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ADVANCES IN CLINICAL CHEMISTRY. 114

Advances in Clinical Chemistry, Volume 112 highlights new advances in the field, with this new volume presenting interesting chapters on a variety of timely topics, including Heterogeneity in Major Depressive Disorder: The need for Biomarker-based and Personalized Treatments, Advances in exosome ana...

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Detalles Bibliográficos
Clasificación:Libro Electrónico
Formato: Electrónico eBook
Idioma:Inglés
Publicado: [S.l.] : ELSEVIER ACADEMIC PRESS, 2023.
Temas:
Acceso en línea:Texto completo
Tabla de Contenidos:
  • Intro
  • Advances in Clinical Chemistry
  • Copyright
  • Contents
  • Contributors
  • Preface
  • Chapter One: Biosensors for saliva biomarkers
  • 1. Introduction
  • 2. Saliva as a noninvasive diagnostic fluid
  • 3. Biomarkers in human saliva
  • 4. Biosensors for saliva biomarkers
  • 4.1. Bacterial and viral biomarkers
  • 4.2. Cancer biomarkers
  • 4.3. Cardiac biomarkers
  • 4.4. Protein and other biomarkers
  • 4.5. Drugs and toxic compound biomarkers
  • 5. Conclusions and future perspectives
  • References
  • Chapter Two: Biochemistry and pathophysiology of the Transient Potential Receptor Vanilloid 6 (TRPV6) calcium channel
  • 1. Introduction
  • 2. The TRPV6 gene
  • 3. Physiology of TRPV6
  • 3.1. Tissue expression
  • 3.2. Regulation of TRPV6 activity
  • 3.3. Channel properties
  • 4. Analytical methods
  • 4.1. Measurement of intracellular Ca
  • 4.2. Measurement of ion currents
  • 4.3. The 3-dimensional structure of TRPV6
  • 4.3.1. X-ray crystallography
  • 4.3.2. Single particle cryogenic-electron microscopy (cryo-EM)
  • 4.3.3. Nuclear magnetic resonance (NMR) spectroscopy
  • 5. Molecular structure and mechanics of TRPV6
  • 5.1. Structure
  • 5.2. Inactivation of the TRPV6 channel by Ca-bound calmodulin
  • 5.2.1. CaM interaction with TRPV6
  • 5.2.2. Proposed mechanism of channel closure
  • 5.3. Proteins associated with TRPV6
  • 6. Establishing the roles of TRPV6 in vivo
  • 7. TRPV6 deficiency due to gene mutations
  • 7.1. Inherited deficiencies in humans
  • 7.1.1. Transient hyperparathyroidism of the newborn (OMIM 618188)
  • 7.1.2. Non-alcoholic chronic pancreatitis (CP)
  • 7.1.3. Calcium kidney stone formation
  • 7.2. TRPV6 deficiency in zebra fish
  • 7.3. TRPV6 deficiency in mouse models
  • 8. TRPV6 in intestinal Ca absorption
  • 8.1. Active transcellular absorption
  • 8.2. Paracellular absorption
  • 8.2.1. Intercellular junctions.
  • 8.2.2. A possible role for TRPV6 in intestinal paracellular Ca absorption?
  • 8.3. Regulation of intestinal Ca transport by 1,25 (OH)2D3
  • 9. TRPV6 deficiency in pregnancy
  • 9.1. TRPV6 in the normal placenta
  • 9.2. Effects of TRPV6 deficiency on the placenta
  • 9.3. TRPV6 in pre-eclamptic toxemia
  • 9.4. Bone abnormalities in fetuses and neonates with TRPV6 deficiency
  • 10. Male infertility in TRPV6 deficiency
  • 11. Alopecia in TRPV6-deficient mice
  • 12. TRPV6 in cancers
  • 12.1. Overview
  • 12.1.1. TRPV6 in tumor growth and metastasis
  • 12.1.2. TRPV6 in epithelial-mesenchymal transition (EMT)
  • 12.2. TRPV6 in breast cancer
  • 12.3. TRPV6 in prostate cancer
  • 12.4. TRPV6 in colon cancer
  • 13. Concluding remarks
  • References
  • Chapter Three: Protein glycation in diabetes mellitus
  • 1. Introduction
  • 2. Diabetes mellitus
  • 3. Protein glycation
  • 4. Glucose and Hyperglycemia
  • 5. Glycated hemoglobin
  • 5.1. History and clinical significance of HbA1c
  • 5.2. HbA1c Standardization
  • 5.3. Limitations of HbA1c
  • 6. Glycated albumin
  • 6.1. GA. Background
  • 6.2. GA as an indicator of hyperglycemia
  • 6.3. GA as a predictor of diabetes complications
  • 6.4. Limitations of GA
  • 7. Other glycated proteins
  • 8. Application of proteomics workflows for glycated proteins
  • 9. Conclusion
  • References
  • Chapter Four: Biomarkers of oxidative stress and reproductive complications
  • 1. Introduction
  • 2. Free radicals in biology and health: ROS and RNS
  • 3. Biomarkers measuring evidence of the direct chemical impact of free radicals in biological systems
  • 3.1. Lipid oxidation products
  • 3.1.1. Initial intermediates
  • 3.1.2. Lipid hydroperoxides
  • 3.1.3. Isoprostanes (IsoPs)
  • 3.1.4. Isolevuglandins (IsoLGs)
  • 3.1.5. Isofurans (IsoFs)
  • 3.1.6. F4-neuroprostanes (F4-NPs) and neurofurans (NFs)
  • 3.1.7. Malondialdehyde.
