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Diabetes: Oxidative Stress and Dietary Antioxidants, Second Edition, builds on the success of the first edition, covering updated research on the science of oxidative stress in diabetes and the potentially therapeutic usage of natural antioxidants in the diet and food matrix. The processes within the science of oxidative stress are not described in isolation, but rather in concert with other processes, such as apoptosis, cell signaling and receptor mediated responses. This approach recognizes that diseases are often multifactorial and oxidative stress is a single component of this. Since the publication of the first edition, the science of oxidative stress and free radical biology continues to rapidly advance with thousands of the research articles on the topic. New sections in this update cover the role of dietary advanced glycation end products (AGEs) in causing OS in diabetes, oxidative stress and diabetes-induced bone metabolism, and oxidative stress and diabetic foot ulcer. - Saves clinicians and researchers time in quickly accessing the very latest details on a broad range of diabetes and oxidation issues - Combines the science of oxidative stress and the putative therapeutic usage of natural antioxidants in the diet, its food matrix or plant - Includes preclinical, clinical and population studies to help endocrinologists, diabetologists, nutritionists, dieticians and clinicians map out key areas for research and further clinical recommendations
This book provides a contemporary resource on one of the major players in retinal diseases – the Retinal Pigment Epithelium (RPE). Throughout the book, the physiological and the pathological function of the RPE are covered on equal terms, to help readers to understand the RPE as a whole. Moreover, the development of RPE in diagnostics and therapy are covered, as well as some practical knowledge about RPE experimental models. Retinal Pigment Epithelium in Health and Disease highlights new findings of RPE research and includes the state-of-the-art knowledge of each RPE topic presented. This important feature sets this book apart from other publications, with the chapters following a design which leads from the general to the specific, to give a precise collection of the facts known. The chapters are written by well-known experts that are currently active in the field as consultants, basic scientists, and group leaders, providing expert guidance on the current aspects and future outlooks of this topic.
This book investigates the various processes that are affected by the age of an organism. Several new tools for the analysis of biological aging have been introduced recently, and this volume provides methods and protocols for these new techniques in addition to its coverage of established procedures. Researchers seeking new technology and techniques will find this volume of tremendous benefit as they move towards new directions.
Extracellular Vesicles, Volume 645 in the Methods in Enzymology series, continues the legacy of this premier serial with quality chapters authored by leaders in the field. Chapters in this new release include Genetic labeling of extracellular vesicle exosomes for studying biogenesis and uptake in living mammalian cells, Fluorescent Labeling of Extracellular Vesicles, Isolation of extracellular vesicles from lymph, Transgenic rats for tracking body fluid/tissue-derived extracellular vesicles, Isolation of amniotic extracellular vesicles, Urinary extracellular vesicle isolation, Immunocapture-based ELISA to Characterize and Quantify Extracellular Vesicles in Both Cell Culture Supernatants and Body Fluids, and much more. Provides the authority and expertise of leading contributors from an international board of authors Presents the latest release in the Methods in Enzymology series
The blinding diseases of inherited retinal degenerations have no treatments, and age-related macular degeneration has no cures, despite the fact that it is an epidemic among the elderly, with 1 in 3-4 affected by the age of 70. The RD Symposium will focus on the exciting new developments aimed at understanding these diseases and providing therapies for them. Since most major scientists in the field of retinal degenerations attend the biennial RD Symposia, they are known by most as the “best” and “most important” meetings in the field. The volume will present representative state-of-the-art research in almost all areas of retinal degenerations, ranging from cytopathologic, physiologic, diagnostic and clinical aspects; animal models; mechanisms of cell death; candidate genes, cloning, mapping and other aspects of molecular genetics; and developing potential therapeutic measures such as gene therapy and neuroprotective agents for potential pharmaceutical therapy. While advances in these areas of retinal degenerations will be described, there will be many new topics that either were in their infancy or did not exist at the time of the last RD Symposium, RD2014. These include the role of inflammation and immunity, as well as other basic mechanisms, in age-related macular degeneration, several new aspects of gene therapy, and revolutionary new imaging and functional testing that will have a huge impact on the diagnosis and following the course of retinal degenerations, as well as to provide new quantitative endpoints for clinical trials. The retina is an approachable part of the central nervous system (CNS), and there is a major interest in neuroprotective and gene therapy for CNS diseases and neurodegenerations, in general. It should be noted that with successful and exciting initial clinical trials in neuroprotective and gene therapy, including the restoration of sight in blind children, the retinal degeneration therapies are leading the way towards new therapeutic measures for neurodegenerations of the CNS. Many of the successes recently reported in these areas of retinal degeneration sprang from collaborations established at previous RD Symposia, and many of those will be reported at the RD2018 meeting and included in the proposed volume. We anticipate the excitement of those working in the field and those afflicted with retinal degenerations will be reflected in the volume.
