Makowski Advances in Clinical Chemistry

1. Auflage 2009
ISBN: 978-0-08-095099-0
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: 6 - ePub Watermark

E-Book, Englisch, 199 Seiten

Volume 48 in the internationally acclaimed Advances in Clinical Chemistry contains chapters submitted from leading experts from academia and clinical laboratory science. Authors are from a diverse field of clinical chemistry disciplines and diagnostics ranging from basic biochemical exploration to cutting-edge microarray technology.
* Leading experts from academia and clinical laboratory science * Volume emphasizes novel laboratory advances with application to clinical laboratory diagnostics and practical basic science studies

Autoren/Hrsg.

Makowski, Gregory

Inhaltsverzeichnis

1;Front Cover;1
2;Advances in Clinical Chemistry;4
3;Copyright Page;5
4;Contents;6
5;Contributors;10
6;Preface;12
7;Chapter 1: Clinical validation of biomarkers for predicting risk;14
7.1;2. Introduction;15
7.2;3. RR/OR Ratios as Diagnostic Tools;16
7.3;4. ROC Plots/Curves as a Diagnostic Tool;17
7.4;5. Comparison of RR/OR with ROC curves;20
7.5;6. Distributions;22
7.6;7. Bayesian Principles;22
7.7;8. Weaknesses of ROC Analysis;25
7.7.1;8.1. Diagnostic Models;25
7.7.2;8.2. Prognostic Models;26
7.8;9. Weaknesses of RR/OR;26
7.9;10. Stand-Alone versus Synergic Biomarkers;28
7.10;11. Techniques for Improving Stratification of Synergic Biomarkers;28
7.11;12. Criteria for Identifying Testing of Clinical Consequence;29
7.12;13. Discussion;32
7.13;14. Conclusions;33
7.14;Glossary of Expressions and Explanations;34
7.15;Acknowlegement;35
7.16;References;35
8;Chapter 2: The potential role of heat shock proteins in cardiovascular disease: Evidence from in vitro and in vivo studies;40
8.1;2. Introduction;41
8.1.1;2.1. Discovery of the HSPs, Their Classification and Their Functions;41
8.1.2;2.2. Atherosclerosis;41
8.1.2.1;2.2.1. Atherosclerosis and the Role of Inflammation;43
8.1.2.2;2.2.2. Atherosclerosis and the Role of Infection;44
8.1.2.3;2.2.3. Autoimmunity in Atherogenesis;47
8.2;3. HSPs and Atherogenesis;47
8.2.1;3.1. HSPs and Animal Models of Atherogenesis;49
8.2.1.1;3.1.1. Mouse and Rat;49
8.2.1.2;3.1.2. Rabbit;49
8.2.2;3.2. Modulation of HSP Expression in Cells Involved in Atherogenesis In Vitro;51
8.2.2.1;3.2.1. Endothelial Cells;52
8.2.2.2;3.2.2. Smooth Muscle Cells;56
8.2.2.3;3.2.3. Cardiac Myocytes;56
8.2.2.4;3.2.4. Monocyte/Macrophages;57
8.2.2.5;3.2.5. Lymphocytes;57
8.2.2.6;3.2.6. HSPs and Apoptosis;57
8.2.3;3.3. Soluble or Circulating HSPs;57
8.3;4. HSPs and Autoimmunity in Atherogenesis;58
8.3.1;4.1. General Consideration;58
8.3.2;4.2. Molecular Mimicry and Relation to Infection;60
8.3.3;4.3. Antibodies to HSPs and Infections;60
8.3.4;4.4. Antibodies to HSPs and Cardiovascular Risk Factors;61
8.3.4.1;4.4.1. Animal Models;61
8.3.4.2;4.4.2. Human Studies;61
8.3.5;4.5. Antibody Titers to HSPs and Their Relationship to CVD Burden;67
8.3.5.1;4.5.1. Observational Studies;67
8.3.5.2;4.5.2. Prospective Studies;68
8.3.6;4.6. Changes in Titers of HSP Antibodies During Acute Coronary Syndromes;69
8.4;5. Therapeutic Implications;71
8.5;6. Conclusions;72
8.6;References;72
9;Chapter 3: The Emerging Role of Symmetric Dimethylarginine in Vascular Disease;86
9.1;2. Introduction;87
9.2;3. Synthesis, Transport, and Metabolism of ADMA and SDMA;88
9.2.1;3.1. Synthesis;88
9.2.2;3.2. Transport and Metabolism;90
9.3;4. ADMA and the Cardiovascular System;91
9.3.1;4.1. Endothelial Function and Hemodynamics;91
