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"Anticarbohydrate antibodies provides a cohesive overview of current knowledge on the immunological recognition of carbohydrates by the adaptive immune system. The text provides fundamental insight needed for advancing clinically relevant diagnostics and therapeutic applications. "

"Many persons have a constellation of major risk/actors, life-habit risk factors, and emerging risk factors that constitute a condition called the Metabolic Syndrome. Eight components characteristic of the Metabolic Syndrome are: I. insulin resistance (with or without glucose intolerance), 2. hyperinsulinemia, 3. abdominal obesity, 4. raised blood pressure, 5. atherogenic dyslipidemia (T Triglyceride, T Postprandial lipemia, Small dense LDL or Type B pattern), 6. procoagulant state (t Fibrinogen, T PAI-1), 7. hyperuricemia, 8. endothelial dysfunction ft Albumin excretion rate, etc).Among the single etiologic factors being considered are: 1. a genetic defect in one or more components of the insulin action cascade leading to insulin resistance, 2. malnutrition during fetal development, and 3. abdominal obesity. It is possible that these three factors could be in some way interrelated. Several mechanisms implicated in the development of insulin resistance in obesity can be shortly postulated below. TNF-a oversecreted by the enlarged fat cells impairs insulin action by inhibiting insulin receptor signaling, possibly by increasing IRS-l serine phosphorylation GLUT-4 expression and translocation to the cell surface will be impaired by TNF-a.Leptin released from visceral adipocytes may inhibit insulin action in the liver by impairing insulin receptor signaling, leading to reduced down-regulation of PEPCK, the rate-limiting enzyme in gluconeogenesis. Glucose-stimulated insulin released from pancreatic fi-cell is also impaired by leptin through STAT-3 production stimulated by leptin via leptin receptor on the surface membrane of fl-cell, and then STAT-3 stimulates the opening of K+Arp-channels, and consequently insulin release will be inhibited.Resistin, as well as TNF-a and leptin released by adipocytes, decrease insulin sensitivity and to be suggested to inhibit adipogenesis; insulin administration rapidly increases resistin levels to normal in adipose tissue. Potential therapeutic beneficial effects of metformin for obesity and insulin resistance may be selectively categorized into 3 groups. In carbohydrate metabolism, metformin prevents pancreatic j3-cellfrom gluco-and lipotoxicity, increases insulin receptor binding, and increases insulin receptor tyrosine kinase (IRTK) activity.Metformin increases oral glucose-induced GLP-l amide levels in obese non-diabetic subjects; metformin is able to inhibit GLP-l degradation induced by dipeptidyl-peptidase IV. GLP-l is a gastrointestinal hormone, which stimulates insulin secretion and promotes satiety, and hence GLP-l and dipeptyl-peptidase IV-inhibitor can be proposed as therapeutic goals for the treatment of patients with Type 2-DM (T2DM) and obesity.In lipid metabolism, metformin may improve lipid profile. Several vasoprotective effects also belong to Metformin, f.e. 4. Hyperinsulinemia, J- Fibrinogen, -I PAl-I, -I FactorXHIa which functions to stabilize fibrin, 4- Platelet aggregation, i Capillary permeability, -I SMC-Fibroblast activity, and i Carbonyl stress (pathway to AGE formation).Conclusion: Obesity and insulin resistance are two major components of the metabolic syndrome, which predispose individuals to the development of T2DM and coronary heart disease. TNF-a and leptin, which are oversecreted by enlarged fat cells, play pivotal roles in the molecular defects of insulin action in obesity-linked insulin resistance. Pleio-tropic properties (vasoprotective effects) of metformin beyond carbohydrate and lipid effects may contribute to the beneficial therapeutic tools for obesity-linked insulin resistance."

"he book describes how the balance between pro- and anti-inflammatory molecules is related to health and disease. It is suggested that many diseases are initiated and their progress is influenced by inflammatory molecules and a decrease in the production and/or action of anti-inflammatory molecules and this imbalance between pro- and anti-inflammatory molecules seems to have been initiated in the perinatal period. This implies that strategies to prevent and manage various adult diseases should start in the perinatal period. An alteration in the metaolism of essential fatty acids and their anti-inflammatory molecules such as lipoxins, resolvins, protecitns, maresins and nitrolipids seems to play a major role in the pathobiology of several adult diseases. Based on these concepts, novel therapeutic approaches in the management of insulin resistance, obesity, type 2 diabetes mellitus, metabolic syndrome, cancer, lupus, rheumatoid arthritis and other auto-immune diseases are presented. Based on all these evidences, a unified concept that several adult diseases are due to an alteration in the balance between pro- and anti-inflammatory molecules is discussed and novel methods of their management are presented."

"This book is a collection of the most current practices relevant to the clinical molecular laboratorian. It begins with an introductory section on techniques and procedure. It then presents four separate sections on infectious disease, oncology, pre/post-natal, and identity testing, with specific chapters clearly outlining clinical protocols used in daily practice."

"Environmental toxicology is the third volume of a three-volume set on molecular, clinical and environmental toxicology that offers a comprehensive and in-depth response to the increasing importance and abundance of chemicals of daily life. By providing intriguing insights far down to the molecular level, this three-volume work covers the entire range of modern toxicology with special emphasis on recent developments and achievements. "

""Molecular Neuropharmacology offers a clear, thorough explanation of the molecular functioning of the nervous system in normal and disease states. More than three hundred full-color illustrations along with didactic text boxes provide an in-depth understanding of nerve cell receptors, their effectors and second messenger targets, and the molecular genetics that are often impacted by these systems. You will also learn how malfunction of these molecular systems relates to human disease and the corresponding medical treatment." "Molecular Neuropharmacology is the most relevant, well-written resource available to help you make the connection between neuropharmacology and clinical neuroscience."--BOOK JACKET."

"Molecular Neuropharmacology offers a clear, thorough explanation of the molecular functioning of the nervous system in normal and disease states. More than three hundred full-color illustrations along with didactic text boxes provide an in-depth understanding of nerve cell receptors, their effectors and second messenger targets, and the molecular genetics that are often impacted by these systems. You will also learn how malfunction of these molecular systems relates to human disease and the corresponding medical treatment." "Molecular Neuropharmacology is the most relevant, well-written resource available to help you make the connection between neuropharmacology and clinical neuroscience."--BOOK JACKET."