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دانلود کتاب Clinical Applications of Biomolecules in Disease Diagnosis: A Comprehensive Guide to Biochemistry and Metabolism

دانلود کتاب کاربردهای بالینی بیومولکول ها در تشخیص بیماری: راهنمای جامع بیوشیمی و متابولیسم

Clinical Applications of Biomolecules in Disease Diagnosis: A Comprehensive Guide to Biochemistry and Metabolism

مشخصات کتاب

Clinical Applications of Biomolecules in Disease Diagnosis: A Comprehensive Guide to Biochemistry and Metabolism

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نویسندگان: , ,   
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ISBN (شابک) : 9789819747221, 9789819747238 
ناشر: Springer 
سال نشر: 2024 
تعداد صفحات: 457 
زبان: English 
فرمت فایل : PDF (درصورت درخواست کاربر به PDF، EPUB یا AZW3 تبدیل می شود) 
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فهرست مطالب

Preface
	Key Features
	Organization of the Book
Acknowledgements
Contents
Editors and Contributors
About the Editors
Contributors
1: Introduction to Clinical Applications of Biomolecules in Disease Diagnosis
	1.1	 Introduction
	1.2	 Clinically Important Biomarkers and Related Disorders
		1.2.1	 Carbohydrates
		1.2.2	 Proteins
		1.2.3	 Nucleic Acids
		1.2.4	 Lipids
		1.2.5	 Enzymes
		1.2.6	 Hormones
		1.2.7	 Vitamins
		1.2.8	 Macro and Microelements
	1.3	 Classification of Biomarkers
		1.3.1	 Molecular and Genetic Biomarkers
		1.3.2	 Biochemical Biomarkers
	1.4	 Omics Science in Clinical Pathology
		1.4.1	 Diagnostic Biomarkers
		1.4.2	 Prognostic Biomarkers
		1.4.3	 Therapeutic Biomarkers
	1.5	 Promising and Valuable Tools for Identification of Biomolecules
	1.6	 Free Radicals and Antioxidants
	1.7	 Advantages and Disadvantages of Biomolecules in Clinical Diagnosis
	1.8	 Future Prospective and Challenges
	1.9	 Conclusions
	References
2: Carbohydrate Metabolism in Health and Diseases
	2.1	 Introduction
	2.2	 Overview of Metabolic Pathways
		2.2.1	 Glycolysis
		2.2.2	 Kreb’s Cycle
		2.2.3	 Oxidative Phosphorylation
	2.3	 Impaired Glucose Metabolism in Metabolic Diseases
	2.4	 Dysregulation of Glucose Uptake and Utilization
	2.5	 Influence of Altered Carbohydrate Metabolism on Metabolic Pathways
	2.6	 Role of Glucose Transporters in Cellular Uptake and Utilization of Carbohydrates
	2.7	 Formation of AGEs Through the Maillard Reaction
	2.8	 Glycoxidation and Lipo-Oxidation Pathways Leading to AGEs Formation
	2.9	 Lipo-Oxidation Pathway
	2.10	 Receptor-Mediated Mechanisms AGEs Uptake and Signaling
	2.11	 Impact of Hyperglycemia and Oxidative Stress on AGEs Accumulation
	2.12	 Receptor for AGE (RAGE) and Its Expression in Various Tissues
	2.13	 Signaling Pathways Activated by RAGE-AGEs Interaction
	2.14	 Cross Talk Between RAGE and Other Receptors in Metabolic Diseases
	2.15	 Role of AGEs in the Progression of Diabetes
	2.16	 Future Perspective
	References
3: Protein Metabolism and Its Profiling for the Diagnosis of Metabolic Disorders
	3.1	 Introduction
		3.1.1	 Amino Acid Metabolism
	3.2	 Protein Metabolic Disorders
		3.2.1	 Aromatic Amino Acid Disorders
			3.2.1.1	 Phenylketonuria (PKU)
			3.2.1.2	 Alkaptonuria
			3.2.1.3	 Tyrosinemia Type I
			3.2.1.4	 Tyrosinemia Type II
			3.2.1.5	 Tyrosinemia Type III
			3.2.1.6	 Albinism
				3.2.1.6.1 Ocular Albinism (OA1)
