Buch, Englisch, 330 Seiten, Format (B × H): 163 mm x 241 mm, Gewicht: 644 g
Reihe: Frontiers in Neuroscience
Buch, Englisch, 330 Seiten, Format (B × H): 163 mm x 241 mm, Gewicht: 644 g
Reihe: Frontiers in Neuroscience
ISBN: 978-0-8493-0119-3
Verlag: CRC Press
Approximately half a million Americans suffer brain ischemic episodes every year. These brain strokes are the third leading cause of death in the United States and the number-one cause of permanent disability. Over the past decade, we have made extensive attempts to understand the biological mechanisms that underlie stroke-induced neuronal injury. Providing a detailed description of the techniques and theories employed in both basic and clinical research, New Concepts in Cerebral Ischemia delineates the mechanisms underlying neuronal damage induced by ischemia. The book covers methods to elucidate the pathogenesis of ischemia, technologies used in the design of specific strategies to protect neurons from further injury, and new approaches to treat patients with acute ischemic episodes. It includes methods and therapeutic approaches for neuronal protection against acute and chronic ischemic episodes and describes new animal models for ischemia research including the application of transgenic animals.
Zielgruppe
Academic and Postgraduate
Autoren/Hrsg.
Fachgebiete
Weitere Infos & Material
Gender Differences in Post-Ischemic and Post-Traumatic Brain Injury. Neonatal Hypoxic-Ischemic Insults and Its Mechanism. Neural Stem Cell Biology Provides Insights into New Therapeutic Strategies for Hypoxic-Ischemic Brain-Injury. Cellular and Molecular Mechanisms of Ischemic Tolerance. Excitotoxicity, Oxidative Stress, and Apoptosis in Ischemic Neuronal Death. Immediate and delayed Factors Causing Neuronal Death after Ischemic and Excitotoxic Insults. Mechanism of Zinc-Induced Neuronal Death. Cerebral Ischemia and Adenosine. Calpain and Caspase in Ischemic and Traumatic Brain Injury. The Potential Role of Hyperbaric Oxygen Therapy as an Adjunctive Treatment Modality for Stroke. Brain Inflammation, Cytokines, and p38AP Kinase Signaling in Stroke.