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The role of ROS/RNS signaling in cardiovascular functions and diseases is increasingly emerging in the last decades. The involvement of ROS/RNS in the control of a large number of cardiovascular functions like the regulation of the vascular tone, the control of blood pressure or myocyte excitation-contraction coupling and force development has been broadly investigated and in part clarified. On the other hand, many efforts have been focused in clarifying the redox mechanisms involved in cardiovascular diseases like ischemia/reperfusion injury, diabetes-associated cardiovascular dysfunctions, atherosclerosis or hypertension, just to mention the major ones. However, in most cases the two levels of investigation remain separate and not interlaced, failing in the attempt to provide a unified vision of the pathophysiologic mechanisms of cardiovascular diseases. The major aim of the Research Topic has been to collect original papers and review articles dealing with the issue from basic to translation research point of views. The topic includes contributions that highlight different interesting aspects of cardiovascular biology with an integrated approach useful for the development of new ideas and advancements in the field of redox signaling in the control of normal cardiovascular functions and their disruption in diseases.
This book presents current understanding of the importance of modern immunology in the etiopathogenesis of human diseases and explores how this understanding is impacting on diagnosis, prognosis, treatment, and prophylaxis. As the core of modern immunology, the “danger/injury model” is introduced and addressed throughout the book. Volume I of the book describes the network of damage-associated molecular pattern molecules (DAMPs) and examines the central role of DAMPs in cellular stress responses and associated regulated cell death, the promotion and resolution of inflammation, the activation of innate lymphoid cells and unconventional T cells, the stimulation of adaptive immunity, and tissue repair. The significance of DAMPs in a wide range of human diseases will then be explored in Volume II of the book, with discussion of the implications of injury-induced innate immunity for present and future treatments. This book is written for professionals from all medical and paramedical disciplines who are interested in the introduction of innovative data from immunity and inflammation research into clinical practice. The readership will include practitioners and clinicians such as hematologists, rheumatologists, traumatologists, oncologists, intensive care anesthetists, endocrinologists such as diabetologists, psychiatrists, neurologists, pharmacists, and transplantologists.
The authors also provide a comparative survey of the properties of genomes (genome size, gene families, synteny, and polymorphism) for prokaryotes as well as the main eukaryotic models.
This cutting-edge resource includes up-to-date information on zebrafish physiology and the tools used to study it, not only as a model species for studies of other vertebrates but with application for studies of human disease and aquatic toxicology. The utility of zebrafish for physiological research is based on several key features including i) a "fully" sequenced genome, ii) rapid (~3 month) generation times), iii) their capacity to produce large numbers of externally fertilized eggs, iv) optical transparency of embryos and larvae, and v) the applicability of reverse and forward genetics to assess gene function. Gene knockdown in embryos and the production of transgenic strains are now standard techniques being used to assess physiology. This book will be of keen interest not only to the typical readers of Fish Physiology but also to biomedical researchers, toxicologists and developmental biologists. - Integrates and synthesizes the biology of the zebrafish under one cover - Features contributions from the leading researchers in their fields - Reaches a wider audience of researchers and biologists with its broad inclusion of subjects relating to zebrafish physiology
This is the premier, single-source reference on redox biochemistry, a rapidly emerging field. This reference presents the basic principles and includes detailed chapters focusing on various aspects of five primary areas of redox biochemistry: antioxidant molecules and redox cofactors; antioxidant enzymes; redox regulation of physiological processes; pathological processes related to redox; and specialized methods. This is a go-to resource for professionals in pharmaceuticals, medicine, immunology, nutrition, and environmental fields and an excellent text for upper-level students.
