experimental types of Arthritis in Animals as Screening exams for medicines to regard Arthritis in Man.- A. Introduction.- B. merits and drawbacks of types of Arthritis—Comparison With Acute Models.- C. Adjuvant-Induced Arthritis.- I. First commentary. First Use as a monitor for anti inflammatory/ Antirheumatic Drugs.- II. Production.- 1. Adjuvant.- 2. direction of Injection.- three. Species edition and pressure Variation.- four. Time process the Disease.- III. Aetiology.- 1. function of Lymphatic System.- 2. Immunological Mechanisms.- three. Histology.- four. Lysosomal Enzymes.- IV. Assessment.- 1. actual Assessment—Gross Measurements.- 2. Physiological/Functional Parameters.- three. Biochemical Parameters.- four. interval of Dosing of Compounds.- V. impression of Drugs.- 1. Non-Steroid anti inflammatory Drugs.- 2. Steroid anti inflammatory Drugs.- three. Gold, Chloroquine, and Penicillamine.- four. Immunosuppressant Drugs.- five. Antilymphocytic Serum, Antigens.- 6. Non-Specific Inhibition.- 7. The impression of Adjuvant Arthritis on Drugs.- D. Arthritis Produced via Intra-Articular Injection of Antigens and Antibodies.- E. Arthritis Produced by means of Intra-Articular Injection of Lysosome Labilisers.- F. Arthritis caused by way of Infectious Agents.- E. Conclusions.- References.- 24 Antagonism of Bradykinin Bronchoconstriction via anti inflammatory Drugs.- A. Introduction.- B. construction of Kinins and different Mediators of Anaphylaxis within the Lungs.- I. In vitro.- II. In vivo.- III. unencumber of Catecholamines in vivo.- C. motion of Bradykinin on Lung Function.- I. Bronchial gentle Muscle in vitro and in vivo.- II. Pulmonary Circulation.- D. liberate of Prostaglandins and Precursors From Lungs by way of Bradykinin.- E. activities of Prostaglandins within the Lungs.- I. Bronchial tender Muscle.- F. interplay of Bradykinin With Prostaglandins within the Lungs.- I. As a Mediator.- II. As a Potentiator.- III. As a Mediator of Vascular Leakage.- G. Metabolism of Kinins within the Pulmonary Circulation.- H. Inhibition of Bronchoconstriction by way of anti inflammatory Acids.- I. In vivo and in vitro Studies.- II. comparability With different Bronchoconstrictor Agents.- I. attainable activities and Interactions of Kinins and Prostaglandins in Asthma.- J. precis and Conclusions.- References.- 25 Interference of anti inflammatory medicines With Hypotension.- A. Interference of Non-Steroidal anti inflammatory medicines With Hypotensive results of strength Inflammatory Mediators.- I. Kinin Peptides.- II. Prostaglandins.- B. Interference by means of Non-Steroidal anti inflammatory medications With the Hypotensive results of brokers That unencumber power Inflammatory Mediators.- I. Proteolytic Enzymes.- 1. Kininogenases.- 2. Thrombin.- three. different Proteolytic Enzymes.- II. Inhibition of Hypotension because of ingredients That turn on Plasma Kininogenase.- 1. Carrageenin.- 2. different Activators of Plasma Kininogenase.- III. Phospholipase A2.- C. Interference of anti inflammatory medicinal drugs With Hypotensive Responses to Lipid Derivatives.- I. results of Arachidonic Acid on Arterial Blood Pressure.- 1. Mechanism of motion of Arachidonic Acid on Blood Pressure.- II. results of Fatty Acids except Prostaglandin Precursors.- III. gradual Reacting Substance C.- 1. Mechanism of motion of sluggish Reacting Substance C.- D. Interference of Non-Steroidal anti inflammatory brokers With results of Miscellaneous Agents.- I. Adenosine Nucleotides.- II. Collagen.- III. Anaphylatoxin.- IV. Depressor energetic Substance (DAS).- V. Platelet Clumping Substance.- VI. Barium Sulphate and different Particulate Materials.- E. Interference of Non-Steroidal anti inflammatory brokers With Hypotension in Endotoxin Shock.- I. Dogs.- II. Cats.- III. different Animal Species.- F. Mechanism of motion of Hypotensive brokers vulnerable to Inhibition by way of Non-Steroid anti inflammatory Drugs.