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Stroke is a leading cause of death in developed countries. However, current therapeutic strategies for stroke have been largely unsuccessful. One possible explanation is that research and pharmacological management have focused on very early events in brain ischemia. New research has shown that brain ischemia and trauma elicit strong inflammatory reactions driven by both external and brain cells. The recognition of inflammation as a fundamental response to brain ischemia provides novel opportunities for new anti-inflammatory therapies. For the first time, an international body of researchers presents the latest findings about the cellular and humoral aspects of immune and inflammatory reactions in the brain. The work may have an impact on the treatment of neuroinjuries and ancillary brain diseases, and increase the understanding of the roles infections and immune reactions play in the brain milieu.
The successful treatment of acute stroke remains one of the major challenges in clinical medicine. Over the last decades, the understanding of stroke pathophysiology has greatly improved, while the therapeutic options in stroke therapy remain very limited. Today, hyperacute mechanisms of damage, such as excitotoxicity, can be discriminated from delayed ones, such as inflammation and apoptosis. Targeting of inflammation has already been successfully applied in various stroke models, but translation into a clinically efficacious strategy has not been achieved so far. In this book, leading experts in basic cerebrovascular research as well as stroke treatment review the current evidence for and against an important role for inflammation in stroke, and explore the potential of treating or modulating inflammation in stroke therapy.
Stroke is a leading cause of death in developed countries. However, current therapeutic strategies for stroke have been largely unsuccessful. One possible explanation is that research and pharmacological management have focused on very early events in brain ischemia. New research has shown that brain ischemia and trauma elicit strong inflammatory reactions driven by both external and brain cells. The recognition of inflammation as a fundamental response to brain ischemia provides novel opportunities for new anti-inflammatory therapies. For the first time, an international body of researchers presents the latest findings about the cellular and humoral aspects of immune and inflammatory reactions in the brain. The work may have an impact on the treatment of neuroinjuries and ancillary brain diseases, and increase the understanding of the roles infections and immune reactions play in the brain milieu.
Ischemic stroke is a devastating clinical event. Increasing evidence suggests that inflammatory mechanisms are involved in the progression of post ischemic-induced brain injury. Cerebral ischemia is accompanied by a marked inflammatory reaction that is initiated by ischemia-induced expression of cytokines, adhesion molecules, and other inflammatory mediators, including prostanoids, extracellular proteases, reactive oxygen species and nitric oxide, leading to the accumulation of inflammatory cells, such as leukocytes and microglia. The inflammatory reaction, which has a rapid onset and continues after the stroke, is thought to acutely contribute to the evolution of tissue injury. Many compounds have been identified in cerebral ischemia, which are known to promote and sustain inflammatory responses. Better understanding of the role of the post ischemic-induced inflammatory response and its potential for modulation might have profound implications for patient treatment. Pre-clinical studies suggest that interventions that are aimed at attenuating such inflammation reduce the progression of brain damage that occurs during the late stages of cerebral ischemia. In particular, strategies that block the activity of inflammation-related enzymes reduce ischemic damage with an extended therapeutic window. In this review, a summary of the available literature on the inflammatory responses after cerebral ischemia and ischemic stroke is presented along with discussion of some of the emerging opportunities for potential therapeutic strategies. Although at the moment, clinical trials using anti-inflammatory strategies did not show benefit in patients with ischemic stroke, there is a strong rationale for continuing to explore the efficacy of anti-inflammatory therapies in the treatment of the late stages of cerebral ischemia. It is plausible that in the near future, additional strategies using neuroprotective drug cocktails that target inflammation could offer exciting new promise in the therapeutic approach to ischemic stroke.
