Advances in Clinical Chemistry

 
 
Academic Press
  • 1. Auflage
  • |
  • erschienen am 12. Oktober 2015
  • |
  • 324 Seiten
 
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978-0-12-803315-9 (ISBN)
 
Advances in Clinical Chemistry, Volume 72, the latest installment in this internationally acclaimed series contains chapters authored by world-renowned clinical laboratory scientists, physicians, and research scientists. The serial discusses the latest and most up-to-date technologies related to the field of clinical chemistry and is the benchmark for novel analytical approaches in the clinical laboratory.
  • Contains the expertise of international contributors
  • Provides the latest cutting-edge technologies in the field
  • Authored by world-renowned clinical laboratory scientists, physicians, and research scientists
0065-2423
  • Englisch
  • USA
Elsevier Science
  • 5,88 MB
978-0-12-803315-9 (9780128033159)
0128033150 (0128033150)
weitere Ausgaben werden ermittelt
  • Front Cover
  • Advances in Clinical Chemistry
  • Copyright
  • Contents
  • Contributors
  • Preface
  • Chapter One: Metabolic Syndrome and Menopause: Pathophysiology, Clinical and Diagnostic Significance
  • 1. Introduction
  • 2. Menopause Definition
  • 3. MetS in Peri- and Postmenopausal Women
  • 3.1. Definitions of MetS
  • 3.2. Prevalence of MetS in Postmenopausal Women
  • 3.3. The Pathophysiology of MetS
  • 3.4. The Age or Menopausal Status as the Leading and Independent Causes of MetS
  • 3.5. Effects of Surgical and Natural Menopause on MetS
  • 3.6. Effects of Reproductive Factors on MetS in Postmenopausal Women
  • 4. Effect of Menopause on MetS Components and the Role of Sex Hormones
  • 4.1. Effect of Menopause on the Body Composition
  • 4.1.1. Relationship Between Sex Hormones and the Body Composition After Menopause
  • 4.1.2. Metabolically Healthy Obese and Metabolically Abnormal but Normal-Weight Postmenopausal Women
  • Metabolically Healthy but Obese Postmenopausal Women
  • Metabolically Obese but Normal-Weight Postmenopausal Women
  • 4.2. Effect of Menopause on IR and Glucose Metabolism
  • 4.2.1. Relation Between Sex Hormones and IR After Menopause
  • 4.3. Effect of Menopause on Lipid Metabolism and the Role of Sex Hormones
  • 4.3.1. High-Density Lipoprotein Cholesterol
  • 4.3.2. TC and Low Density Lipoprotein Cholesterol
  • 4.3.3. Triglycerides
  • 4.4. Effect of Menopause on BP
  • 4.4.1. The Role of Sex Hormones for Hypertension Development
  • 4.4.2. The Role of Obesity and Inflammation State for Hypertension Development
  • 5. Other Biomarkers Related to MetS in Postmenopausal Women
  • 5.1. Inflammatory Markers
  • 5.2. Adipocytokines
  • 5.3. Oxidative Stress and Iron Metabolism
  • 6. MetS: A Risk Factor for Diseases Related to Menopause
  • 6.1. Type 2 Diabetes
  • 6.2. Cardiovascular Diseases
  • 6.3. Breast Cancer
  • 6.4. Osteoporosis
  • 7. Effect of Hormone Replacement Therapy on MetS Components and Cardiovascular Events
  • 7.1. Effect of Hormone Replacement Therapy on MetS and Diabetes Type 2
  • 7.2. Effect of Hormone Replacement Therapy on Cardiovascular Events
  • 8. Dietary Patterns and Risk of MetS in Postmenopausal Women
  • 8.1. Low-Energy Diet