- I. Structure-Activity Correlations.- 1. Thiol and Anti-Oxidant Compounds.- II. Stereospecificity.- III. Mechanism of motion of Hypotensive brokers topic to Inhibition via Non-Steroidal anti inflammatory Drugs.- 1. Bradykinin.- 2. Collagen.- three. Carrageenin.- four. Adenosine Nucleotides.- IV. Conclusions.- 1. Relevance of Hypotensive Responses to irritation and to review of Inflammatory Events.- 2. Multisequential Activation and Acute Hypotensive Responses: customers of Research.- References.- 26 Antagonism of ache and Hyperalgesia.- A. Introduction.- I. Terminology.- II. historic creation to Analgesic trying out in Hyperalgesic Animals.- B. Non-Hyperalgesic gentle Analgesic Assays.- I. Stretching Tests.- C. review of gentle Analgesia in Humans.- I. medical Avaluation of gentle Analgesic Agents.- D. Conclusion.- References.- 27 Inhibition of phone Migration in vivo and Granuloma Formation.- A. common Introduction.- I. Mechanisms of telephone Migration.- II. The series of mobilephone Migration.- III. destiny of Emigrated Cells.- 1. Polymorphs.- 2. Mononuclear Cells.- IV. Granuloma Formation and Evolution.- B. versions for Leucocyte Emigration in vivo.- I. Generalities.- II. Histological Method.- III. phone assortment From Cavities.- 1. average Cavities.- 2. synthetic Cavities.- IV. cellphone assortment From Early Granulomata.- V. phone Labelling.- C. versions for Granuloma Formation in vivo.- I. Cotton-Pellet Granuloma.- II. Granuloma Pouch.- III. Carrageenin Granuloma.- IV. Plastic Ring Granuloma.- V. filter out Paper Granuloma.- D. Inhibition of mobile Migration in vivo.- I. Steroids.- 1. Neutrophils.- 2. Mononuclear Cells.- II. Non-Steroid anti inflammatory Drugs.- III. Immunosuppressive Agents.- IV. Endogenous Substances.- E. Inhibition of Granuloma Formation.- I. Steroid anti inflammatory Drugs.- II. Non-Steroid anti inflammatory Drugs.- III. Immunosuppressive Agents.- IV. Endogenous Substances.- F. Conclusions.- References.- 28 Inhibition of Fever.- A. Introduction.- B. Pathogenesis of Fever.- I. Exogenous and Endogenous Pyrogen.- II. website of motion of Pyrogens.- III. Mechanism of motion of Pyrogens.- 1. switch in Set-Point or Gain?.- 2. function of Prostaglandins.- three. function of Monoamines and Cyclic-AMP.- four. Ionic Mechanisms in Fever.- C. Antipyretics.- I. attainable websites of motion of Antipyretics.- 1. Inactivation of Bacterial Pyrogen (Site I).- 2. Inhibition of Endogenous Pyrogen creation or unlock (Site II).- three. Inhibition of Endogenous Pyrogen job (Site III).- four. entry of Endogenous Pyrogen to the vital apprehensive approach (Site IV).- five. Hypothalamic Thermoregulatory Centres (Site V).- 6. Suppression of warmth construction (Site VI).- II. attainable Mechanisms of Antipyretic Action.- 1. Inhibition of Prostaglandin Synthesis/Release.- 2. aggressive Antagonism among Pyrogens and Antipyretics for a Receptor Site.- three. Alteration within the job of Neurones within the Hypothalamus.- III. Antipyresis.- D. Inhibition of Fever by means of different Means.- I. elevated warmth Loss.- II. Monoamine Blockade and Depletion.- III. Cholinergic Blockade.- E. Conclusion.- References.- 29 overview of the Toxicity of anti inflammatory Drugs.- A. Introduction.- I. historic Overview.- B. overview of Toxicity in Man.- I. Gastrointestinal Tract.- II. vital anxious System.- III. Dermatological Disorders.- IV. Haematopoietic System.- V. Ocular Disturbances.- VI. Renal facet Effects.- VII. Miscellaneous part Effects.- C. equipment Used to guage Toxicity in Animals.- I. Gastrointestinal.- II. Kidney.- III. Haematopoietic System.- IV. Liver.- V. Skin.- VI. Eye.- VII. crucial anxious System.- D. Correlation of Experimental versions With scientific Toxicity.- I. Non-Steroid anti inflammatory Drugs.- 1. Salicylates.- 2. Indomethacin.- three. Phenylbutazone.