Complex and unexplained phenomena tend to foster unorthodox perspectives. This publication is an example, as is a prior publication that emphasized the concept that intermediary metabolism might play a significant and determining role in hepatocyte proliferation and 1 tumorigenesis. Formulation of this hypothesis was based on an attempt to clarify several poorly understood phenomena; including the observations: 1) that xenobiotic peroxisome proliferators such as the fibrate hypolipidemic agents induce hepatocyte proliferation and carcinogenesis in rodents; 2) that benign and malignant liver tumors complicate the human syndrome of glycogen storage disease type I (glucose-6-phosphatase deficiency); and 3) that in this same syndrome, administration of glucose exerts an anti-tumor effect. Fatty acid and glucose metabolism are tightly linked in a we- established and profoundly inportant interplay. This connection, together with the fact that peroxisome proliferator-induced hepatocyte proliferation and carcinogenesis reflects inhibition of mitochondrial carnitine palmitoyltransferase-I and fatty acid oxidation, suggested the possibility that regulation of fatty acid metabolism could prove to be a pivotal determinant in the control of cell growth. In 1993, the year in which the paper cited above was published, insight into the importance of growth factors and signal transduction pathways in cell cycle regulation was increasing rapidly, but metabolic and energetic aspects of cell proliferation had attracted relatively little attention. Despite this, the concept seemed inescapable that the two seemingly distinct and unrelated determinants — signal transduction and metabolism — were integrally linked.
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Robert K. Ockner, M.D., Professor of Medicine at the University of California, San Francisco, graduated from Pomona College and Harvard Medical School, and completed clinical and research training at Boston City Hospital, National Institutes of Health, and Massachusetts General Hospital. He is former Director of the UCSF Division of Gastroenterology and the UCSF Liver Center, and served as Editor of Gastroenterology, Co-Editor of Progress in Liver Diseases, and Associate Editor of the Journal of Lipid Research. He and colleagues initially identified and characterized the cytosolic fatty acid binding proteins.
INTEGRATION OF METABOLISM,
ENERGETICS, AND SIGNAL TRANSDUCTION
Unifying Foundations in Cell Growth and Death, Cancer,
Atherosclerosis, and Alzheimer Disease
ROBERT K. OCKNER
"Dr. Ockner has written a fascinating and original book which explores potential metabolic links to neurodegeneration. He takes a fresh look at metabolic pathways involving interaction between astrocyte and neuron that are important for brain health and may play a significant role in the pathogenesis of Alzheimer disease and other normal and pathological phenomena. Dr. Ockner has a distinguished research career in fatty acid metabolism and the fatty acid binding proteins and writes with clarity upon this under-explored aspect of the brain in health and disease. Not only is his book important for understanding links between systemic and cerebral metabolism in neurodegeneration, but is a must read for scientists with an interest in the connection between metabolic pathways and brain function."
— Dr. Bruce Miller,
Professor of Neurology
Clinical director of the Memory and Aging Center
University of California, San Francisco
"I find this book to be a commendable and comprehensive undertaking as it encompasses an evaluation of a wide area of scientific research. Researchers working in lipid metabolism to those interested in mitochondrial energetics and in the mechanisms of signal transduction pathways in cancer and Alzheimer disease will benefit from this book."
—M.A.Q. Siddiqui,
Professor and Chairman of the Department of Anatomy and Cell Biology
SUNY Downstate, Brooklyn, NY
Robert K. Ockner, M.D. is Professor of Medicine at the University of California, San Francisco, and is former Director of the UCSF Liver Center and Division of Gastroenterology. He and colleagues initially identified and characterized the cytosolic fatty acid binding proteins. He is a graduate of the Harvard Medical School and completed clinical and research training at Boston City Hospital, National Institutes of Health, and Massachusetts General Hospital.
