This volume deals with many of the recent advances made in uncovering the molecular and cellular basis of apoptosis and elaborates on how this accumulating knowledge is helping us to understand the significance of apoptosis in pathogenesis of diseases arising from inappropriate cell death. Further, mechanistic aspects of cell death and role of apoptosis in disease is covered.

The brain is the most complex organ in our body. Indeed, it is perhaps the most complex structure we have ever encountered in nature. Both structurally and functionally, there are many peculiarities that differentiate the brain from all other organs. The brain is our connection to the world around us and by governing nervous system and higher function, any disturbance induces severe neurological and psychiatric disorders that can have a devastating effect on quality of life. Our understanding of the physiology and biochemistry of the brain has improved dramatically in the last two decades. In particular, the critical role of cations, including magnesium, has become evident, even if incompletely understood at a mechanistic level. The exact role and regulation of magnesium, in particular, remains elusive, largely because intracellular levels are so difficult to routinely quantify. Nonetheless, the importance of magnesium to normal central nervous system activity is self-evident given the complicated homeostatic mechanisms that maintain the concentration of this cation within strict limits essential for normal physiology and metabolism. There is also considerable accumulating evidence to suggest alterations to some brain functions in both normal and pathological conditions may be linked to alterations in local magnesium concentration. This book, containing chapters written by some of the foremost experts in the field of magnesium research, brings together the latest in experimental and clinical magnesium research as it relates to the central nervous system. It offers a complete and updated view of magnesiums involvement in central nervous system function and in so doing, brings together two main pillars of contemporary neuroscience research, namely providing an explanation for the molecular mechanisms involved in brain function, and emphasizing the connections between the molecular changes and behavior. It is the untiring efforts of those magnesium researchers who have dedicated their lives to unraveling the mysteries of magnesiums role in biological systems that has inspired the collation of this volume of work.

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This book discusses properties of apoptosis and other cell death modalities in cancer pathogenesis and treatment. Its nine chapters discuss modulation of anti-tumor inflammatory and immune responses, effects on the tumor microenvironment, to strategies for improving pro-apoptotic therapies, mechanisms and implications for disease pathogenesis, axl and mer receptor tyrosine kinases, immunogenic apoptotic cell death and anti-cancer immunity and cancer cell death-inducing radiotherapy. This book places the onco-biology of apoptosis in clear and objective perspective through an expertly synthesized series of reviews. Apoptosis in Cancer Pathogenesis and Anti-cancer Therapy is a deft and thorough exploration of cutting-edge research in apoptosis and anti-cancer mechanisms from basic biology to oncology. It highlights a rapidly growing field within cancer research and is essential reading for oncologists, biochemists and advanced graduate students alike.

Apoptosis, or cell death, can be pathological, a sign of disease and damage, or physiological, a process essential for normal health. This book, with contributions from experts in the field, provides a timely compilation of reviews of mechanisms of apoptosis. The book is organized into three convenient sections. The first section explores the different processes of cell death and how they relate to one another. The second section focuses on organ-specific apoptosis-related diseases. The third section explores cell death in non-mammalian organisms, such as plants. This comprehensive text is a must-read for all researchers and scholars interested in apoptosis.

Clinical Perspectives and Targeted Therapies in Apoptosis: Drug Discovery, Drug Delivery, and Disease Prevention provides comprehensive coverage, from basic cell biology, to modern assessment techniques for apoptosis in all major disease areas. Chapters provide an introduction to the fundamentals of cell biology, biochemical mechanisms, and the pathophysiological consequences of apoptosis. In addition, the book covers the tools and techniques used to quantify apoptosis and the significance of apoptosis in drug discovery, drug delivery, and its applications in disease prevention. Finally, the book provides a comprehensive compilation of the apoptosis targeting drugs that recently underwent clinical trials. This combination of fundamentals, along with applications in drug discovery, drug delivery, and clinical research make this book a useful resource for those in both academia and industry who are engaged in pharmaceutical, biomedical and biotechnology research.

The Janeway's Immunobiology CD-ROM, Immunobiology Interactive, is included with each book, and can be purchased separately. It contains animations and videos with voiceover narration, as well as the figures from the text for presentation purposes.

This volume focuses on apoptotic and non-apoptotic programmed cell death, including necroptosis, pyroptosis, and ferroptosis, and presents recent findings in the field. It discusses the crucial role that apoptotic and non-apoptotic cell death play in various pathological conditions, such as skin diseases, inflammatory bowel diseases, and virus infections. Further, it highlights the mechanisms underlying the recognition and clearance of dead cells, and the subsequent biological responses triggered by phagocytosed macrophages and factors released from dying cells. Offering insights into cell death, it is a valuable resource for researchers and clinicians developing novel strategies to treat various diseases that are closely associated with cell death.