Endotoxins are potentially toxic compounds produced by Gram-negative bacteria including some pathogens. Unlike exotoxins, which are secreted in soluble form by live bacteria, endotoxins are comprised of structural components of bacteria. Endotoxins can cause a whole-body inflammatory state, sepsis, leading to low blood pressure, multiple organ dysfunction syndrome and death. This book brings together contributions from researchers in the forefront of these subjects. It is divided into two sections: the first dealing with how endotoxins are synthesized and end up on the bacterial surface. The second discussed how endotoxins activate the Toll-like receptor TLR4 and, in turn, how TLR4 generates the molecular signals leading to infectious and inflammatory diseases. The way endotoxins interact with the host cells is fundamental to understanding the mechanism of sepsis, and recent research on these aspects of endotoxins has served to illuminate previously undescribed functions of the innate immune system. This volume presents a description of endotoxins according to their genetic constitution, structure, function and mode of interaction with host cells.

The last few years have witnessed an explosion of both interest and knowledge about apoptosis, the process by which a cell actively commits suicide. The number of publications on the topic has increased from nothing in the early 1980s to more than 10,000 papers annually today. It is now well recognized that apoptosis is essential in many aspects of normal development and is required for maintaining tissue homeostasis. The idea that life requires death seems somewhat paradoxical, but cell suicide is essential for an animal to survive. For example, without selective destruction of "non-self" T cells, an animal would lack immunity. Similarly, meaningful neural connections in the brain are whittled from a mass of cells. Further, developmental cell remodeling during tissue maturation involves programmed cell death as the major mechanism for functional and structural safe transition of undifferentiated cells to more specialized counterparts. Apoptosis research, with roots in biochemistry, developmental and cell biology, genetics, and immunology, embraces this long-ignored natural law. Failure to properly regulate apoptosis can have catastrophic consequences. Cancer and many diseases (AIDS, Alzheimer's disease, Parkinson's disease, heart attack, stroke, etc. ) are thought to arise from deregulation of apoptosis. As apoptosis emerges as a key biological regulatory mechanism, it has become harder and harder to keep up with new developments in this field.

The subject for a volume on the fat-soluble vitamins needs no justification considering the importance of this group of nutrients and the rate of expan sion of our knowledge of its role in cell biology, genetics, and disease. The level of our understanding has clearly moved from knowing what fat soluble vitamins do to how they perform their functions. Hand in hand with a knowledge of their molecular mechanisms of action is the recognition that vitamins are used sparingly, and regeneration processes operate in certain cases to recycle vitamins from their metabolites. We have divided the volume into alphabetical sections beginning with vitamin A and the carotenoids through vitamins D, E, F, and K, and ending with coenzyme Q. The contributors are all acknowledged experts in their particular fields and have made significant contributions to published research results. All have worked assiduously to deliver the product of their labors on a restricted time scale and to provide the most up-to date information on their respective topics. We are truly grateful for their indulgence."

The fluid-mosaic model of membrane structure formulated by Singer and Nicolson in the early 1970s has proven to be a durable concept in terms of the principles governing the organization of the constituent lipids and proteins. During the past 30 or so years a great deal of information has accumulated on the composition of various cell membranes and how this is related to the dif ferent functions that membranes perform. Nevertheless, the task of explaining particular functions at the molecular level has been hampered by lack of struc tural detail at the atomic level. The reason for this is primarily the difficulty of crystallizing membrane proteins which require strategies that differ from those used to crystallize soluble proteins. The unique exception is bacteriorhodopsin of the purple membrane of Halobacterium halobium which is interpolated into a membrane that is neither fluid nor in a mosaic configuration. To date only 50 or so membrane proteins have been characterised to atomic resolution by diffraction methods, in contrast to the vast data accumulated on soluble proteins. Another factor that has been difficult to explain is the reason why the lipid compliment of membranes is often extremely complex. Many hundreds of different molecular species of lipid can be identified in some membranes. Remarkably, the particular composition of each membrane appears to be main tained within relatively narrow limits and its identity distinguished from other morphologically-distinct membranes.

The book is the first thorough overview of the first important steps to develop a worldwide virtual observatory so that, in the future, it could be easier to "dial-up" a part of the sky than wait many months to access a telescope. The articles in this book present details on the status of the first efforts to develop a standardized framework for the virtual observatory, including steps towards completion and deployment of technical infrastructure, uptake by data providers worldwide, and utilization by the scientific community.