				3.2.1.6.2 Hermansky-Pudlak Syndrome (HPS)
				3.2.1.6.3 Chediak-Higashi Syndrome (CHS)
				3.2.1.6.4 Angelman Syndrome (AS) and Prader-Willi Syndrome (PWS)
		3.2.2	 Branched-Chain Amino Acid (BCAA) Disorders
		3.2.3	 Sulfur-Containing Amino Acid Disorders
			3.2.3.1	 Cystathioninuria
			3.2.3.2	 Cystinuria
		3.2.4	 Urea Cycle Disorders (UCDs)
			3.2.4.1	 Hyperornithinemia-Hyperammonemia-Homocitrullinuria (HHH) Syndrome
		3.2.5	 Protein Deficient Disorders
			3.2.5.1	 Kwashiorkor
			3.2.5.2	 Marasmus
	3.3	 Diagnostic Techniques for Amino Acid Metabolic Disorders
		3.3.1	 Quantitative Analysis
		3.3.2	 Newborn Screening
		3.3.3	 Ion Exchange Chromatography
		3.3.4	 Reverse-Phase High-Performance Liquid Chromatography (RP-HPLC)
		3.3.5	 Tandem Mass Spectrometry
	3.4	 Conclusions
	References
4: Disorders of Lipid Metabolism
	4.1	 Introduction
	4.2	 Normal Lipid Metabolism
	4.3	 Primary Lipid Metabolic Disorders
		4.3.1	 Hypertriglyceridemia
			4.3.1.1	 Familial Hypertriglyceridemia
			4.3.1.2	 Familial Combined Hyperlipidemia
			4.3.1.3	 Congenital Lipoprotein Lipase Deficiency
			4.3.1.4	 Apoprotein C-II Deficiency
			4.3.1.5	 Familial Dysbetalipoproteinemia
		4.3.2	 Hypercholesterolemia
			4.3.2.1	 Homozygous Familial Hypercholesterolemia
			4.3.2.2	 Dysbetalipoproteinemia
			4.3.2.3	 Sitosterolemia
			4.3.2.4	 Polygenic Hypercholesterolemia
			4.3.2.5	 Familial Combined Hyperlipidemia
		4.3.3	 Hyperalphalipoproteinemia (HALP)
		4.3.4	 Hypolipoproteinemia
			4.3.4.1	 Hypoalphalipoproteinemia
			4.3.4.2	 Hypobetalipoproteinemia
			4.3.4.3	 Abetalipoproteinemia (ABL)
			4.3.4.4	 Tangier Disease
	4.4	 Secondary Lipid Metabolic Disorders
		4.4.1	 Cardiovascular Diseases (CVDs)
		4.4.2	 Obesity
		4.4.3	 Diabetes
		4.4.4	 Hypothyroidism
		4.4.5	 Gaucher Disease
		4.4.6	 Tay-Sachs Disease
		4.4.7	 Chronic Kidney Disease (CKD)
		4.4.8	 Liver Cholestasis
		4.4.9	 Other Diseases
	4.5	 Conclusions
	References
5: Nucleic Acid Metabolism and Disorders
	5.1	 Introduction
	5.2	 Purine Metabolism
		5.2.1	 Purine Nucleotide Biosynthesis
		5.2.2	 Salvage Pathway for Purine Nucleotide Synthesis
		5.2.3	 Purine Nucleotide Degradation
	5.3	 Disorders of Purine Metabolism
		5.3.1	 Gout
			5.3.1.1	 Treatment
		5.3.2	 Lesch-Nyhan’s Disease/Syndrome
			5.3.2.1	 Treatment
		5.3.3	 Adenine Phosphoribosyltransferase Deficiency
			5.3.3.1	 Treatment
		5.3.4	 Phosphoribosyl Pyrophosphate (PRPP) Synthetase Superactivity
			5.3.4.1	 Treatment
		5.3.5	 Adenosine Deaminase (ADA) Deficiency
			5.3.5.1	 Treatment
		5.3.6	 Purine Nucleoside Phosphorylase Deficiency
			5.3.6.1	 Treatment
		5.3.7	 Xanthine Oxidase Deficiency: Hereditary Xanthinuria
			5.3.7.1	 Treatment
		5.3.8	 Adenylosuccinate Lyase (ADSL) Deficiency
			5.3.8.1	 Treatment
		5.3.9	 Myoadenylate Deaminase Deficiency (MADD)
			5.3.9.1	 Treatment
		5.3.10	 Thiopurine Methyltransferase (TPMT) Deficiency
			5.3.10.1	 Treatment
		5.3.11	 Deoxyguanosine Kinase (DGUOK) Deficiency
			5.3.11.1	 Treatment
	5.4	 Pyrimidine Metabolism
		5.4.1	 Pyrimidine Nucleotide Biosynthesis
		5.4.2	 Catabolism of Pyrimidine Nucleotides
	5.5	 Disorders of Pyrimidine Metabolism
		5.5.1	 UMP Synthase Deficiency
			5.5.1.1	 Treatment
		5.5.2	 Dihydropyrimidine Dehydrogenase (DPD) Deficiency
			5.5.2.1	 Treatment
		5.5.3	 Dihydropyrimidinase (DHP) Deficiency