Cover art by Sadie McFarlane
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Buch. Condizione: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -Complex and unexplained phenomena tend to foster unorthodox perspectives. This publication is an example, as is a prior publication that emphasized the concept that intermediary metabolism might play a significant and determining role in hepatocyte proliferation and 1 tumorigenesis. Formulation of this hypothesis was based on an attempt to clarify several poorly understood phenomena; including the observations: 1) that xenobiotic peroxisome proliferators such as the fibrate hypolipidemic agents induce hepatocyte proliferation and carcinogenesis in rodents; 2) that benign and malignant liver tumors complicate the human syndrome of glycogen storage disease type I (glucose-6-phosphatase deficiency); and 3) that in this same syndrome, administration of glucose exerts an anti-tumor effect. Fatty acid and glucose metabolism are tightly linked in a we- established and profoundly inportant interplay. This connection, together with the fact that peroxisome proliferator-induced hepatocyte proliferation and carcinogenesis reflects inhibition of mitochondrial carnitine palmitoyltransferase-I and fatty acid oxidation, suggested the possibility that regulation of fatty acid metabolism could prove to be a pivotal determinant in the control of cell growth. In 1993, the year in which the paper cited above was published, insight into the importance of growth factors and signal transduction pathways in cell cycle regulation was increasing rapidly, but metabolic and energetic aspects of cell proliferation had attracted relatively little attention. Despite this, the concept seemed inescapable that the two seemingly distinct and unrelated determinants - signal transduction and metabolism - were integrally linked. 416 pp. Englisch. Codice articolo 9780306484711
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Buch. Condizione: Neu. Neuware -Complex and unexplained phenomena tend to foster unorthodox perspectives. This publication is an example, as is a prior publication that emphasized the concept that intermediary metabolism might play a significant and determining role in hepatocyte proliferation and 1 tumorigenesis. Formulation of this hypothesis was based on an attempt to clarify several poorly understood phenomena; including the observations: 1) that xenobiotic peroxisome proliferators such as the fibrate hypolipidemic agents induce hepatocyte proliferation and carcinogenesis in rodents; 2) that benign and malignant liver tumors complicate the human syndrome of glycogen storage disease type I (glucose-6-phosphatase deficiency); and 3) that in this same syndrome, administration of glucose exerts an anti-tumor effect. Fatty acid and glucose metabolism are tightly linked in a we- established and profoundly inportant interplay. This connection, together with the fact that peroxisome proliferator-induced hepatocyte proliferation and carcinogenesis reflects inhibition of mitochondrial carnitine palmitoyltransferase-I and fatty acid oxidation, suggested the possibility that regulation of fatty acid metabolism could prove to be a pivotal determinant in the control of cell growth. In 1993, the year in which the paper cited above was published, insight into the importance of growth factors and signal transduction pathways in cell cycle regulation was increasing rapidly, but metabolic and energetic aspects of cell proliferation had attracted relatively little attention. Despite this, the concept seemed inescapable that the two seemingly distinct and unrelated determinants ¿ signal transduction and metabolism ¿ were integrally linked.Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg 416 pp. Englisch. Codice articolo 9780306484711
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Buch. Condizione: Neu. Druck auf Anfrage Neuware - Printed after ordering - Complex and unexplained phenomena tend to foster unorthodox perspectives. This publication is an example, as is a prior publication that emphasized the concept that intermediary metabolism might play a significant and determining role in hepatocyte proliferation and 1 tumorigenesis. Formulation of this hypothesis was based on an attempt to clarify several poorly understood phenomena; including the observations: 1) that xenobiotic peroxisome proliferators such as the fibrate hypolipidemic agents induce hepatocyte proliferation and carcinogenesis in rodents; 2) that benign and malignant liver tumors complicate the human syndrome of glycogen storage disease type I (glucose-6-phosphatase deficiency); and 3) that in this same syndrome, administration of glucose exerts an anti-tumor effect. Fatty acid and glucose metabolism are tightly linked in a we- established and profoundly inportant interplay. This connection, together with the fact that peroxisome proliferator-induced hepatocyte proliferation and carcinogenesis reflects inhibition of mitochondrial carnitine palmitoyltransferase-I and fatty acid oxidation, suggested the possibility that regulation of fatty acid metabolism could prove to be a pivotal determinant in the control of cell growth. In 1993, the year in which the paper cited above was published, insight into the importance of growth factors and signal transduction pathways in cell cycle regulation was increasing rapidly, but metabolic and energetic aspects of cell proliferation had attracted relatively little attention. Despite this, the concept seemed inescapable that the two seemingly distinct and unrelated determinants - signal transduction and metabolism - were integrally linked. Codice articolo 9780306484711
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