Our understanding of the function of natural killer (NK) cells has dramatically changed in recent years. The discovery of NK receptors specific for MHC class I molecules, and the study of the role of co-stimulatory and adhesion molecules have led to an understanding of how NK cells recognize tumor and virally infected cells that have lost expression of MHC class I molecules or have altered distribution of normal cell surface molecules. Such recognition events lead to intracellular signals which can be either stimulatory or inhibitory. This book provides an insight into how NK cells develop, how they learn to distinguish altered cells from normal cells, and into their biological role in controlling infections and tumors.

At first glance the destruction of a target cell by a killer cell seems to be a simple endeavor. A closer look, however, reveals the complex mechanisms underlying this task. Killer cells are able to specifically recognize altered or infected cells. A transient contract with target cells has to be established to allow the delivery of lethal molecules or signals. The killer cell then disengages from the damaged cell and moves away to kill other target cells. After the eradication of the target cells, the number or activity of activated killer cells has to be reduced to avoid nonspecific killing of innocent cells. In 1992, Herman Eisen concluded, in his introductory remarks in the most recent volume on lymphocyte cytotoxicity (EISEN 1993): "Given the immense amount of effort made in the past decade to understand these (lytic) mechanisms, it seems surprising that a consensus about the principal mechanisms has not been reached." Since that time, advances made in the field of cell-mediated cytolysis are so significant that our knowledge regarding the lytic mechanisms has been considerably augmented. Much of this is due to studies with transfectants and mutants-either naturally occurring or generated by gene targeting. It is now clear that there are two predominant pathways which act hand in hand and lead to efficienttarget cell destruction.

Current Topics in Membranes provides a systematic, comprehensive, and rigorous approach to specific topics relevant to the study of cellular membranes. Each volume is a guest edited compendium of membrane biology. This series has been a mainstay for practicing scientists and students interested in this critical field of biology. Articles covered in the volume include ENaC Proteins in Vascular Smooth Muscle Mechanotransduction; Regulation of the Mechano-Gated K2P Channel TREK-1 by Membrane Phospholipids; MechanoTRPs and TRPA1; TRPC; The Cytoskeletal Connection to Ion Channels as a Potential Mechanosensory Mechanism. Lessons From Polycystin-2 (TRPP2); Lipid Stress at Play: Mechanosensitivity of Voltage-Gated Channels; Hair Cell Mechanotransduction: The Dynamic Interplay between Structure and Function; Pharmacology of Hair Cell MS Channels; Hair Cell Mechanotransduction; Models of Hair Cell Mechanotrasduction; Touch; Mechanosensitive Ion Channels in Dystrophic Muscle; Mechanotransduction in Endothelial Cells;MS Channels in Tumor Cell Migration; Mechanosensitive Channels in Regulating Smooth Muscle Contraction in the GI; Mechanosensitive Ion Channels in Blood-Pressure-Sensing Baroreceptor Neurons.

In this manuscript, practitioners and students who are concerned with sports and rehabilitation medicine, kinesiology, as well as coaches and athletes, are introduced to numerous concepts, including mechanotransduction, inflammation, pro- and anti-inflammatory cytokines, calpains, the extracellular matrix, neutrophils and macrophages, and their relevance to stretching, particularly stretching intensity. Although the quantitative parameters of training, duration, and frequency are important, it is the qualitative criterion of intensity (“how much”) that the author suggests is ultimately of greater concern. Intensity, the rate and magnitude of force, may be responsible for the proper recovery, regeneration, and adaptation of the musculoskeletal tissues from training, competition, or rehabilitation from injuries. Research suggests that too much force results in the stimulation of an inflammatory response, one associated with a biochemical feedback emerging from a mechanical stimulus. The intent of this manuscript is twofold: to initiate the discussion of the importance of stretching intensity with regard to proper recovery, regeneration, and adaptation, and to suggest that researchers need to explore its potential role in addressing numerous inflammatory (RA) and non-inflammatory (OA, recurrent tendinitis etc.) musculoskeletal conditions as well.