Molecular biology has driven a powerful reductionist, or “molecule-c- tric,” approach to biological research in the last half of the 20th century. Red- tionism is the attempt to explain complex phenomena by defining the functional properties of the individual components of the system. Bloom (1) has referred to the post-genome sequencing era as the end of “naïve reductionism. ” Red- tionist methods will continue to be an essential element of all biological research efforts, but “naïve reductionism,” the belief that reductionism alone can lead to a complete understanding of living organisms, is not tenable. Organisms are clearly much more than the sum of their parts, and the behavior of complex physiological processes cannot be understood simply by knowing how the parts work in isolation. Systems biology has emerged in the wake of genome sequencing as the s- cessor to reductionism (2–5). The “systems” of systems biology are defined over a wide span of complexity ranging from two macromolecules that interact to carry out a specific task to whole organisms. Systems biology is integrative and seeks to understand and predict the behavior or “emergent” properties of complex, multicomponent biological processes. A systems-level characteri- tion of a biological process addresses the following three main questions: (1) What are the parts of the system (i. e.
Methodology and applications of redox proteomics The relatively new and rapidly changing field of redox proteomics has the potential to revolutionize how we diagnose disease, assess risks, determine prognoses, and target therapeutic strategies for people with inflammatory and aging-associated diseases. This collection brings together, in one comprehensive volume, a broad array of information and insights into normal and altered physiology, molecular mechanisms of disease states, and new applications of the rapidly evolving techniques of proteomics. Written by some of the finest investigators in this area, Redox Proteomics: From Protein Modifications to Cellular Dysfunction and Diseases examines the key topics of redox proteomics and redox control of cellular function, including: * The role of oxidized proteins in various disorders * Pioneering studies on the development of redox proteomics * Analytical methodologies for identification and structural characterization of proteins affected by oxidative/nitrosative modifications * The response and regulation of protein oxidation in different cell types * The pathological implications of protein oxidation for conditions, including asthma, cardiovascular disease, diabetes, preeclampsia, and Alzheimer's disease Distinguished by its in-depth discussions, balanced methodological approach, and emphasis on medical applications and diagnosis development, Redox Proteomics is a rich resource for all professionals with an interest in proteomics, cellular physiology and its alterations in disease states, and related fields.
This book describes how systems biology, pharmacogenomic and behavioral approaches, as applied to neurodevelopmental toxicology, provide a structure to arrange information in a biological model. Authors review and discuss approaches that can be used as effective tools to dissect mechanisms underlying pharmacological and toxicological phenomena associated with the exposure to drugs or environmental toxicants during development. This book presents cross-cutting research tools and animal models, along with applications to the studies associated with potential anesthetic-induced developmental neurotoxicity; the developmental basis of adolescent or adult onset of disease; risk assessment of methyl mercury and its effects on neurodevelopment; challenges in the field to identify environmental factors of relevance to autism; and the strategy and progress of epilepsy research.
This book provides a cutting-edge review of polyglutamine disorders. It primarily focuses on two main aspects: (1) the mechanisms underlying the pathologies’ development and progression, and (2) the therapeutic strategies that are currently being explored to stop or delay disease progression. Polyglutamine (polyQ) disorders are a group of inherited neurodegenerative diseases with a fatal outcome that are caused by an abnormal expansion of a coding trinucleotide repeat (CAG), which is then translated in an abnormal protein with an elongated glutamine tract (Q). To date, nine polyQ disorders have been identified and described: dentatorubral-pallidoluysian atrophy (DRPLA); Huntington’s disease (HD); spinal–bulbar muscular atrophy (SBMA); and six spinocerebellar ataxias (SCA 1, 2, 3, 6, 7, and 17). The genetic basis of polyQ disorders is well established and described, and despite important advances that have opened up the possibility of generating genetic models of the disease, the mechanisms that cause neuronal degeneration are still largely unknown and there is currently no treatment available for these disorders. Further, it is believed that the different polyQ may share some mechanisms and pathways contributing to neurodegeneration and disease progression.
Protein degradation has been identified as a major mechanism for the regulation of cellular functions. Not surprisingly, its deregulation is implied in almost any pathological condition. This book describes how aged proteins are eliminated during cell metabolism, how cell proliferation is regulated by protein degradation and how its deregulation can contribute to the development of cancer, how protein degradation is modified during normal and abnormal aging, in particular with regard to Alzheimer's disease and other degenerative diseases of the brain and central nervous system. Attempts aiming at correcting these pathologies by interfering with deviations of the normal pathway of protein degradation are also treated.