Pathophysiology of Ischemia-Reperfusion Injury and Use of Fingolimod in Cardioprotection is a deep examination into the mechanisms of myocardial ischemiareperfusion injury and role of fingolimod as a cardioprotective agent through its antioxidant, anti-apoptotic and anti-inflammatory effects. Dr. Ahmed explore the physiology and pathophysiology of myocardial metabolism under normal and ischemic conditions and focused on pharmacological cardioprotection. They provide a concise, yet rigorous discussion of Ischemia-Reperfusion Injury, Myocardial Ischemia during Circulatory Arrest, Myocardial Reperfusion, Myocardial Protection related to Ischemia-Reperfusion Injury and Role of Fingolimod in Cardioprotection.Pathophysiology of Ischemia-Reperfusion Injury and Use of Fingolimod in Cardioprotection is ideal for researchers, cardiovascular scientists, and clinical pharmacologists to further work in this challenging area and apply this knowledge to clinical trials for cardioprotection. - Provides detailed and critical analysis of the latest research in the field from molecular basis to potential clinical relevance - Examines the effect of fingolimod/sphingosine 1-phosphate in cardioprotection, pointing to future myocardial preventative strategies

For decades we have known that the overgrowth, hardening and scarring of tissues (so-called fibrosis) represents the final common pathway and best histological predictor of disease progression in most organs. Fibrosis is the culmination of both excess extracellular matrix deposition due to ongoing or severe injury, and a failure to regenerate. An inadequate wound repair process ultimately results in organ failure through a loss of function, and is therefore a major cause of morbidity and mortality in disease affecting both multiple and individual organs. Whilst the pathology of fibrosis and its significance are well understood, until recently we have known little about its molecular regulation. Current therapies are often indirect and non-specific, and only slow progression by a matter of months. The recent identification of novel therapeutic targets, and the development of new treatment strategies based on them, offers the exciting prospect of more efficacious therapies to treat this debilitating disorder. This Research Topic therefore compromises several up-to-date mini-reviews on currently known and emerging therapeutic targets for fibrosis including: the Transforming Growth Factor (TGF)-family; epigenetic factors; Angiotensin II type 2 (AT2) receptors; mineralocorticoid receptors; adenosine receptors; caveolins; and the sphingosine kinase/sphingosine 1-phosphate and notch signaling pathways. In each case, mechanistic insights into how each of these factors contribute to regulating fibrosis progression are described, along with how they can be targeted (by existing drugs, small molecules or other mimetics) to prevent and/or reverse fibrosis and its contribution to tissue dysfunction and failure. Two additional reviews will discuss various anti-fibrotic therapies that have demonstrated efficacy at the experimental level, but are not yet clinically approved; and the therapeutic potential vs limitations of stem cell-based therapies for reducing fibrosis while facilitating tissue repair. Finally, this Research Topic concludes with a clinical perspective of various anti-fibrotic therapies for cardiovascular disease (CVD), outlining limitations of currently used therapies, the pipeline of anti-fibrotics for CVD and why so many anti-fibrotic drugs have failed at the clinical level.

New updated edition first published with Cambridge University Press. This new edition includes 29 chapters on topics as diverse as pathophysiology of atherosclerosis, vascular haemodynamics, haemostasis, thrombophilia and post-amputation pain syndromes.

'Inflammation book' is published under the aegis of the Society of Inflammation Research, which is an endeavor to disseminate knowledge about inflammation. This book provides the latest information on cutting-edge research concerning inflammation, its fundamentals including the direct and indirect determinants, besides the advanced management protocols employed in clinical practice. This volume of the book deals with basic molecular aspects of antibody response in various inflammatory conditions like sepsis, organ transplantation, role of lipid metabolism in inflammation, followed by detailed description on certain disease entities caused due to inflammation. Each topic is dealt in detail i

This updated second edition of Acute Ischemic Stroke: Imaging and Intervention provides a comprehensive account of the state of the art in the diagnosis and treatment of acute ischemic stroke. The basic format of the first edition has been retained, with sections on fundamentals such as pathophysiology and causes, imaging techniques and interventions. However, each chapter has been revised to reflect the important recent progress in advanced neuroimaging and the use of interventional tools. In addition, a new chapter is included on the classification instruments for ischemic stroke and their use in predicting outcomes and therapeutic triage. All of the authors are internationally recognized experts and members of the interdisciplinary stroke team at the Massachusetts General Hospital and Harvard Medical School. The text is supported by numerous informative illustrations, and ease of reference is ensured through the inclusion of suitable tables. This book will serve as a unique source of up-to-date information for neurologists, emergency physicians, radiologists and other health care providers who care for the patient with acute ischemic stroke.

With upwards of 4.5 million deaths worldwide each year, and more than one tenth of these occurring in those with no previously documented heart disease, sudden arrhythmic death (SAD) is both a major public health burden and a highly emotive issue for society at large. Recent years have witnessed a marked expansion in our knowledge of the physiology underlying SAD, both in the context of hereditary and acquired cardiac disorders. Thanks largely to work in genetically modified animals, the growth in our understanding of mechanisms underlying arrhythmia in the hereditary channelopathies has been particularly marked. Our growing knowledge of the fundamental mechanisms underlying SAD has so far failed to spur substantial developments in clinical practice. Despite a large body of work in both humans and animals, it remains impossible to confidently identify those at high risk of SAD, making pre-emptive therapy a challenge. What is more, with the thankful exception of the implantable cardioverter-defibrillators and pharmacological agents in very specific situations, there has been depressingly little progress in finding new and effective therapies. This Research Topic aims to go some way towards bridging the gap between advances in basic science and the development and delivery of new therapies. It brings together original research contributions and review articles from key opinion leaders in the field, focusing on the direct clinical implications of the basic science research now and in the future