			5.5.3.1	 Treatment
		5.5.4	 β-Ureidopropionase Deficiency
		5.5.5	 Pyrimidine 5′-Nucleotidase Deficiency
			5.5.5.1	 Treatment
		5.5.6	 Cytosolic 5′-Nucleotidase Superactivity
		5.5.7	 Thymidine Phosphorylase Deficiency
		5.5.8	 Dihydroorotate Dehydrogenase (DHO) Deficiency
		5.5.9	 Cytidine Deaminase (CDA) Deficiency
		5.5.10	 Thymidine Kinase 2 Deficiency
	5.6	 Diagnosis of Inborn Errors of Purine and Pyrimidine Metabolism
	5.7	 Conclusions
	References
6: Vitamins and Their Impact on Human Health
	6.1	 Introduction
	6.2	 Structure and Physio-chemical Properties
		6.2.1	 Vitamin A
		6.2.2	 Vitamin D
		6.2.3	 Vitamin E
		6.2.4	 Vitamin K
		6.2.5	 Vitamin C
		6.2.6	 Vitamin B1
		6.2.7	 Vitamin B2
		6.2.8	 Vitamin B3 (Niacin)
		6.2.9	 Vitamin B5 (Pantothenic Acid)
		6.2.10	 Vitamin B6 (Pyridoxine)
		6.2.11	 Vitamin B7 (Biotin)
		6.2.12	 Vitamin B9 (Folate)
		6.2.13	 Vitamin B12 (Cobalamin)
	6.3	 Dietary Sources and Its Bioavailability
	6.4	 Vitamins Influences Human Health
	6.5	 Summary
	References
7: Electrolytes and Acid-Base Disorders
	7.1	 Introduction to Electrolytes and Acid-Base Homeostasis
	7.2	 Electrolytes
		7.2.1	 Role of HCO3−/CO2 Buffer in Acid-Base Homeostasis
		7.2.2	 Major Ions Present in the Human Body
		7.2.3	 Role of Major Ions in the Human Body
		7.2.4	 Electrolytes as Osmotic Regulators
			7.2.4.1	 Role of Electrolytes
			7.2.4.2	 Regulatory Mechanisms
	7.3	 Buffers
		7.3.1	 Introduction to Buffers
		7.3.2	 Role of Buffers
			7.3.2.1	 Maintaining Homeostasis
				7.3.2.1.1 Blood pH Regulation
				7.3.2.1.2 Acid-Base Balance
				7.3.2.1.3 Respiratory Regulation
			7.3.2.2	 Regulation of Enzymatic Functions
	7.4	 Maintenance of Plasma Osmolality
		7.4.1	 Plasma and Plasma Osmolality
		7.4.2	 Composition of Plasma
			7.4.2.1	 Water
			7.4.2.2	 Inorganic Substances
			7.4.2.3	 Organic Substances
			7.4.2.4	 Gases
		7.4.3	 Measurement of Osmolality
		7.4.4	 Mechanisms to Maintain Plasma Osmolality
			7.4.4.1	 Posterior Pituitary/Renal Systems
			7.4.4.2	 Renin Angiotensin Aldosterone System
			7.4.4.3	 Functions Angiotensin 2
	7.5	 Renal Regulation of Acid-Base Balance
		7.5.1	 Major Organs Involved in the Acid-Base Balance Regulation
			7.5.1.1	 Lungs
			7.5.1.2	 Kidneys
				7.5.1.2.1 Role of Kidneys
	7.6	 Metabolic Acidosis and Alkalosis
		7.6.1	 Metabolic Acidosis
		7.6.2	 Metabolic Alkalosis
	7.7	 Electrolyte Disorders
		7.7.1	 Understanding Electrolyte Disorders
		7.7.2	 Factors Causing Electrolyte Imbalance
		7.7.3	 Common Electrolyte Disorders
			7.7.3.1	 Hyponatremia
			7.7.3.2	 Hypernatremia
			7.7.3.3	 Hypokalemia
			7.7.3.4	 Hyperkalemia
			7.7.3.5	 Hypocalcemia and Hypercalcemia
	7.8	 Conclusions
	References
8: Metabolism of Macro-elements (Calcium, Magnesium, Sodium, Potassium, Chloride and Phosphorus) and Associated Disorders
	8.1	 Introduction
	8.2	 Metabolic Regulation, Functions, and Disorders of Calcium Metabolism
		8.2.1	 Metabolic Disorders of Calcium
			8.2.1.1	 Hypocalcemia
			8.2.1.2	 Hypercalcemia
			8.2.1.3	 Malignancy and Hyperparathyroidism
			8.2.1.4	 Hyperparathyroidism
			8.2.1.5	 Calcium-Sensing Receptor (CaSR) Associated Disorders
				8.2.1.5.1 Familial Hypocalciuric Hypercalcemia (FHH)
				8.2.1.5.2 Neonatal Severe Hyperparathyroidism (NSHPT)
				8.2.1.5.3 Autosomal Dominant Hypocalcemia (ADH)