- four. Arylalkanoic Acids.- five. Gold.- II. Steroids.- E. Summary.- References.- Pharmacology of the anti inflammatory Agents.- 30 Prostaglandin Synthetase Inhibitors I.- A. Introduction.- B. Inhibiton of Synthetase by way of Substrate Analogues and Fatty Acid Derivatives.- I. Unsaturated Fatty Acids.- II. Bicyclic Analogues.- C. legislation of Enzymic elements: Co-Factors, Stimulation, and Catabolism.- I. legislation of Biosynthesis.- II. Catabolic Enzymes.- D. Inhibition by means of Non-Steroid anti inflammatory Agents.- I. an summary of Structure-Activity Relationship.- 1. Correlation of PG Syntheatase Inhibition With anti inflammatory Action.- 2. basic Structure-Activity Relationship.- II. Salicylates.- III. Indomethacin, Sulindac, and Congeners.- IV. Substituted Aryl Aliphatic Acids.- V. Fenamates.- VI. different Acidic anti inflammatory Agents.- VII. Non-Acidic anti inflammatory Agents.- E. results of Corticosteroids.- F. Inhibition and Stimulation via different Pharmacological Agents.- I. Anti-Arthritic and comparable Compounds.- II. Psychotropic Drugs.- III. Sulphydryl Reagents and Derivatives.- IV. Hormones and Mediators.- V. Inactive Pharmacological Agents.- G. the quest for brand new Inhibitors.- I. present learn Trend.- II. Biochemical and Physiological Specificity.- III. Pharmacodynamic and Metabolic Control.- IV. Multiple-Action Inhibitors.- V. artificial and Physicochemical Approaches.- H. Pharmacokinetics of Prostaglandin Synthetase Inhibitors.- I. Conclusion.- References.- 31 Mode of motion of anti inflammatory brokers that are Prostaglandin Synthetase Inhibitors.- A. Mediators and Inflammatory Responses.- B. Mechanism of anti inflammatory Action.- I. motion on Step 1: Diminution of the potential of Tissue Cells to reply to Inflammatory Mediators.- 1. elevated Dilatation and Vascular Permeability.- 2. ache and Hyperalgesia.- three. elevated Fibroblast Proliferation and Secretion.- II. motion on Step 2: Pharmacological Receptor Antagonism.- III. motion on Step three: Inhibition of Extracellular Enzymic actions Which Generate Inflammatory Mediators or reason damage to cellphone Membranes and/or Tissue Components.- IV. motion on Step four: Inhibition of the discharge of Intracellular Lytic Enzymes or Mediator-Genases or kept Receptor-Mediators.- V. motion on Step five: Inhibition of the Synthesis of Inflammatory Mediators.- 1. Prostaglandin Synthesis and Release.- 2. Prostaglandins and Inflammatory indicators and Symptoms.- three. Correlation among in vitro Inhibition of Prostaglandin Synthesis and anti inflammatory Activity.- four. Inhibition of Prostaglandin Synthesis in vivo and Inflammatory symptoms and Symptoms.- VI. motion on Step 6: Inhibition of phone Migration.- VII. motion on Step 7: Inhibition of the new release of the powerful Inflammatory Trauma.- C. Side-Effects of anti inflammatory medications that are Prostaglandin Synthetase Inhibitors.- D. Theories and Theories.- References.- 32 Penicillamine and medication With a particular motion in Rheumatoid Arthritis.- A. category of Antirheumatic Drugs.- B. Penicillamine.- I. activities in Man.- II. attainable Mode of motion and results in Animal Models.- C. Gold Salts.- D. Chloroquine and different Antimalarials.- E. Levamisole.- F. different Imidazole Derivatives.- G. Immunosuppressives.- H. Alclofenac.- I. Steroids.- J. Summary.- References.- 33 Antagonists of Histamine, 5-Hydroxytryptamine and SRS—A.- A. category of Antihistamines.- B. Histamine H1 Antagonists: Structure-Activity Relationships.- C. Histamine H1 Antagonists: Inhibition of Responses to Histamine fascinated by Inflammatory and Anaphylactic Reactions.- I. Guinea Pig.- II. Rat.- III. Rabbit.- IV. Mouse.- V. Man.- D. Histamine H2 Antagonists: Chemical Considerations.- E. Inhibition of Cardiovascular Responses to Histamine by way of H1 and H2 Antagonists.