A distinction between primary and secondary brain damage of vari ous origin, particularly in acute lesions, such as head injury and ische mia is not entirely new. The concept is of practical significance, be cause it is the foremost intention of all clinical efforts to prevent, or at least attenuate the development of secondary sequelae. Primary dam age to nervous elements usually cannot be influenced by treatment. Its prevention is the objective of prophylactic measures. The current volume gathered prominent scientists and clinicians from various fields to pro vide a competent introduction and survey of the various aspects involved in secondary brain damage. It was attempted to provide criteria for the distinction between the primary and secondary phenomena on a morpho logical and functional level, on the basis of the kinetics involved and, most importantly, regarding the different specific manifestations, such as disturbances of microcirculation, aspects of the blood-brain barrier, and of cellular structure and function at a molecular level. Although it was not expected that a grand unifying hypothesis will be reached recon cilable with the many, occasionally opposing views on such a complex subject, nevertheless, the present volume attains an appropriate result. It can best be described as a mosaic of many different pieces which only as an ensemble reflect the current state of the art.
Recent research has revealed the importance of immunological mechanisms and inflammation in delaying damage and/or promoting repair after an acute injury to the central nervous system. This book provides a comprehensive and up-to-date overview of the role of immunological mechanisms and therapies for treating acute neurological injuries such as cerebral ischemia, hemorrhage, and brain and spinal cord trauma. In several sections, the contributing authors provide a review of immunological mechanisms involved in neurological injury and of various translational and clinical research aimed at harnessing those mechanisms for better patient outcomes.
Toole's Cerebrovascular Disorders was the first modern book devoted to care of the stroke, originally published more than 40 years ago. This is a completely revised and updated sixth edition of the highly respected standard for stroke diagnosis and treatment. Dr James Toole has stayed on as a consultant for the text, and Drs E. Steve Roach, Kerstin Bettermann, and Jose Biller have reworked Dr Toole's book to include chapters on genetics, pregnancy-related stroke, and acute treatments. The practical focus of the book has not changed, retaining its emphasis on bedside diagnosis and treatment. Easily accessible both for stroke specialists and residents, the sixth edition has been modernized to keep pace with the rapid expansion of knowledge in stroke care and includes evidence-based recommendations, the latest technology and imaging, and risk factors. The text is supplemented with more than 200 images, many in color.
Stroke is a cerebrovascular event resulting in cell death in the brain, neurological deficits, and other complications. Stroke is one of the most common causes of death and disability worldwide, but in spite of its prevalence, treatments remain extremely limited. Neuroinflammation after stroke is an appealing therapeutic target, because of its prolonged time course and because it includes multifaceted responses which may either exacerbate or mitigate neuronal death and facilitate injury resolution and repair. Microglia are the brain's resident macrophage population and are central to the neuro-immune response after stroke by becoming activated in response to cellular damage, initiating inflammation, releasing chemokines and pro-inflammatory signaling molecules, clearing dead cells and debris, and secreting growth factors to promote tissue repair. Furthermore, microglia recruit peripheral immune cells into the injured brain, such as monocyte-derived macro-phages, which also contribute to these aspects of the neuro-immune response. Chapter 1 provides an overview of the events in the neuroinflammatory response to ischemic stroke and highlights current knowledge and controversies about microglial functions in post-stroke neuroinflammation. Much is still unknown about which microglial functions are most important to the overall immune response after stroke, and how those functions change over time. Particularly little is known about the pivotal role that microglia play in initiating neuroinflammation after stroke, and the different signals which regulate the microglial and macrophage response. The sympathetic nervous system is activated after stroke, and previous studies indicate that sympathetic neurotransmitters inhibit inflammatory activities of immune cells primarily by acting on beta2-adrenergic receptors. In Chapter 2, I use pharmacological stimulation of beta2-adrenergic signaling and genetic knockout of the beta2-adrenergic receptor from microglia and macrophages to evaluate the extent to which beta2-adrenergic receptor signaling modulates the activation and inflammatory functions of these cells following ischemic stroke. In Chapter 3, I leverage gene expression profiling of ribosome-associated mRNA from microglia to characterize the microglial transcriptional profile in the early response phase after stroke compared to the later sub-acute phase. This work reveals robust pro-inflammatory signaling of microglia during the initiation of post-stroke neuroinflammation and demonstrates that this response changes over time. This analysis also identified several genes strongly upregulated during the acute and sub-acute micro-glial inflammatory responses, and Chapter 4 describes ongoing work to investigate the functional role of some of these molecules in stroke recovery and neuro-immune signaling. Chapter 5 provides a summary of the findings reported in this dissertation, and de-scribes ongoing work and future studies.