			8.2.1.6	 Nutritional Rickets and Osteomalacia
			8.2.1.7	 Osteoporosis
			8.2.1.8	 Tumor-Induced Osteomalacia (TIO)
			8.2.1.9	 Tumoral Calcinosis
			8.2.1.10	 Milk-Alkali Syndrome or Calcium-Alkali Syndrome
			8.2.1.11	 Paget’s Disease of Bone
			8.2.1.12	 Neonatal Hypocalcemia
			8.2.1.13	 Hypoparathyroidism
			8.2.1.14	 Thyrotoxicosis
			8.2.1.15	 Hungry Bone Syndrome (HBS)
	8.3	 Metabolic Regulation, Functions, and Disorders of Phosphate Metabolism
		8.3.1	 Metabolic Disorders of Phosphate
			8.3.1.1	 Hypophosphatemia
			8.3.1.2	 Hyperphosphatemia
			8.3.1.3	 Hypoparathyroidism
			8.3.1.4	 Familial Hypophosphatemia (X-linked Hypophosphatemia)
			8.3.1.5	 Oncogenic Osteomalacia
			8.3.1.6	 Hyperphosphatemic Familial Tumoral Calcinosis (HFTC)
			8.3.1.7	 Fanconi Syndrome
			8.3.1.8	 Tertiary Hyperparathyroidism
			8.3.1.9	 Hereditary Hypophosphatemic Rickets with Hypercalciuria (HHRH)
			8.3.1.10	 Vitamin D-Resistant Rickets
			8.3.1.11	 Autosomal Dominant Hypophosphatemic Rickets (ADHR)
	8.4	 Metabolic Regulation and Functions of Magnesium
		8.4.1	 Metabolic Disorders of Magnesium
			8.4.1.1	 Hypomagnesemia
			8.4.1.2	 Hypermagnesemia
			8.4.1.3	 Renal Magnesium Wasting
			8.4.1.4	 Familial Hypomagnesemia with Hypercalciuria and Nephrocalcinosis (FHHNC)
			8.4.1.5	 Primary Aldosteronism
	8.5	 Metabolic Regulation, Functions, and Disorders of Sodium Metabolism
		8.5.1	 Metabolic Disorders of Sodium
			8.5.1.1	 Hyponatremia
			8.5.1.2	 Hypernatremia
			8.5.1.3	 Hypovolemia and Edema
			8.5.1.4	 Vomiting and Diarrhea
			8.5.1.5	 Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
			8.5.1.6	 Diabetes Insipidus
			8.5.1.7	 Addison’s Disease
	8.6	 Metabolic Regulation, Functions, and Disorders of Potassium Metabolism
		8.6.1	 Metabolic Disorders of Potassium
			8.6.1.1	 Hypokalemia
			8.6.1.2	 Hyperkalemia
			8.6.1.3	 Gitelman Syndrome
			8.6.1.4	 Bartter Syndrome
			8.6.1.5	 Medication Induced Disorder
			8.6.1.6	 Kidney Disease
			8.6.1.7	 Addison’s Disease
			8.6.1.8	 Diabetic Ketoacidosis
			8.6.1.9	 Acid-Base Disorders
			8.6.1.10	 Conn’s Syndrome (Primary Hyperaldosteronism)
			8.6.1.11	 Hereditary Periodic Paralysis
			8.6.1.12	 Hyperthyroid Periodic Paralysis
	8.7	 Metabolic Regulation, Functions, and Disorders of Chloride Metabolism
		8.7.1	 Metabolic Disorders of Chloride
			8.7.1.1	 Hypochloremia
			8.7.1.2	 Hyperchloremia
			8.7.1.3	 Cystic Fibrosis
			8.7.1.4	 Dehydration
			8.7.1.5	 Diabetic Ketoacidosis (DKA)
			8.7.1.6	 Renal Tubular Acidosis (RTA)
			8.7.1.7	 Addison’s Disease
			8.7.1.8	 Bartter Syndrome
	8.8	 Conclusions
	References
9: Metabolism of Essential Trace Elements and Associated Disorders
	9.1	 Introduction
	9.2	 Iron Metabolism
		9.2.1	 Systemic Iron Homeostasis
		9.2.2	 Recycling and Absorption
		9.2.3	 Circulating Iron
		9.2.4	 Cellular Iron Homeostasis
		9.2.5	 Disorders
			9.2.5.1	 Iron Deficiency
			9.2.5.2	 Iron Overload
			9.2.5.3	 Iron and Liver Disease
			9.2.5.4	 Iron and Diabetes Mellitus
			9.2.5.5	 Iron and Cardiovascular Disease
			9.2.5.6	 Iron and Neurodegenerative Diseases
			9.2.5.7	 Iron and Cancer
			9.2.5.8	 Iron and Kidney Disease
			9.2.5.9	 Iron and Bone Disorders
	9.3	 Iodine Metabolism
		9.3.1	 Iodine Trapping
		9.3.2	 Iodine Synthesis and Secretion
		9.3.3	 Oxidation of Iodine