  • 8.2. Vitamin D
  • 8.3. Antioxidants and Soy Isoflavones
  • 8.4. Omega-3 Fatty Acids
  • 9. Association Between Physical Activity and MetS in Postmenopausal Women
  • 10. Conclusions
  • References
  • Chapter Two: Homocysteine in Chronic Kidney Disease
  • 1. Introduction
  • 2. Causes of Hyperhomocysteinemia
  • 3. Homocysteine-Induced Oxidation
  • 4. Are Oxidation Reactions the Sole Culprit for Renal Failure?
  • 5. Changes in Methylation Pattern
  • 6. Redox Switches
  • 6.1. S-Cysteinylation
  • 6.2. S-Glutathionylation
  • 6.3. S-Homocysteinylation of Metallothionein
  • 6.4. S-Sulfhydration
  • 7. Conclusion
  • References
  • Chapter Three: Lung Cancer Biomarkers
  • 1. Introduction
  • 1.1. What Are Biomarkers?
  • 1.2. Why Do We Need Biomarkers for Screening and Diagnostics in Addition to Imaging Modalities?
  • 2. Biomarker Development in Biological Fluids (Body Fluids)
  • 2.1. What Molecules Can Be Biomarkers for Lung Cancers?
  • 3. Publication Trend in "Lung Cancer biomarkers"
  • 4. Lung Cancer Biomarkers at Limited Clinical Usage
  • 4.1. Protein Tumor Markers
  • 4.1.1. Cytokeratin 19 Fragment
  • 4.1.2. Carcinoembryonic Antigen
  • 4.1.3. SCC Antigen
  • 4.1.4. Neuron-Specific Enolase
  • 4.1.5. Progastrin-Releasing Peptide
  • 4.1.6. Epidermal Growth Factor Receptor
  • 5. Lung Cancer Biomarkers in Clinical Trials
  • 6. Lung Cancer Biomarkers in Validation Phases
  • 6.1. Protein Biomarkers
  • 6.1.1. Serum Amyloid A
  • 6.1.2. Haptoglobin
  • 6.1.3. Plasma Kallikrein (KLKB1)
  • 6.1.4. Complement Components: C9 and C4d
  • 6.1.5. Tumor M2-Pyruvate Kinase
  • 6.1.6. C-Reactive Protein
  • 6.1.7. Cip1 (p21)-Interacting Zinc Finger Protein (Ciz1)
  • 6.1.8. Insulin-Like Growth Factor-Binding Protein-2
  • 6.1.9. Progesterone Receptor Membrane Component 1/Sigma-2 Receptor
  • 6.1.10. Peroxiredoxin 1
  • 6.1.11. Endoglin (CD105)
  • 6.1.12. Matrix Metalloproteinase-1
  • 6.1.13. Urokinase Plasminogen Activator Receptor
  • 6.1.14. Serum Paraoxonase 1 (Pon1)
  • 6.2. miRNA as Lung Cancer Biomarkers
  • 6.3. DNA Methylation-Based (Epigenetic) Lung Cancer Biomarkers in Body Fluids
  • 7. Circulating Tumor Cells
  • 8. Additional Molecular Markers in Other Biological Fluids of Lung Cancer Patients
  • 8.1. Sputum
  • 8.2. Bronchoalveolar Lavage
  • 8.3. Saliva
  • 8.4. Pleural Effusion
  • 8.5. Exhaled Breath Concentrate-Volatile Organic Compound
  • 9. Conclusion
  • Acknowledgments
  • References
  • Chapter Four: SEPT9: A Specific Circulating Biomarker for Colorectal Cancer
  • 1. Introduction
  • 2. The Role of Septin9
  • 3. SEPT9 and Colorectal Cancer
  • 3.1. DNA Methylation in Cancer
  • 3.2. The Roles of SEPT9 Gene in Carcinogenesis
  • 3.3. SEPT9 Gene Methylation in Colorectal Cancer
  • 3.3.1. Gene Methylation Markers in CRC Detection
  • 3.3.2. Hypermethylation at CpG Island 3 (CGI3) of SEPT9 Transcript V2 Is Specific for CRC Carcinogenesis and Is the Targe...
  • 3.3.3. Validation of SEPT9 Gene Methylation Assay for CRC Detection
  • 4. Clinical Applications of SEPT9 Gene Methylation Assay in CRC Detection and Screening
  • 4.1. Application of SEPT9 Gene Methylation Assay in CRC Early Detection
