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Chronic inflammation predisposes to some forms of cancer and the host response to malignant disease shows several parallels with inflammation and wound healing. The cells involved in inflammation are detected in a range of common cancers, together with the inflammatory cytokines and members of the chemokine ligand/receptor systems. Neutralization or deletion of the gene for some inflammatory cytokines confers resistance to tumour induction and experimental metastasis. Over-expression of such cytokines in tumour cells may enhance malignant potential. Certain chemokines are likely to subvert antitumour immunity by favouring development of ineffective Type 2 responses. Tumour cells may even utilize chemokine receptors in homing to lymph nodes and other organs. Thus, the cells, cytokines and chemokines found in tumours are more likely to contribute to tumour growth, progression and immunosuppression than they are to mount an effective host antitumour response. This book draws together contributions from an international group of scientists and clinicians from diverse disciplines, ranging from epidemiology to immunology, cell biology, molecular oncology, molecular medicine and pharmacology to debate these and related issues. Topics covered include the epidemiological links between cancer and inflammation, the parallels between inflammation and cancer, the role of inflammation in cancer, inflammatory genes as risk factors for cancer initiation and progression, inflammation and cancer angiogenesis, and preventative and therapeutic strategies. Related Novartis Foundation symposia: 252 Generation and Effector Functions of Regulatory Lymphocytes Chair: Jean-François Bach 254 Immunoinformatics: Bioinformatic Strategies for Better Understanding of Immune Function Chair: Hans-Georg Rammensee

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Inflammatory bowel disease (IBD) comprises a group of idiopathic diseases of the intestine characterized by chronic inflammation of the bowel with periods of exacerbation and remission. Although the exact cause of IBD remains undetermined, the condition appears to be related to a combination of genetic and environmental factors resulting in an aberrant activation of the mucosal immune system. This book contains a series of interdisciplinary discussions between clinical and basic scientists focusing on key issues such as: Epithelial cell and molecular biology, including apoptosis, necrosis and cell survival The role of bacterial milieu and mucosal bacteria in the IBD and of prebiotic and probiotic therapy The progress towards the identification of susceptibility genes and phenotype-determining genes The pharmacogenetics of IBD Mucosal immunology and therapeutic strategies stemming therefrom

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Drawing together contributions from a diverse group of international experts in the field, this collection of papers examines the biology and pathology of elastin at the molecular level. Topics include the structure, ultrastructure and function of elastin; elastin regulation; elastin's role in aging, lung development and disease and atherosclerosis; as well as related aspects of pharmacology and nutrition.

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The ability at the molecular level to keep track of time is a property shared by organisms ranging from the simplest unicells to humans. The primary feature of these biological clocks is their ability to entrain to environmental stimuli. The dominant stimulus comes from environmental light cues, which requires the existence of photopigments sensitive to light. The exact identity of the molecules involved in circadian photoreception has remained elusive. The classical view of the circadian system is of diverse physiological rhythms regulated by a centralized clock structure. This book presents evidence that challenges this view. Experiments in both vertebrate and invertebrate systems demonstrate that the circadian timing system is dispersed throughout the animal and suggest that possibly every cell contains an autonomous clock mechanism. A variety of tissues and cells contain have been shown to maintain an oscillation when placed in vitro and removed from any external cues or signals that originate from the classical clock structures and/or the environment. This book draws together contributions from an international and interdisciplinary group of experts whose work is focused on all aspects of the topic. Coverage includes the mechanisms of light signalling to the vertebrate clock, the connections between central and peripheral clocks, circadian gene expression patterns and output pathways of clock mechanisms.

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Insect-Plant Interactions and Induced Plant Defence Chair: John A. Pickett, 1999 This book examines the sophisticated mechanisms that plants use to defend themselves against attack by insects and pathogens, focusing on the networks of plant signalling pathways that underlie these defences. In response to herbivory, plants release a complex blend of as many as 100 volatile chemicals, known as semiochemicals ('sign chemicals'). These act as an airborne SOS signal, revealing the presence of the herbivore to the predators and parasitoids that are its natural enemies. Plants also have endogenous defence mechanisms that can be induced in response to pathogens, and separate chapters deal with systemic acquired resistance, phytoalexins, and the interacting pathways in pathogen and pest resistance. The book discusses underlying biochemical mechanisms by which plant stress leads to the biosynthesis of chemical signals from pools of secondary metabolite precursors, or even from the primary metabolism source. Finally, consideration is given to the possibilities for exploiting these signalling pathways by plant molecular genetics. The use of plant signals and their analogues to switch on defence pathways in crop plants is covered in depth. Bringing together contributions from entomologists, chemical ecologists, molecular biologists and plant physiologists this book is truly interdisciplinary, and will be essential reading for anyone with an interest in agricultural pest control.