		9.3.4	 Iodination of the Tyrosine
		9.3.5	 Secretion
		9.3.6	 Disorders
			9.3.6.1	 Iodine Deficiency Disorders (IDD)
				9.3.6.1.1 Goiter
			9.3.6.2	 Endemic Cretinism
	9.4	 Copper Metabolism
		9.4.1	 Absorption
		9.4.2	 Transportation and Secretion
		9.4.3	 Disorders
			9.4.3.1	 Menkes Disease (MD)
			9.4.3.2	 Wilson Disease
			9.4.3.3	 Occipital Horn Syndrome (OHS)
	9.5	 Fluoride Metabolism
		9.5.1	 Absorption
		9.5.2	 Distribution
		9.5.3	 Secretion
		9.5.4	 Excretion
		9.5.5	 Disorders
			9.5.5.1	 Dental Fluorosis
	9.6	 Zinc Metabolism
		9.6.1	 Zinc Transporters (ZnTs)
		9.6.2	 Role of Metallothionein
		9.6.3	 Homeostasis
		9.6.4	 Excretion
		9.6.5	 Disorders
			9.6.5.1	 Acrodermatitis Enteropathica (AE)
			9.6.5.2	 Total Parenteral Nutrition (TPN)
			9.6.5.3	 Penicillamine Therapy
			9.6.5.4	 Zinc and Growth
			9.6.5.5	 GI Disorders
	9.7	 Manganese (Mn) Metabolism
		9.7.1	 Absorption
		9.7.2	 Distribution and Regulation
		9.7.3	 Elimination
		9.7.4	 Disorders
			9.7.4.1	 HMNDYT1-SLC30A10 Deficiency
			9.7.4.2	 CDG2N-SLC39A8 Deficiency
	9.8	 Magnesium Metabolism
		9.8.1	 Absorption and Transport
		9.8.2	 Excretion
		9.8.3	 Disorders
			9.8.3.1	 Hypomagnesium
			9.8.3.2	 Hypermagnesium
	9.9	 Cobalt Metabolism
	9.10	 Chromium Metabolism
		9.10.1	 Absorption
		9.10.2	 Blood Transport
		9.10.3	 Excretion
	9.11	 Conclusions
	References
10: Enzymes and Their Clinical Applications
	10.1	 Introduction
	10.2	 Properties of Enzymes
		10.2.1	 Catalytic Properties
		10.2.2	 Specificity
		10.2.3	 Enzymes Regulation
	10.3	 Enzymes in Clinical Diagnosis
		10.3.1	 Bone Diseases
			10.3.1.1	 Alkaline Phosphatase (ALP)
			10.3.1.2	 Leukocyte Esterase
		10.3.2	 Autoimmune Disorders
			10.3.2.1	 Lysozyme
			10.3.2.2	 Gelatinase B
			10.3.2.3	 Tartrate-Resistant Acid Phosphatase (TRAP)
			10.3.2.4	 Cathepsin D
		10.3.3	 Cancer
		10.3.4	 Diabetes (Type 2)
		10.3.5	 Gaucher’s Disease (GD)
			10.3.5.1	 Symptoms of Gaucher Disease
			10.3.5.2	 Enzymes Used in Diagnosis of Gaucher Disease
		10.3.6	 Liver Diseases
			10.3.6.1	 Symptoms of Liver Disease
			10.3.6.2	 Enzymes Used in Diagnosis of Liver Diseases
				10.3.6.2.1 Alanine Transaminase (ALT)
				10.3.6.2.2 Aspartate Transaminase (AST)
				10.3.6.2.3 Alkaline Phosphatase (ALP)
				10.3.6.2.4 Gamma-Glutamyl Transferase (GGT)
		10.3.7	 Pancreatitis
			10.3.7.1	 Acute Pancreatitis
			10.3.7.2	 Chronic Pancreatitis
			10.3.7.3	 Symptoms of Pancreatitis
			10.3.7.4	 Enzymes Used in Diagnosis of Pancreatitis
				10.3.7.4.1 Serum and Urinary Amylase
				10.3.7.4.2 Lipase
		10.3.8	 Myocardial Infarction (MI)
			10.3.8.1	 Symptoms
			10.3.8.2	 Enzymes Used in Diagnosis of Myocardial Infarction
				10.3.8.2.1 Creatine Kinase (CK)
				10.3.8.2.2 Lactate Dehydrogenase
		10.3.9	 Renal Disorders
			10.3.9.1	 Chronic Kidney Disease (CKD)
			10.3.9.2	 Polycystic Kidney Disease (PKD)
			10.3.9.3	 IgA Nephropathy
			10.3.9.4	 Interstitial Nephritis
			10.3.9.5	 Lupus Nephritis
			10.3.9.6	 Glomerulonephritis (Glomerular Disease)
			10.3.9.7	 Symptoms of Renal Disorders
			10.3.9.8	 Enzymes Used in Diagnosis of Renal Disorders
	10.4	 Enzyme as Therapeutics
	10.5	 Factors Affecting Enzyme Activities
		10.5.1	 Concentration of Substrate
		10.5.2	 Effect of Temperature
		10.5.3	 Effect of pH
		10.5.4	 Effect of Activator