- F. Chemical and Pharmacological sessions of 5-Hydroxytryptamine Antagonists.- I. Chemical Classes.- II. “M” and “D” Receptors.- III. 201C;Musculotropic” and “Neurotropic” Receptors.- G. Antagonists of 5-Hydroxytryptamine: Inhibition of Responses to 5-HT keen on Inflammatory and Anaphylactic Reactions.- I. Guinea Pig.- II. Rat.- III. Rabbit.- IV. Mouse.- V. Man.- H. results of Antagonists of Histamine (H1 Receptors) and 5-HT in a number of different types of Inflammation.- I. Guinea Pig.- 1. Thermal and Ultraviolet Injury.- 2. neighborhood Anaphylaxis.- three. Systemic Anaphylaxis.- four. Compound 48/80 and Polymyxin B.- five. Bradykinin.- II Rat.- 1. Thermal and Ultraviolet Injury.- 2. neighborhood Anaphylaxis.- three. Systemic Anaphylaxis.- four. Compound 48/80, Polymyxin, Dextran, and Egg White.- five. Turpentine Pleurisy.- 6. Carrageenin Oedema.- 7. Croton Oil.- eight. Bradykinin.- III. Rabbit.- 1. Thermal Injury.- 2. Anaphylactic Reactions.- three. irritation linked to Bacterial Infections.- IV. Mouse.- 1. normal Anaphylaxis.- 2. Cutaneous Anaphylaxis.- three. different neighborhood Inflammatory Reactions.- four. Systemic Reactions concerning Inflammation.- V. Man.- 1. Burns.- 2. Compound 48/80 and Polymyxin.- three. allergy States.- four. Rheumatoid Arthritis and 5-HT Antagonists.- VI. Bovine Anaphylaxis.- I. Antagonists of SRS-A.- I. Non-Steroid anti inflammatory Drugs.- II. Polyphloretin Phosphate (PPP).- III. FPL 55712.- IV. Hydratropic Acids.- J. customers for brand new Drugs.- References.- 34 Inhibitors of the discharge of Anaphylatic Mediators.- A. features of Anti-Allergic brokers Discussed.- B. Cromoglycate and comparable Compounds.- I. identity and Screening.- 1. The Passive Cutaneous Anaphylaxis response (PCA) in Rats.- 2. Lung Anaphylaxis in vivo.- three. Passive Peritoneal Anaphylaxis.- four. Human Tissues in vitro.- five. Rat Tissues in vitro.- II. Structure-Activity Relationships.- III. Anti-Allergic Properties.- 1. Tissue and Species Selectivity.- 2. Inhibition of Mast phone Reactions Provoked via Stimuli except Antigen-Antibody Interactions.- three. Time path Studies.- four. Tachyphylaxis.- IV. reports of the Mechanism of Anti-Allergic Action.- V. different Pharmacological Effects.- VI. Pharmacokinetics.- C. different Inhibitors of Mediator Release.- I. Isosteres of Theophylline.- 1. Structure-Activity Relationships.- 2. Anti-Allergic Properties.- II. Antihistamines and Histamine.- III. Diethylcarbamazine.- 1. Rat Peritoneal Cells in vivo.- 2. Lung Tissue.- three. Human Leucocytes.- four. Passive Cutaneous Anaphylaxis Reactions.- IV. Chlorphenesin.- D. customers for brand spanking new Drugs.- References.- 35 Cytostats With results in persistent Inflammation.- A. Introduction.- B. normal Pharmacology of Cytostats powerful in power Inflammation.- I. “Immunosuppressants”.- 1. Alkylating Agents.- 2. Anti-Metabolites.- II. Microtubular Inhibitors.- 1. Colchicine.- C. a few homes of chosen Compounds.- I. Microtubular Inhibitors.- 1. Cytostatic results of Colchicine.- II. Cyclophosphamide.- 1. Metabolism.- 2. houses of a few Metabolites.- three. web site of Action.- four. a few Side-Effects.- III. Chlorambucil.- 1. Metabolism.- 2. anti inflammatory Effects.- three. Mode of Action.- IV. Methotrexate.- V. Azathioprine.- D. present Problems.- Appendix. Synovectomy and Destruction of Pannus.- References.- Addendum.- 36 regulate of Hyperuricemia.- A. Introduction.- B. Uric Acid Metabolism.- C. Biochemical Pharmacology of Hypouricemic Drugs.- I. medications decreasing Uric Acid Synthesis.- 1. Allopurinol and Oxipurinol.- 2. Thiopurinol.- three. different Inhibitors of Uric Acid Synthesis.- II. Uricosuric Agents.- III. Uricolytic Agents.- D. medical Use of Hypouricemic Drugs.- I. standards for choosing a Hypouricemic Drug.- II. Use of person Hypouricemic Drugs.- III. Toxicity of Hypouricemic Agents.- References.