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This Research Topic assembles original contributions and reviews from an international consortium of PIs related to interactions between pro-inflammatory cytokines and ion channels during acute lung injury and chronic heart failure.
Advances in itch research have elucidated differences between itch and pain but have also blurred the distinction between them. There is a long debate about how somatic sensations including touch, pain, itch, and temperature sensitivity are encoded by the nervous system. Research suggests that each sensory modality is processed along a fixed, direct-line communication system from the skin to the brain. Itch: Mechanisms and Treatment presents a timely update on all aspects of itch research and the clinical treatment of itch that accompanies many dermatological conditions including psoriasis, neuropathic itch, cutaneous t-cells lymphomas, and systemic diseases such as kidney and liver disease and cancer. Composed of contributions from distinguished researchers around the world, the book explores topics such as: Neuropathic itch Peripheral neuronal mechanism of itch The role of PAR-2 in neuroimmune communication and itch Mrgprs as itch receptors The role of interleukin-31 and oncostatin M in itch and neuroimmune communication Spinal coding of itch and pain Spinal microcircuits and the regulation of itch Examining new findings on cellular and molecular mechanisms, the book is a compendium of the most current research on itch, its prevalence in society, and the problems associated with treatment.
Volume I.A An outbreak of a respiratory disease first reported in Wuhan, China in December 2019 and the causative agent was discovered in January 2020 to be a novel betacoronovirus of the same subgenus as SARS-CoV and named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Coronavirus disease 2019 (COVID-19) has rapidly disseminated worldwide, with clinical manifestations ranging from mild respiratory symptoms to severe pneumonia and a fatality rate estimated around 2%. Person to person transmission is occurring both in the community and healthcare settings. The World Health Organization (WHO) has recently declared the COVID-19 epidemic a public health emergency of international concern. The ongoing outbreak presents many clinical and public health management challenges due to limited understanding of viral pathogenesis, risk factors for infection, natural history of disease including clinical presentation and outcomes, prognostic factors for severe illness, period of infectivity, modes and extent of virus inter-human transmission, as well as effective preventive measures and public health response and containment interventions. There are no antiviral treatment nor vaccine available but fast track research and development efforts including clinical therapeutic trials are ongoing across the world. Managing this serious epidemic requires the appropriate deployment of limited human resources across all cadres of health care and public health staff, including clinical, laboratory, managerial and epidemiological data analysis and risk assessment experts. It presents challenges around public communication and messaging around risk, with the potential for misinformation and disinformation. Therefore, integrated operational research and intervention, learning from experiences across different fields and settings should contribute towards better understanding and managing COVID-19. This Research Topic aims to highlight interdisciplinary research approaches deployed during the COVID-19 epidemic, addressing knowledge gaps and generating evidence for its improved management and control. It will incorporate critical, theoretically informed and empirically grounded original research contributions using diverse approaches, experimental, observational and intervention studies, conceptual framing, expert opinions and reviews from across the world. The Research Topic proposes a multi-dimensional approach to improving the management of COVID-19 with scientific contributions from all areas of virology, immunology, clinical microbiology, epidemiology, therapeutics, communications as well as infection prevention and public health risk assessment and management studies.
Murray and Nadel’s Textbook of Respiratory Medicine has long been the definitive and comprehensive pulmonary disease reference. Robert J. Mason, MD now presents the fifth edition in full color with new images and highlighted clinical elements. The fully searchable text is also online at www.expertconsult.com, along with regular updates, video clips, additional images, and self-assessment questions. This new edition has been completely updated and remains the essential tool you need to care for patients with pulmonary disease. Consult this title on your favorite e-reader, conduct rapid searches, and adjust font sizes for optimal readability. Compatible with Kindle®, nook®, and other popular devices. Master the scientific principles of respiratory medicine and its clinical applications. Work through differential diagnosis using detailed explanations of each disease entity. Learn new subjects in Pulmonary Medicine including Genetics, Ultrasound, and other key topics. Grasp the Key Points in each chapter. Search the full text online at expertconsult.com, along with downloadable images, regular updates, more than 50 videos, case studies, and self-assessment questions. Consult new chapters covering Ultrasound, Innate Immunity, Adaptive Immunity, Deposition and Clearance, Ventilator-Associated Pneumonia. Find critical information easily using the new full-color design that enhances teaching points and highlights challenging concepts. Apply the expertise and fresh ideas of three new editors—Drs. Thomas R. Martin, Talmadge E. King, Jr., and Dean E. Schraufnagel. Review the latest developments in genetics with advice on how the data will affect patient care.