  • 3.1.8. 4-hydroxy-2-trans-nonenal (4-HNE)
  • 3.2. Protein oxidation products
  • 3.2.1. Carbonyl groups
  • 3.2.2. Advanced glycation end products (AGEs) and advanced lipoxidation end products (ALEs)
  • 3.2.3. Advanced oxidation protein products (AOPP)
  • 3.2.4. Ischemia-modified albumin (IMA)
  • 3.2.5. Oxidized low-density lipoproteins (oxLDL)
  • 3.2.6. Oxidized sulfur-containing amino acids
  • 3.2.7. 3-Nitrotyrosine (3-NT)
  • 3.3. Products of the oxidation of nucleic acids
  • 3.4. Oxidation of uric acid: Allantoin
  • 3.5. Total antioxidant capacity
  • 3.6. Oxidation-reduction potential (ORP)
  • 3.7. Novel biomarkers of oxidative stress
  • 3.7.1. Osmotic fragility of red blood cells
  • 3.7.2. Exosomes
  • 3.7.3. Heart rate variability and oxidative stress severity
  • 3.7.4. Reactive oxygen metabolites (ROM) and biological antioxidant potential (BAP)
  • 4. Oxidative stress and healthy pregnancy
  • 4.1. Oxidative stress and embryonic development
  • 4.2. Role of oxidative stress during early embryogenesis
  • 4.3. Placental oxidative stress
  • 5. Oxidative stress in reproductive complications
  • 5.1. Male infertility
  • 5.2. Female infertility
  • 5.3. Endometriosis
  • 5.4. Polycystic ovarian syndrome
  • 5.5. Ovarian torsion
  • 5.6. Assisted reproductive techniques
  • 5.7. Preeclampsia
  • 5.8. Intrauterine growth restriction
  • 5.9. Miscarriages
  • 5.10. Gestational diabetes mellitus
  • 5.11. Premature rupture of membranes
  • 6. Summary and future perspectives
  • Acknowledgments
  • References
  • Chapter Five: Cortisol: Analytical and clinical determinants
  • 1. Cortisol biochemistry and metabolism
  • 2. Evolution of cortisol assays
  • 3. Cortisol measurement in serum
  • 3.1. Pre-analytic considerations
  • 3.2. Analytical considerations
  • 3.3. Free serum cortisol
  • 4. Cortisol measurement in urine
  • 4.1. Pre-analytic considerations.
  • 4.2. Analytical considerations
  • 5. Cortisol measurement in saliva
  • 5.1. Pre-analytic considerations
  • 5.2. Analytic considerations
  • 6. Cortisol measurement in hair
  • 6.1. Pre-analytic considerations
  • 6.2. Analytic considerations
  • 7. Clinical value of cortisol measurement
  • 8. Summary
  • References
  • Chapter Six: Hemophilia A: Emicizumab monitoring and impact on coagulation testing
  • 1. Introduction
  • 2. Emicizumab
  • 2.1. Development of emicizumab
  • 2.2. Mechanism of action
  • 3. Clinical studies of emicizumab
  • 3.1. HAVEN studies
  • 3.2. Other studies
  • 3.3. Summary of clinical studies
  • 4. Laboratory testing
  • 4.1. Effect of emicizumab on clinical laboratory testing
  • 4.2. APTT, FVIII and FVIII inhibitors testing
  • 4.3. Effect of emicizumab on the measurement of APTT, FVIII and FVIII inhibitors
  • 4.4. Measurement of FVIII and FVIII inhibitors in the presence of emicizumab
  • 4.5. Effect of emicizumab on other coagulation laboratory assays
  • 4.6. Monitoring plasma emicizumab levels
  • 4.7. Measurement of anti-drug antibodies
  • 4.8. Global testing
  • 4.9. General principle of VEM
  • 4.10. General principle of TGA
  • 4.11. General principle of CWA
  • 4.12. Performance issues and limitations of VEM, TGA, and CWA
  • 4.13. VEM, TGA, and/or CWA monitoring of emicizumab therapy
  • 5. Guidelines for monitoring emicizumab in the clinical laboratory
  • 6. The future
  • 7. Conclusion
  • References
  • Index.