Since its discovery in 1957, Coenzyme Q has piqued the interest of scientists from a wide range of disciplines because of its bioenergetics, vitamin-like behavior, and interactions with antioxidant vitamins E and C. Coenzyme Q: Molecular Mechanisms in Health and Disease is a comprehensive treatise on this often-studied coenzyme. International experts cover the research that led to its emergence as an exciting, new dietary supplement.

The present volume summarizes the latest developments in various areas of CoQ research. New concepts on extramitochondrial functions of CoQ are discussed in two chapters, while recent discoveries in biosynthetic pathways for CoQ based on molecular genetic approaches are presented in another chapter.

Further chapters explore the role of CoQ as an antioxidant, revealing the need for additional research in this exciting area.

This book will be of extreme interest to biochemists, biophysicists, molecular and cell biologists, as well as nutritionists and biomedical health workers.

The book is the first thorough overview of the first important steps to develop a worldwide virtual observatory so that, in the future, it could be easier to "dial-up" a part of the sky than wait many months to access a telescope. The articles in this book present details on the status of the first efforts to develop a standardized framework for the virtual observatory, including steps towards completion and deployment of technical infrastructure, uptake by data providers worldwide, and utilization by the scientific community.

The subject for a volume on the fat-soluble vitamins needs no justification considering the importance of this group of nutrients and the rate of expan sion of our knowledge of its role in cell biology, genetics, and disease. The level of our understanding has clearly moved from knowing what fat soluble vitamins do to how they perform their functions. Hand in hand with a knowledge of their molecular mechanisms of action is the recognition that vitamins are used sparingly, and regeneration processes operate in certain cases to recycle vitamins from their metabolites. We have divided the volume into alphabetical sections beginning with vitamin A and the carotenoids through vitamins D, E, F, and K, and ending with coenzyme Q. The contributors are all acknowledged experts in their particular fields and have made significant contributions to published research results. All have worked assiduously to deliver the product of their labors on a restricted time scale and to provide the most up-to date information on their respective topics. We are truly grateful for their indulgence."

The last few years have witnessed an explosion of both interest and knowledge about apoptosis, the process by which a cell actively commits suicide. The number of publications on the topic has increased from nothing in the early 1980s to more than 10,000 papers annually today. It is now well recognized that apoptosis is essential in many aspects of normal development and is required for maintaining tissue homeostasis. The idea that life requires death seems somewhat paradoxical, but cell suicide is essential for an animal to survive. For example, without selective destruction of "non-self" T cells, an animal would lack immunity. Similarly, meaningful neural connections in the brain are whittled from a mass of cells. Further, developmental cell remodeling during tissue maturation involves programmed cell death as the major mechanism for functional and structural safe transition of undifferentiated cells to more specialized counterparts. Apoptosis research, with roots in biochemistry, developmental and cell biology, genetics, and immunology, embraces this long-ignored natural law. Failure to properly regulate apoptosis can have catastrophic consequences. Cancer and many diseases (AIDS, Alzheimer's disease, Parkinson's disease, heart attack, stroke, etc. ) are thought to arise from deregulation of apoptosis. As apoptosis emerges as a key biological regulatory mechanism, it has become harder and harder to keep up with new developments in this field.

Endotoxins are potentially toxic compounds produced by Gram-negative bacteria including some pathogens. Unlike exotoxins, which are secreted in soluble form by live bacteria, endotoxins are comprised of structural components of bacteria. Endotoxins can cause a whole-body inflammatory state, sepsis, leading to low blood pressure, multiple organ dysfunction syndrome and death. This book brings together contributions from researchers in the forefront of these subjects. It is divided into two sections. The first deals with how endotoxins are synthesized and end up on the bacterial surface. The second discussed how endotoxins activate TLR4 and, in turn, how TLR4 generates the molecular signals leading to infectious and inflammatory diseases. The way endotoxins interact with the host cells is fundamental to understanding the mechanism of sepsis, and recent research on these aspects of endotoxins has served to illuminate previously undescribed functions of the innate immune system. This volume presents a description of endotoxins according to their genetic constitution, structure, function and mode of interaction with host cells.