Many physiological conditions such as host defense or aging and pathological conditions such as neurodegenerative diseases, and diabetes are associated with the accumulation of high levels of reactive oxygen species and reactive nitrogen species. This generates a condition called oxidative stress. Low levels of reactive oxygen species, however, which are continuously produced during aerobic metabolism, function as important signaling molecules, setting the metabolic pace of cells and regulating processes ranging from gene expression to apoptosis. For this book we would like to recruit the experts in the field of redox chemistry, bioinformatics and proteomics, redox signaling and oxidative stress biology to discuss how organisms achieve the appropriate redox balance, the mechanisms that lead to oxidative stress conditions and the physiological consequences that contribute to aging and disease.
Ion channel dysfunction in humans leads to impairment of the excitable processes necessary for the normal function of several tissues, such as muscle and brain. It follows that an increasing number of human diseases have been associated with malfunctioning ion channels, many of which have a genetic component. This volume of Advances in Genetics presents a broad and comprehensive overview of the inherited channelopathies in humans, including clinical, genetic and molecular aspects of these conditions. Keeping true to the scope of the serial, novel genomic and modeling research approaches and a review of potential therapeutic approaches for each of these conditions are also incorporated.
Bacterial pathogenicity factors are functionally diverse. They may facilitate the adhesion and colonization of bacteria, influence the host immune response, assist spreading of the bacterium by e.g. evading recognition by immune cells, or allow bacteria to dwell within protected niches inside the eukaryotic cell. Exotoxins can be single polypeptides or heteromeric protein complexes that act on different parts of the cells. At the cell surface, they may insert into the membrane to cause damage; bind to receptors to initiate their uptake; or facilitate the interaction with other cell types. For example, bacterial superantigens specifically bind to major histocompatibility complex (MHC) II molecules on the surface of antigen presenting cells and the T cell receptor, while cytolysins cause pore formation. For intracellular activity, exotoxins need to be translocated across the eukaryotic membrane. Gram-negative bacteria can directly inject effector proteins in a receptor-independent manner by use of specialized needle apparatus such as bacterial type II, III, or type IV secretion systems. Other methods of translocation include the phagocytic uptake of bacteria followed by toxin secretion, or receptor-mediated endocytosis which allows the targeting of distinct cell types. Receptor-based uptake is initiated by the binding of heteromeric toxin complexes to the cell surface and completed by the translocation of the effector protein(s) across the endosomal membrane. In the cytosol, toxins interact with specific eukaryotic target proteins to cause post-translational modifications that often result in the manipulation of cellular signalling cascades and inflammatory responses. It has become evident that the actions of some bacterial toxins may exceed their originally assumed cytotoxic function. For example, pore-forming toxins do not only cause cytolysis, but may also induce autophagy, pyroptosis, or activation of the MAPK pathways, resulting in adjustment of the host immune response to infection and modification of inflammatory responses both locally and systemically. Other recently elucidated examples of the immunomodulatory function of cell death-inducing exotoxins include TcdB of Clostridium difficile which activates the inflammasome through modification of cellular Rho GTPases, or the Staphyloccocus d-toxin which activates mast cells. The goal of this research topic was to gather current knowledge on the interaction of bacterial exotoxins and effector proteins with the host immune system. The following 16 research and review articles in this special issue describe mechanisms of immune modification and evasion and provide an overview over the complexity of bacterial toxin interaction with different cells of the immune system.