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The complement system is a multi-tasking gatekeeper of innate immunity thatintricately interacts with other key defense systems, such as the endothelial barrier,contact activation and coagulation systems, in maintaining tissue immunosurveillanceand homeostasis. Its rapid and forceful activation in the bloodstream not onlyensures the effective containment of microbial infections through potent cytolyticmechanisms, but also alerts the adaptive immune compartment to ensure the mountingof a proper humoral immune response against foreign antigens. However, there isa lurking ‘dark side’ that can lead complement astray, fueling a self-perpetuatingvicious cycle of inflammation, exuberant immune ...
Neuroinflammation is associated with a wide spectrum of acute and chronic diseases of the central and peripheral nervous system. It causes secondary damage, which is a major determinant for progression and outcome. Activated complement is suspected to be a key player to neuroinflammation. Complement is an important evolutionary ancient system for host anti-microbial aid. It serves the innate immunity and interfaces with the adaptive immunity. Complement recognizes non-cognate or altered-self antigens and devours 'unwanted' cells or cell compartments. Activation of complement leads to opsonisation of a target, inflammation by the release of anaphylatoxins, and damage of the target by the assembled membrane attack complex. Because complement can harm self-tissue, activation is tightly controlled by regulators. However, complement activation might be excessive and uncontrolled at sites of damage contributing to neuroinflammation leading to neurodegeneration.
This book equips dental care providers with a thorough understanding of the emerging therapies that promise to revolutionize the clinical management of periodontal diseases. Existing therapies targeted to the oral microbiome alone often fail to provide favorable clinical outcomes. Local inflammation and tissue destruction may persist and periodontal tissue regeneration is not predictably achieved. In recognition of these shortcomings, current research efforts are focused on understanding the biological interactions between the host and the resident microbiome and identifying key molecules and molecular pathways that can be used for more targeted, individualized therapies that will restrain oral inflammation and restore periodontal tissue homeostasis. This book introduces novel concepts and molecules that are currently being tested in preclinical and clinical models. Readers will find detailed information from leading experts on specific therapeutic strategies targeting the host immune and inflammatory system, the oral microbiome, and regeneration.
This is a revised and very expanded version of the previous second edition of the book. "Pharmacokinetic and Pharmacodynamic Data Analysis" provides an introduction into pharmacokinetic and pharmacodynamic concepts using simple illustrations and reasoning. It describes ways in which pharmacodynamic and pharmacodynamic theory may be used to give insight into modeling questions and how these questions can in turn lead to new knowledge. This book differentiates itself from other texts in this area in that it bridges the gap between relevant theory and the actual application of the theory to real life situations. The book is divided into two parts; the first introduces fundamental principles of ...
The third component of complement, C3, is one of the most versatile proteins and an important participant in immune surveillance and immune response pathways. Its multifunctio nality is based on its ability to interact specifically with multiple serum complement proteins, cell surface receptors, and mem brant;-associated regulatory proteins. One of its most intriguing strategies of interaction with cell surfaces is the covalent binding of activated C3 through the internal thioester. The field has expanded over the past 10 years and a wealth of information has accumulated. C3 from various species and many of the human C3 binding proteins have been cloned and expressed. Numerous cellular respo...
The first International Conference on Oral Mucosal Immunity and Microbiome (OMIM) aimed to highlight cutting-edge basic and translational research from an oral immunological and microbiological perspective. Oral diseases with a microbial etiology are the most prevalent chronic diseases of humans. Whilst not life-threatening, they can significantly compromise quality of life, are associated with increased risk for certain systemic diseases, and pose heavy financial burdens to national health systems. Hence, periodontal and peri-implant diseases, dental caries, root canal infections and mucosal infections are significant global public health problems. In this book global experts summarize and discuss the latest progress made in oral mucosal immunity and the oral microbiome. Target audience is basic and/or translational researchers with expertise in host immunity and microbiome research, and interest in oral health and disease. This volume provides a much needed quantum leap in the field, by joining forces to address gaps at the oral mucosal immunity-microbiome cross-talk.
The Mosaic of Autoimmunity: The Novel Factors of Autoimmune Diseases describes the multifactorial origin and diversity of expression of autoimmune diseases in humans. The term implies that different combinations of factors in autoimmunity produce varying and unique clinical pictures in a wide spectrum of autoimmune diseases. Most of the factors involved in autoimmunity can be categorized into four groups: genetic, immune defects, hormonal and environmental factors. In this book, the environmental factors are reviewed, including infectious agents, vaccines as triggers of autoimmunity, smoking and its relationship with rheumatoid arthritis, systemic lupus erythematosus, thyroid disease, multiple sclerosis and inflammatory bowel diseases. An entirely new syndrome, the autoimmune/inflammatory syndrome induced by adjuvants (ASIA), is also included, along with other diseases that are now recognized as having an autoimmune etiopathogenesis.