	10.6	 Advantages and Disadvantages of Use of Enzymes in Clinical Diagnosis
		10.6.1	 Advantages
		10.6.2	 Disadvantages
	10.7	 Future Prospectives and Challenges
	10.8	 Conclusions
	References
11: Hormonal Manifestations of Endocrine Diseases
	11.1	 Introduction
	11.2	 Pineal Gland
		11.2.1	 Pineal Gland Calcification
		11.2.2	 Seasonal Affective Disorder
		11.2.3	 Jet Lag and Shift Work Sleep Disorder
		11.2.4	 Pineal Gland Tumors
	11.3	 Thymus
		11.3.1	 Myasthenia Gravis
		11.3.2	 Thymic Carcinomas and Thymomas
	11.4	 Pituitary Gland and Hypothalamus
		11.4.1	 Kallmann Syndrome and Isolated/Idiopathic Hypogonadotropic Hypogonadism
		11.4.2	 Hypopituitarism
		11.4.3	 Hyperpituitarism
		11.4.4	 Pituitary Tumors
		11.4.5	 Diabetes Insipidus
		11.4.6	 Prolactinoma
		11.4.7	 Pituitary Apoplexy
		11.4.8	 Therapy for Pituitary Gland Disorders
	11.5	 Thyroid Gland
		11.5.1	 Hypothyroidism
		11.5.2	 Hyperthyroidism
		11.5.3	 Treatment and Management
	11.6	 Adrenal Glands
	11.7	 Pancreas
		11.7.1	 Clinical Significance of Insulin
		11.7.2	 Diabetes Mellitus
		11.7.3	 Hyperinsulinemia
		11.7.4	 Glucagon
	11.8	 Placenta and Pregnancy-Associated Endocrine Diseases
		11.8.1	 Gestational Diabetes Mellitus.
		11.8.2	 Pregnancy-Associated Endocrine Disorders
			11.8.2.1	 Preterm Labor and Birth
			11.8.2.2	 Pituitary Tumor in Pregnancy
			11.8.2.3	 Overt Thyroid Dysfunction
	11.9	 Gonads
	11.10	 Secondary Endocrine Organs
	11.11	 Additional Endocrine Cancers and the Role of Hormones in Cancer
	11.12	 Summary
	References
12: Biomolecular Components of Blood and Their Role in Health and Diseases
	12.1	 Introduction
	12.2	 Blood
		12.2.1	 Characteristics of Blood
		12.2.2	 Components of Blood
			12.2.2.1	 Blood Plasma
			12.2.2.2	 Plasma Proteins
				12.2.2.2.1 Albumin
				12.2.2.2.2 Globulins
				12.2.2.2.3 Fibrinogen
			12.2.2.3	 Erythrocytes
				12.2.2.3.1 Shape and Structure of Erythrocytes
				12.2.2.3.2 Hemoglobin
				12.2.2.3.3 Leukocytes and Platelets
					12.2.2.3.3.1 Classification of Leukocytes
						Granular Leukocytes
							Neutrophils
							Eosinophils
							Basophils
						Agranular Leukocytes
							Lymphocytes
							Monocytes
							Platelets
		12.2.3	 Functions of Blood
			12.2.3.1	 Transportation
			12.2.3.2	 Defense
			12.2.3.3	 Maintenance of Homeostasis
		12.2.4	 Complete Blood Count (CBC)
	12.3	 Blood and Its Related Diseases
		12.3.1	 Anemia
			12.3.1.1	 Iron Deficiency Anemia
			12.3.1.2	 Vitamin Deficiency Anemias
			12.3.1.3	 Hemolytic Anemias
			12.3.1.4	 Immune Hemolytic Anemia
			12.3.1.5	 Hereditary Spherocytosis
			12.3.1.6	 Sickle Cell Anemia
			12.3.1.7	 Thalassemia
			12.3.1.8	 Anemia of Chronic Disease
			12.3.1.9	 Aplastic Anemia
		12.3.2	 Multiple Myeloma
		12.3.3	 Thrombocytopenia
		12.3.4	 Disseminated Intravascular Coagulation (DIC)
		12.3.5	 Hemophilia
		12.3.6	 Myeloproliferative Neoplasms
			12.3.6.1	 Symptoms of Specific MPNs
		12.3.7	 Leukemia
			12.3.7.1	 Acute Lymphoblastic Leukemia (ALL)
			12.3.7.2	 Acute Myeloid Leukemia (AML)
			12.3.7.3	 Chronic Lymphocytic Leukemia (CLL)
			12.3.7.4	 Chronic Myeloid Leukemia (CML)
		12.3.8	 Lymphoma
	12.4	 Conclusions
	References
13: Free Radicals and Their Relation to Diseases and Protection Against Them
	13.1	 Introduction
		13.1.1	 Free Radicals
