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The successful previous volume on this topic provided a detailed benchwork manual for the most commonly used animal models of acute neurological injuries including cerebral ischemia, hemorrhage, vasospasm, and traumatic brain and spinal cord injuries. Animal Models of Acute Neurological Injuries II: Injury and Mechanistic Assessments aims to collect chapters on assessing these disorders from cells and molecules to behavior and imaging. These comprehensive assessments are the key for understanding disease mechanisms as well as developing novel therapeutic strategies to ameliorate or even prevent damages to the nervous system. Volume 2 examines global cerebral ischemia, focal cerebral ischemia, and neonatal hypoxia-ischemia, as well as intensive sections covering traumatic brain injury and spinal cord injury. Designed to provide both expert guidance and step-by-step procedures, chapters serve to increase understanding in what, why, when, where, and how a particular assessment is used. Accessible and essential, Animal Models of Acute Neurological Injuries II: Injury and Mechanistic Assessments will be useful for trainees or beginners in their assessments of acute neurological injuries, for experienced scientists from other research fields who are interested in either switching fields or exploring new opportunities, and for established scientists within the field who wish to employ new assessments.
Cerebral preconditioning is a phenomenon wherein a mild insult or stress induces cellular and tissue adaptation or tolerance to a later, severe injury, therefore reflecting the efficacy of endogenous mechanisms of cerebrovascular protection. Initially identified for rapid cardiac protection, preconditioning has expanded to all aspects of CNS protection from ischemia, trauma and potentially neurodegeneration. Many different stimuli or stressors have been identified as preconditioning agents, suggesting a downstream convergence of mechanisms and underscoring the potential for translational application of preconditioning in the clinic. Moreover, the fundamental mechanisms responsible for preconditioning-induced tolerance will help in the design novel pharmacological approaches for neuroprotection. While stroke and many other brain injuries are not predictable, in some populations (e.g., metabolic syndrome, patients undergoing carotid endarterectomy, aneurysm clipping, or with recent TIAs) the risk for stroke is identifiable and significant, and preconditioning may represent a useful strategy for neuroprotection. For unpredictable injuries, post-conditioning the brain - or inducing endogenous protective mechanisms after the initial injury - can also abrogate the extent of injury. Finally, remote pre- and post-conditioning methods have been developed in animals, and are now being tested in clinical trials, wherein a brief, noninjurious stress to a noncerebral tissue (i.e., skeletal muscle) can provide protection to the CNS and thereby allows clinicians the opportunity to circumvent concerns regarding the direct preconditioning of neurological tissues.
Stroke is a major cause of death and disability in the U.S. and worldwide. A variety of pathophysiologic episodes or cellular medications occur following a stroke, and knowledge of these aftermath events can lead to potential therapeutic strategies that may reverse or attenuate stroke injury. Cellular events that occur following stroke include the excessive releases of excitatory amino acids, alterations in the genomic responses, mitochondrial injury producing reactive oxygen and nitrogen species (ROS), and secondary injury, often in the setting of reperfusion.
This volume sets a basis for effective translational research. Authored by experts in the field of translational stroke research, each chapter specifically addresses one or more components of preclinical stroke research. The emphasis is placed on target identification and drug development using state-of-the-art in vitro and in vivo assays, in combination with in vitro toxicology assays, AMDE and clinical design.
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