  • 4.1.1. Sensitivity, Specificity, PPV, and NPV of the SEPT9 Assay in CRC Detection
  • 4.1.2. The Positive Detection Rate in All CRC Stages
  • 4.1.3. Detection of Precancerous Diseases and Other Colonic Diseases
  • 4.2. Comparison of SEPT9 Gene Methylation Assay with Other CRC Detection Markers or Methods
  • 4.2.1. SEPT9 Assay Exhibited Similar or Better Performance Than Fecal Immunoassay or DNA Assay
  • 4.2.2. SEPT9 Assay Is More Sensitive Than Any Existing Single Glycoprotein Marker in CRC Detection
  • 4.2.3. Combined Use of SEPT9 Assay with Other CRC Detection Assays
  • 4.3. Application of FOBT, Colonoscopy, and SEPT9 Gene Methylation Assay in CRC Screening
  • 4.4. Application of SEPT9 Gene Methylation Assay in the Assessment of CRC Recurrence, Surgery, Chemotherapy, and Long-Ter...
  • 4.5. Detection of Other Cancers by SEPT9 Gene Methylation Assay
  • 4.6. Automated SEPT9 Assay in Future CRC Screening
  • 5. Conclusions
  • Acknowledgments
  • References
  • Chapter Five: Glycated Serum Albumin and AGE Receptors
  • 1. Introduction
  • 2. Protein Glycation
  • 2.1. Historical Development
  • 2.2. Chemical Principles of Protein Glycation
  • 2.3. Glycation Products Derived from Lysine Side Chains
  • 2.4. Glycation Products Derived from Arginine Side Chains
  • 2.5. Glycation Products Leading to Intra- or Intermolecular Cross-Linkage
  • 3. Glycated Serum Albumin-GA
  • 3.1. In Vivo and In Vitro Glycation in Human Serum Albumin
  • 3.2. Methods of Measuring Albumin Glycation
  • 3.2.1. Fructosamine Enzymatic Assay
  • 3.2.2. Glycated Albumin Enzymatic Assay
  • 3.2.3. Fructosamine Colorimetric Assay
  • 3.2.4. Ion-Exchange Chromatography
  • 3.2.5. Boronate Affinity Chromatography
  • 3.2.6. Enzyme-Linked Boronate Immunoassay (ELBIA)
  • 3.2.7. Antibodies
  • 3.2.8. Mass Spectrometry
  • 3.2.9. Fluorescence Spectrometry
  • 3.2.10. Raman Spectroscopy
  • 3.3. Sites of Glycation in Human Serum Albumin
  • 3.4. Structural Consequences of Albumin Glycation
  • 3.5. Effect of Glycation of Albumin on Drug Binding
  • 3.6. Storage of Samples for Glycation Analysis
  • 4. AGE Receptors
  • 4.1. Scavenger Receptors
  • 4.1.1. MSR1
  • 4.1.2. CD36
  • 4.1.3. SCARB1
  • 4.1.4. OLR1
  • 4.1.5. STAB1 and STAB2
  • 4.1.6. AGE Uptake By Other Scavenger Receptors
  • 4.2. AGE Receptors: AGE-R1, AGE-R2, and AGE-R3
  • 4.3. RAGE
  • 4.3.1. AGE-RAGE Signaling in Endothelial Cells
  • 4.3.2. AGE-RAGE Signaling in Vascular Smooth Muscle Cells
  • 4.3.3. AGE-RAGE Signaling in Inflammatory Cells
  • 5. Glycated Albumin as a Clinical Marker
  • 5.1. Glycated Hemoglobin HbA1c
  • 5.2. Glycated Serum Albumin-GA
  • 5.3. Measurement of Glycated Serum Proteins and Serum Fructosamine
  • 6. Conclusion
  • References
  • Chapter Six: Polycyclic Aromatic Hydrocarbons: Part I. Exposure
  • 1. Introduction
  • 2. PAH Distribution and Exposure
  • 3. The Concept of Biomarkers
  • 3.1. Biomarkers of Exposure
  • 3.2. Biomarkers of Effect
  • 3.3. Biomarkers of Susceptibility
  • 4. The Concept of Toxicokinetics
  • 5. Toxicokinetics of PAH
  • 5.1. Absorption
  • 5.2. Distribution
  • 5.3. Metabolism
  • 5.4. Excretion
  • References
  • Index
  • Back Cover

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