		13.1.2	 Types of Free Radicals
		13.1.3	 Formation of Free Radicals
			13.1.3.1	 Endogenous Formation of Free Radicals
			13.1.3.2	 Exogenous Generation of Free Radicals
	13.2	 Free Radicals Associated with DNA Damage
		13.2.1	 Superoxide Radical
		13.2.2	 Hydroxyl Radical
		13.2.3	 Alkoxyl Radical and Peroxyl Radical
		13.2.4	 Nitric Oxide and Nitrogen Dioxide
		13.2.5	 Peroxynitrite
		13.2.6	 Mechanism of Free Radical-Induced DNA Damage
	13.3	 Free Radicals and Lipid Peroxidation
		13.3.1	 Mechanism of Lipid Peroxidation
			13.3.1.1	 Initiation, Propagation, and Termination Phases
		13.3.2	 Consequences of Lipid Peroxidation
	13.4	 Free Radicals and Protein Damage
		13.4.1	 Oxidative Protein Damage
		13.4.2	 Nitrosative Protein Damage
		13.4.3	 Carbonyl Protein Damage
		13.4.4	 Fragmentation of Proteins Damage
		13.4.5	 Consequences of Protein Damage
			13.4.5.1	 Altered Protein Function
			13.4.5.2	 Protein Aggregation and Misfolding
	13.5	 Impact of Free Radicals and Its Relation to Various Metabolic Disorders
		13.5.1	 Cardiovascular Diseases
		13.5.2	 Neurodegenerative Diseases
		13.5.3	 Aging
		13.5.4	 Respiratory Diseases
	13.6	 Scavengers of Free Radicals
		13.6.1	 Antioxidant Enzymes
		13.6.2	 Non-enzymatic Antioxidants
	13.7	 Strategies to Mitigate Free Radicals Induced Damage
		13.7.1	 Antioxidant Therapies
		13.7.2	 Diet and Nutrition
		13.7.3	 Lifestyle Modifications
		13.7.4	 Antioxidant Supplementation
		13.7.5	 Modulation of Protein Quality Control
	13.8	 Conclusions and Future Perspective
	References
14: Clinical Biochemistry of Cancer
	14.1	 Introduction
	14.2	 Types of Cancer
	14.3	 Other Types of Cancer
		14.3.1	 Adenocarcinoma
			14.3.1.1	 Symptoms
				14.3.1.1.1 Breast Cancer
				14.3.1.1.2 Lung Cancer
				14.3.1.1.3 Pancreatic Cancer
				14.3.1.1.4 Colon Cancer
			14.3.1.2	 Treatment
			14.3.1.3	 Risk Factors
		14.3.2	 Skin Cancer
			14.3.2.1	 Symptoms
			14.3.2.2	 Treatment
			14.3.2.3	 Risk Factors
		14.3.3	 Squamous Cell Carcinoma
			14.3.3.1	 Symptoms
			14.3.3.2	 Treatment
			14.3.3.3	 Risk Factors
		14.3.4	 Sarcoma
			14.3.4.1	 Types of Sarcomas
				14.3.4.1.1 Bone Sarcomas
				14.3.4.1.2 Soft Tissue Sarcomas
			14.3.4.2	 Causes of Sarcoma
	14.4	 Characteristics of Cancer Development and Biomarkers
		14.4.1	 Cancer Biomarkers
		14.4.2	 Clinical Classification of Cancer Biomarkers
			14.4.2.1	 Screening and Diagnostic Biomarkers
			14.4.2.2	 Prognostic Biomarkers
			14.4.2.3	 Tumour Staging and Grading Systems
			14.4.2.4	 Predictive Biomarkers
	14.5	 General Aspects of Cancer
	14.6	 Oncogene and Tumour Suppressor Genes
		14.6.1	 Gene Variants/Mutations
		14.6.2	 Epigenetic Modifications
			14.6.2.1	 Gene Mutations and Variants
			14.6.2.2	 Changes in Epigenetics
	14.7	 Factors Responsible for Cancer Development
		14.7.1	 Coherent Factors/Environmental Contaminants
			14.7.1.1	 Radiation Exposure
			14.7.1.2	 Chemical Pollutants
			14.7.1.3	 Occupational Hazards
			14.7.1.4	 Endocrine-Disrupting Chemicals (EDC)
	14.8	 Stages of Cancer
	14.9	 Mechanisms of Action
	14.10	 Statistics: International and National
	14.11	 Multiple Omics Approaches in Cancer Research
	14.12	 Health and Toxicity
		14.12.1	 Carcinogenic Chemicals
		14.12.2	 PFOS and PFAS
	14.13	 Surgical Intervention for Cancer Treatment
		14.13.1	 Removal of Entire Tumours