- 37 anti inflammatory Steroids: Mode of motion in Rheumatoid Arthritis and Homograft Reaction.- A. normal Considerations.- B. Scope of the Review.- C. obviously happening anti inflammatory Steroids.- D. artificial anti inflammatory Steroids.- E. organic actions saw With Physiological quantities of Cortisol-Like Steroids.- I. Metabolic Effects.- 1. Gluconeogenesis.- 2. Protein Metabolism.- three. DNA Synthesis.- four. Molecular foundation for Metabolic Effects.- five. Onset and period of Cortisol Action.- 6. Mechanism of motion of Cortisol.- 7. Glycogenosis.- eight. Lipolysis.- nine. dating to anti inflammatory, Anti-Allergic and Anti-Rheumatic Action.- 10. dating to Clinically bad Effects.- eleven. Implications for the Future.- II. Sodium preserving Activity.- III. regulate of Adrenocorticotrophic Hormone (ACTH) Synthesis and Secretion.- 1. Neuroendocrine Control.- 2. adverse suggestions Control.- three. foundation for detrimental suggestions Control.- four. function of Cytoplasmic Steroid Receptors.- five. courting to Clinically fascinating Effects.- 6. dating to Clinically bad Effects.- IV. Cardiovascular Effects.- 1. middle and Peripheral Blood Vessels in Adrenalectomised State.- 2. Microcirculation.- three. dating to anti inflammatory, Anti-Allergic, and Anti-Rheumatic Action.- four. courting to Clinically bad Effects.- five. Pharmacological Implications.- F. Mode of motion in Homograft Reaction.- I. Interference With the advance of Circulating Sensitized Lymphocytes.- II. Effectiveness opposed to irritation because of in the community Sensitized Lymphocytes.- III. Effectiveness opposed to irritation as a result of Circulating Sensitized Lymphocytes.- IV. scientific Relevance of Experimental Observations.- V. Relevance to review of greater Anti-Rejection and Anti-Rheumatic Drugs.- G. Concluding Remarks.- References.- 38 anti inflammatory brokers of Animal Origin.- A. Introduction.- B. Definition and overview of anti inflammatory Activity.- C. Mechanisms of Action.- D. person Agents.- I. Alkoxyglyce

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Inhibition of PG biosynthesis in vitro by acidic anti-inflammatory drugs. Molar ratios represent the relative anti-enzymic potencies of the drugs as compared to the inhibitory potency of aspirin in the same assay system. Most of these assay systems are presented in Table 1. , 1975). The data of PATRONO et al. (1976) refer to the superfused slices of human synovium. The data of DEMBINSKA-KIEC et al. 0 References FLOWER et al. (1972) HAM et al. (1972) DEMBINSKA-KIEC et al. (1975) HAM et al. (1972) TAKEGUCHI and SIH (19~2) FLOWER et al.

1975a). , 1972; KovAcs and GOROG, 1972) and suppress the adhesiveness of leucocytes to plasma-coated glass beads (KOVACS and GOROG, 1972). NSAID do not protect leucocytes against heatinduced lesions of their membranes (KALBHEN and HABIB-MAHMOUD, 1973). 2. Effects on Lysosomal Membrane Extensive reviews have been published on the methods of isolation of lysosomes and assessment of the fragility of their membranes (DINGLE, 1972), as well as on the pharmacological regulation of the lysosomal enzymes secretion (IGNARRO, 1974).

C) Principles of the Methods in vitro Platelet aggregation can be assessed in several types of commercially available aggregometers, according to the principle described by BORN (1962a, b). Light is passed through citrated platelet rich plasma (PRP) being stirred at 37° C. A pro-aggregatory agent is added to PRP and then an increase in light transmission is measured. Special techniques allow evaluation of the shape of platelets. The anti-aggregatory effects of NSAID can be studied either by addition to PRP or by administration of a drug to the PRP donor.

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Anti-Inflammatory Drugs by R. J. Gryglewski (auth.), Dr. John R. Vane, Dr. Sergio H. Ferreira (eds.)

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