Inflammation and Stroke
Published on 13. October 2012
Book
Paperback/Softback
XIII, 356 pages
978-3-0348-9508-8 (ISBN)
Description
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.
More details
Series
Edition
Softcover reprint of the original 1st ed. 2001
Language
English
Place of publication
Basel
Switzerland
Publishing group
Springer Basel
Target group
Professional and scholarly
Research
Illustrations
XIII, 356 p.
Dimensions
Height: 235 mm
Width: 155 mm
Thickness: 21 mm
Weight
569 gr
ISBN-13
978-3-0348-9508-8 (9783034895088)
DOI
10.1007/978-3-0348-8297-2
Schweitzer Classification
Other editions
Additional editions
Giora Z. Feuerstein
Inflammation and Stroke
Book
09/2001
1st Edition
Springer
€85.55
Article exhausted; check different version
Content
New opportunities for stroke prevention and therapeutics: a hope from anti-inflammatory drugs?.- Inflammation in stroke and CNS trauma - experimental and clinical evidence.- Clinical evidence of inflammation as a risk factor in ischemic stroke.- Inflammation as a risk factor for stroke: evidence from experimental models.- Inflammatory and immune responses to CNS injury: beneficial and detrimental components.- Salutary effect of autoimmune T cells after central nervous system injury.- Traumatic brain injury: is head trauma an inflammatory disease?.- Cyclic activation and inactivation of brain vessels involving inflammatory mediators - implications for stroke.- Inflammatory cells in stroke.- Do leukocytes play a role in focal ischemia in the brain? An objective review of the literature.- The role of microglia in ischemic brain injury.- Inflammatory activation of brain cells by hypoxia: transcription factors and signaling pathways.- Inflammatory cytokines, interleukins and chemokines in stroke and CNS trauma.- Cytokine effects on CNS cells: implications for the pathogenesis and prevention of stroke.- Interleukin-10 in cerebral ischemia and stroke.- Chemokines and ischemic stroke.- Biphasic activity of tumor necrosis factor in stroke and brain trauma: interaction with reactive oxygen species.- Interleukin-1 and IL-1 receptor antagonist in stroke: mechanisms and potential therapeutics.- Inflammatory cytokines in CNS trauma.- Inflammation in cerebral thrombosis, angiogenesis and matrix regulation: a new perspective in stroke research and therapeutics.- Microvessel integrin expression during focal cerebral ischemia.- The inflammatory response in focal cerebral ischemia.- Chronic neuronal perturbation mediated by RAGE, a receptor for ?-sheet fibrils and S100/calgranulins.-Mediators of inflammation and blood-brain barrier permeability in cerebral ischemia.- Inflammatory proteases and oxygen radicals in stroke.- The role of metalloproteinases on blood-brain barrier breakdown after ischemic stroke.- Matrix metalloproteinases and their inhibitors in hypoxia/reoxygenation and stroke.- Extracellular matrix-degrading metalloproteinases and neuroinflammation in stroke.- Anti-oxidant strategies to treat stroke.- Inflammatory adhesion molecules, kinins, nitric oxide complement factors and lipid mediators in stroke.- Selectin-and complement-mediated mechanisms of tissue injury in stroke.- The kallikrein-kinin system in ischemic and traumatic brain injury.- Nitric oxide, nitric oxide synthases and cyclooxygenase-2 in experimental focal stroke.