		14.13.2	 Debulking Tumours
		14.13.3	 Reduction of Implications of Cancer Impact
		14.13.4	 Diagnostic Procedures
		14.13.5	 Staging and Assessment
		14.13.6	 Reconstruction and Rehabilitation
		14.13.7	 Combination with Other Treatments
	14.14	 Surgical Operations and Complications
		14.14.1	 Cryosurgery
		14.14.2	 Lasers
		14.14.3	 Hyperthermia
	14.15	 Salient Approaches for Effective Management of Critical Care Patients
		14.15.1	 Early Detection
			14.15.1.1	 Screening Programme
			14.15.1.2	 Genetic Testing
		14.15.2	 Prevention
		14.15.3	 Treatment
		14.15.4	 Supportive Care
	14.16	 Computational Toxicology and Its Benefit for Cancer Therapy
	14.17	 Artificial Intelligence (AI) and Cancer
		14.17.1	 Monitoring and Management of Cancer Patients
	14.18	 Forensic Issues with Cancer Patients
	14.19	 Spices as Potential Agents for Cancer Prevention and Treatment
	14.20	 Futuristic Approaches for Drug Delivery System
	14.21	 Conclusions
	References
15: Outbreak of Deadly Coronavirus (COVID-19) Pandemic: Diagnosis and Management
	15.1	 Introduction
	15.2	 Outbreak of COVID-19
	15.3	 Transmission Modes of SARS-CoV2 (COVID-19)
		15.3.1	 Droplets/Aerosol
		15.3.2	 Fomite Transmission
		15.3.3	 Saliva
		15.3.4	 Vertical Transmission
		15.3.5	 Conjunctival Transmission
		15.3.6	 Sexual Transmission
	15.4	 Structure of SARS-CoV-2
		15.4.1	 Spike(S) Protein
		15.4.2	 Nucleocapsid (N) Protein
		15.4.3	 Envelope Protein
		15.4.4	 Membrane (M) Glycoprotein
	15.5	 Clinical Manifestation
		15.5.1	 Host Immune Response
			15.5.1.1	 Innate Immune Response
			15.5.1.2	 Adaptive Immune Response
	15.6	 Diagnosis
		15.6.1	 Lateral Flow Immunoassay
			15.6.1.1	 Antigen Lateral Flow Tests
			15.6.1.2	 Antibody Lateral Flow Tests
		15.6.2	 Chest X-Ray
		15.6.3	 Chest CT Scan
		15.6.4	 RT-PCR
		15.6.5	 Serological Assay
		15.6.6	 CRISPER-Based Diagnosis
	15.7	 Treatments and Management of COVID-19
		15.7.1	 Antiviral Agents
			15.7.1.1	 Lopinavir/Ritonavir(LPV/r)
			15.7.1.2	 Remdesivir
			15.7.1.3	 Favipiravir
		15.7.2	 Antimalarial Drugs
		15.7.3	 COVID-19 Vaccines
			15.7.3.1	 Whole Virus Vaccine
			15.7.3.2	 Nucleic Acid Vaccines
			15.7.3.3	 Viral Vector Vaccines
			15.7.3.4	 Protein-Based Vaccines
		15.7.4	 Plasma Therapy
		15.7.5	 Cell-Based Therapy
	15.8	 Herbal Remedies
	15.9	 Lesson from COVID-19 Pandemic
		15.9.1	 Vaccine Development
		15.9.2	 Diagnostic Tools
		15.9.3	 Drug Discovery
		15.9.4	 Data Science and Bioinformatics
		15.9.5	 Vaccine Distribution
	15.10	 Strategies for Future Pandemics
	15.11	 Conclusion
	References
16: Techniques for the Identification and Characterization of Biomolecules
	16.1	 Introduction
	16.2	 Carbohydrates
		16.2.1	 Methods of Carbohydrate Extraction and Purification
		16.2.2	 Carbohydrate Purification and Detection Methods
	16.3	 Proteins, Antigens, Antibodies and Enzymes
		16.3.1	 Methods to Isolate and Purify Proteins
		16.3.2	 High-Throughput Methods to Detect Proteins/Amino Acids
	16.4	 Lipids
		16.4.1	 Pretreatments and Lipid Extraction
		16.4.2	 Lipid Detection and Quantification
	16.5	 Identification and Characterization of Nucleic Acids
		16.5.1	 Low- and High-Throughput Methods to Sequence Nucleic Acids
	16.6	 Conclusions
	References




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