The purpose of this Research Topic is to discuss the latest developments in aging and neurodegenerative diseases. Aging represents the major risk factor of the two most relevant neurodegenerative diseases Parkinson’s disease (PD) and Alzheimer’s disease (AD). It is generally accepted that symptoms of PD correlate with the severity of degeneration of dopaminergic substantia nigra neurons. In most cases neuronal loss during aging is not sufficient to cause clinical symptoms but only leads to a preclinical state of PD. However, in a small number of our population, neurodegeneration by aging gets accelerated by individual (e.g. brain injuries), environmental (e.g. toxins) and genetic (e.g. mutations of the alpha-synuclein gene) factors to reach the critical threshold for clinical symptoms during lifetime. Thus, neurodegeneration in PD appears to represent the common final pathway of “normal brain aging” and all other risk factors including genetics and the accumulation of the neurotoxic alpha-synuclein protein. While aging alone is generally agreed to be sufficient for at least the preclinical state of PD, the situation in AD seems to be different. Aging as the major and well documented risk factor of AD has been neglected for decades. Biochemical mechanisms of brain aging and the cognitive deficits of “normal brain aging” were seen as two not related and independent processes not related to AD. AD has always been characterized for decades by the presence of histopathological alterations (extracellular amyloid- containing plaques and intracellular tangles of hyperphosphorylated tau-protein), by neurodegeneration (synaptic deficits and finally neuronal loss), as well as by severe cognitive deficits clinically often accompanied by neuropsychiatric symptoms like delusions, as already described in the first famous patient Auguste D at the Psychiatric Hospital of Frankfurt. If or if not one or both of the two histopathological hallmarks play a causative role remains unclear until now. The discovery of homocygotic risk genes in most of the very rare (probably less than 1%) cases of early onset AD which share increased production of β-amyloid (Aβ) as one (but probably not the only one) common property led to the hypothesis of Aβ as the major causative factor for the development of AD. It was neglected that plaques density in the brain of AD patients did not correlate with presence and severity of clinical symptoms, while synaptic deficits did so even in first observations already published many years ago. Based on the Amyloid hypothesis, many drug treatments to remove Aβ plaques were developed. Even if all seemed to remove Aβ to some extent, all strategies failed to improve the symptoms of dementia. Thus, other concepts to explain the development of clinical symptoms of AD over time are needed. These should include the brain aging process not only as a statistical but also as a causative contributing factor. These concepts should not only relay on cell or animal models but should much more take into account the disease and the patients. A closer look at the situation in PD will certainly be helpful.
This book will contain the proceedings of the XIV International Symposium on Retinal Degeneration (RD2010), held July 13-17, 2010, in Mont-Tremblant, Quebec, Canada. The volume will present representative state-of-the-art research in almost all areas of retinal degenerations, ranging from cytopathologic, physiologic, diagnostic and clinical aspects; animal models; mechanisms of cell death; candidate genes, cloning, mapping and other aspects of molecular genetics; and developing potential therapeutic measures such as gene therapy and neuroprotective agents for potential pharmaceutical therapy.