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140912s2014 flua ob 001 0 eng d |
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|z (OCoLC)899156438
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|a 612.67
|2 23
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|a UAMI
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|a Valentine, R. C.
|q (Raymond Carlyle),
|d 1936-
|e author.
|1 https://id.oclc.org/worldcat/entity/E39PCjwvyjbryvqkV4MR3rPgBq
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|a Human longevity :
|b omega-3 fatty acids, bioenergetics, molecular biology, and evolution /
|c Raymond C. Valentine and David L. Valentine.
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264 |
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|a Boca Raton :
|b CRC Press,
|c 2014.
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300 |
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|a 1 online resource
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|a text
|b txt
|2 rdacontent
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|a still image
|b sti
|2 rdacontent
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|a computer
|b c
|2 rdamedia
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|a online resource
|b cr
|2 rdacarrier
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|a Includes bibliographical references and index.
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|a CIP data; item not viewed.
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|a Front Cover; Contents; Preface; Acknowledgments; About the Authors; Chapter 1: Mitochondrial Hypothesis of Aging Is Undergoing Revision; Chapter 2: Oxidative Stress Defined as a Deadly Free Radical-Mediated Chain Reaction : Case History of Paraquat; Chapter 3: Membranes of Deep-Sea Bacteria as Surrogates for Mitochondrial Membranes of Humans; Chapter 4: Protective Mechanisms for EPA Membranes in C. elegans and Their Relationship to Life Span.
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|a Chapter 5: Remarkable Longevity of Queens of Social Insects Likely Involves Dietary Manipulation to Minimize Levels of Polyunsaturates and Decrease Membrane PeroxidationChapter 6: Membrane Peroxidation Hypothesis Helps Explain Longevity in Birds, Rodents, and Whales; Chapter 7: Did Longevity Help Humans Become Super Humans?; Chapter 8: Mitochondrial Diseases and Aging Have Much in Common; Chapter 9: Revised Mitochondrial Hypothesis of Aging Highlights Energy Deficiency Caused by Errors of Replication (Mutations) of mtDNA; Chapter 10: Benefits of Polyunsaturated Mitochondrial Membranes.
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|a Chapter 11: Mitochondrial Membranes as a Source of Reactive Oxygen Species (ROS)Chapter 12: Mitochondrial Membranes as Major Targets of Oxidation; Chapter 13: Apoptosis Caused by Oxidatively Truncated Phospholipids Can Be Reversed by Several Mechanisms, Especially Enzymatic Detoxification; Chapter 14: Selective Targeting of HUFAs Away from Cardiolipin and Beta-Oxidation Combine to Protect Mitochondrial Membranes against Oxidative Damage; Chapter 15: Oxygen Limitation Protects Mitochondrial Phospholipids, Especially Cardiolipin.
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|a Chapter 16: Uncoupling Proteins (UCPs) of Mitochondria Purposely Waste Energy to Prevent Membrane DamageChapter 17: Mitochondrial Fission Protects against Oxidative Stress by Minting a Continuous Supply of Cardiolipin and Other Polyunsaturated Phospholipids; Chapter 18: Mitophagy Eliminates Toxic Mitochondria; Chapter 19: Longevity Genes Likely Protect Membranes; Chapter 20: Aging as a Cardiolipin Disease That Can Be Treated; Back Cover.
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|a More than 7 billion people inhabit the earth and all of them are subject to aging. This book is aimed at persons interested in a molecular explanation of how our cells age. Human Longevity: Omega-3 Fatty Acids, Bioenergetics, Molecular Biology, and Evolution is built on the proposition that we age as our mitochondria age. It suggests a revised version of Harman's famous hypothesis featuring mitochondrial oxidative and energy stresses as the root causes of aging. Human cells are protected from the ravages of aging by a battery of defensive systems including some novel mechanisms against membran.
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|a ProQuest Ebook Central
|b Ebook Central Academic Complete
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650 |
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|a Aging
|x Genetic aspects.
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|a Mitochondria.
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|a Oxidative stress.
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|a Omega-3 fatty acids
|x Health aspects.
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|a Docosahexaenoic acid.
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|a Cellular Senescence
|x physiology
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|a Docosahexaenoic Acids
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|a Mitochondria
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|a Oxidative Stress
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|a Vieillissement
|x Aspect génétique.
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|a Mitochondries.
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|a Stress oxydatif.
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|a Acide docosahexaénoïque.
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|a Docosahexaenoic acid
|2 fast
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|a Aging
|x Genetic aspects
|2 fast
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|a Mitochondria
|2 fast
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|a Omega-3 fatty acids
|x Health aspects
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|a Oxidative stress
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|a Valentine, David L.,
|e author.
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|i Print version
|z 9781466594869
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856 |
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|u https://ebookcentral.uam.elogim.com/lib/uam-ebooks/detail.action?docID=1604291
|z Texto completo
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|a BATCHLOAD
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|a Askews and Holts Library Services
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