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This book brings together contributions from key investigators in the area of Transient Receptor Potential (TRP) channel structure and function. It covers the structure, function and regulation of mammalian TRP channels and mechanisms of signal transduction. The discussions indicate research that would improve understanding of the role of TRP channels in normal cellular physiology, the involvement of TRP channels in disease states and their potential use as molecular targets for novel therapeutic agents.

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This book draws together contributions from cell and developmental biologists, structural biologists, geneticists and clinical scientists aimed at a better understanding of the cellular and molecular basis of these diseases. Topics include: How nuclear structure and location within a nucleus affect gene expression Chromatin organization and cell differentiation The nature of the interactions between the nuclear envelope and the cytoskeleton The extent to which the cytoskeleton mediates communication between the cell membrane and nucleus in regulating gene expression and whether disruption of such communication might underlie the disease processes It is hoped that a better understanding of the mechanisms leading to disease pathogenesis may ultimately lead to more rational and appropriate treatments.

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Oxygen sensing is a key physiological function of many tissues, but the identity of the sensor, the signalling pathways linking the sensor to the effector, and the endpoint effector mechanisms are all subjects of controversy. This book evaluates the various mediators that have been proposed, including the mitochondria, NAD(P)H oxidases, cytochrome p450 enzymes, and direct effects on enzymes and ion channels. There has been a resurgence of interest in the role of mitochondria, based partly on the ability of mitochondrial inhibitors to mimic hypoxia, but there is little consensus concerning mechanisms. Some favour the view that the primary signalling event is a reduction in cell redox state and reactive oxygen species (ROS) due to general inhibition of the electron transport chain (ETC); others support a key role for complex III of the ETC and an increase in ROS generation, while others doubt either of these components is the key intermediary. All these hypotheses are discussed in the book, together with conceptual problems concerning the ability of mitochondria to respond to physiological hypoxia. The other area of controversy covered in the book is the identity of the endpoint effector(s). Some authors favour K+ channel inhibition, followed by depolarization and Ca2+ entry via L-type channels, while others propose that release of Ca2+ from intracellular stores, or capacitative Ca2+ entry and other voltage-independent pathways may be more important. The book also describes evidence for an endothelium-dependent Ca2+-sensitizing pathway involving Rho and possibly other kinases. While some of these differences can be attributed to variation between tissues, many must be related to differences in interpretation or methodology. In this book, experts in the field of acute oxygen sensing working in different tissues address these controversies and their possible origins, and discuss possible approaches whereby these controversies might be resolved. The book will be of great interest to all those working in fields where oxygen sensing is important, particularly cancer and wound healing, as well as researchers in drug discovery and biotechnology.

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ATP, the intracellular energy source, is also an extremely important cell–cell signalling molecule for a wide variety of cells across evolutionarily diverse organisms. The extracellular biochemistry of ATP and its derivatives is complex, and the multiple membrane receptors that it activates are linked to many intracellular signalling systems. Purinergic signalling affects a diverse range of cellular phenomena, including ion channel function, cytoskeletal dynamics, gene expression, secretion, cell proliferation, differentiation and cell death. Recently, this class of signalling molecules and receptors has been found to mediate communication between neurons and non-neuronal cells (glia) in the central and peripheral nervous systems. Glia are critical for normal brain function, development and response to injury. Neural impulse activity is detected by glia and purinergic signalling is emerging as a major means of integrating functional activity between neurons, glia and vascular cells in the nervous system. These interactions mediate effects of neural activity on the development of the nervous system and in association with injury, neurodegeneration, myelination and cancer. Bringing together contributions from experts in diverse fields, including glial biologists, neurobiologists and specialists in purinergic receptor structure and pharmacology, this book considers how extracellular ATP acts to integrate communication between different types of glia, and between neurons and glia. Beginning with an overview of glia and purinergic signalling, it contains detailed coverage of purine release, receptors and reagents, purinergic signalling in the neural control of glial development, glial involvement in information processing, and discussion of the interactions between neurons and microglia.

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Many different pathological conditions are currently under investigation as therapeutic targets of purines including cancer, cardiovascular conditions, behavioural disorders, inflammation, immunoregulation, and neuroendocrine function. This book draws together research on all aspects of P2 purinoceptors and discusses their use in different therapeutic areas.

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