9.3.2;4.2. Arterial Stiffness, Cardiac Function, Atherosclerosis, and Inflammation;91
9.3.3;4.3. Cardiovascular Outcomes;92
9.4;5. SDMA and the Cardiovascular System;92
9.4.1;5.1. Endothelial Function and Cardiac Function;92
9.4.2;5.2. Cardiovascular Homeostasis;97
9.4.2.1;5.2.1. Renal Function;97
9.4.2.2;5.2.2. Intradialytic Hypotension;99
9.4.3;5.3. Cardiovascular Outcomes;100
9.5;6. Discussion;101
9.6;References;102
10;Chapter 4: Melanocortin-4 Receptor Mutations In Obesity;108
10.1;2. Introduction;109
10.2;3. The Melanocortin System;110
10.3;4. The MC4R;112
10.4;5. Mutations in the MC4R;113
10.5;6. Functional Alterations of MC4R;115
10.6;7. Clinical Phenotype of MC4R-Mutated Individuals;115
10.7;8. Implications of MC4R Mutations in the Clinical Management of Obesity;116
10.8;9. Conclusions;116
10.9;References;117
11;Chapter 5: Proinflammatory cytokines in CRP baseline regulation;124
11.1;2. C-Reactive Protein and Inflammation;125
11.2;3. Demographic, Metabolic, and Socioeconomic Factors;127
11.3;4. Proinflammatory Cytokines;131
11.3.1;4.1. IL-6;131
11.3.2;4.2 IL-1 Family;132
11.3.3;4.3 TNF;134
11.3.4;4.4 IL-17;135
11.4;5. Signaling Through IL Receptors;136
11.5;6. Genetic Polymorphisms;137
11.6;7. Conclusions;137
11.7;Acknowlegement;139
11.8;References;139
12;Chapter 6: Fetal Skin Wound Healing;150
12.1;2. Introduction;151
12.2;3. Development;153
12.2.1;3.1. Fetal Skin;153
12.2.2;3.2. Fetal ECM;153
12.2.3;3.3. Collagen;153
12.2.4;3.4. Hyaluronic Acid;154
12.2.5;3.5. Proteoglycan ECM Modulators;154
12.3;4. Scarless Fetal Wound Repair Specificity;154
12.3.1;4.1. Scarless Fetal Wound Phenotype;154
12.3.2;4.2. Collagen Content;155
12.3.3;4.3. Hyaluronic Acid;156
12.3.4;4.4. ECM Adhesion Proteins;156
12.3.5;4.5. ECM Proteoglycan Modulators;158
12.3.6;4.6. Scarless Repair is Intrinsic to Fetal Skin;159
12.3.7;4.7. Scarless Repair Depends on Gestational Age and Wound Size;159
12.3.8;4.8. Mechanisms of Scarless Repair;160
12.4;5. Stem Cells;160
12.4.1;5.1. Hematopoietic Stem Cells (HSCs);160
12.4.2;5.2. Fetal and Postnatal Epidermal Stem Cells;161
12.4.3;5.3. Dot Cells;162
12.5;6. Cellular Inflammatory Mediators;162
12.5.1;6.1. Platelets;162
12.5.2;6.2. Neutrophils;163
12.5.3;6.3. Fibroblasts;163
12.6;7. Cytokines;164
12.6.1;7.1. Transforming Growth Factor-Beta (TGF-beta);164
12.6.2;7.2. Connective Tissue Growth Factor (CTGF);165
12.6.3;7.3. Vascular Endothelial Growth Factor (VEGF);165
12.6.4;7.4. Fibroblast Growth Factors (FGFs);166
12.6.5;7.5. Platelet Derived Growth Factor (PDGF);166
12.6.6;7.6. Wnts;167
12.6.7;7.7. Interleukins;167
12.6.8;7.8. Molecular Control of Scarless Repair;167
12.6.9;7.9. Perspective;168
12.7;References;168
13;Chapter 7: Clinical Relevance of BNP Measurement in the Follow-Up of Patients with Chronic Heart Failure;176
13.1;2. Background and Aim of the Study;177
13.2;3. Biochemical and Physiological Properties of B-Type Natriuretic Peptides;178
13.3;4. Circulating Levels of B-Type Natriuretic Peptides;180
13.3.1;4.1. Analytical Aspects;180
13.3.2;4.2. Pathophysiological Considerations;181
13.4;5. Variations of Plasma B-Type Natriuretic Peptides, Dependent on Pharmacological Treatment, as Surrogate End-Point for Treatment of Patients with HF;181
13.5;6. Prognostic Relevance of Plasma BNP/NT-proBNP Variations After Treatment;182
13.6;7. Meta-Analysis for Overall Mortality Including All Randomized Clinical Trials;187
13.7;8. BNP-Guided Therapy in Chronic Heart Failure: Instructions for Use;188
13.8;References;189
14;Index;194