4 edition of Neuroprotective Agents and Cerebral Ischaemia, Volume 40 (International Review of Neurobiology.) found in the catalog.
December 27, 1996
by Academic Press
Written in English
|Contributions||Richard C. Green (Editor), Alan J. Cross (Editor), Ronald J. Bradley (Series Editor), Robert Adron Harris (Series Editor), Peter Jenner (Series Editor)|
|The Physical Object|
|Number of Pages||378|
A cute ischemic stroke (AIS) resulted in million deaths globally in according to Feigin et al. 24 They estimated that there were close to 18 million ischemic stroke survivors worldwide in The global stroke burden continues to increase. 24 Recent innovations in the clinical stroke arena include advanced imaging for stroke diagnosis 9 and endovascular mechanical thrombectomy for. Background and purpose: This study explored the correlation between duration of focal ischemia and infarct volume in spontaneously hypertensive rats as a measure of outcome after neuroprotective intervention. Methods: We used 2,3,5-triphenyltetrazolium chloride staining to discriminate infarcted tissue and calculate infarct volume 24 hours after temporary tandem common carotid/middle cerebral.
Cerebral ischemia is a common refractory brain disease that seriously endangers human health. There are 15 million new stroke patients worldwide each year, and six million people die from the disease, among which ischemic stroke accounts for 80% [1,2].Cerebral ischemia-reperfusion (I/R) injury is the damage caused by the recovery of blood supply after a certain period of brain tissue ischemia. Aims: To determine whether or not BM possesses neuroprotective effects against cerebral ischemia induced by permanent middle cerebral artery occlusion (pMCAo), a .
Sodium butyrate (NaB) is a dietary microbial fermentation product of fiber and serves as an important neuromodulator in the central nervous system. In this study, we further investigated that NaB attenuated cerebral ischemia/reperfusion (I/R) injury in vivo and its possible mechanisms. NaB (5, 10 mg/kg) was administered intragastrically 3h after the onset of reperfusion in bilateral. Hypothermia has neuroprotective effects in certain clinical conditions and in animal models of brain insult. Yenari and Han review the mechanisms .
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Purchase Neuroprotective Agents and Cerebral Volume 40 book, Volume 40 - 1st Edition. Print Book & E-Book. ISBNSearch in this book series. Neuroprotective Agents and Cerebral Ischaemia. Edited by A. Richard Green, Alan J. Cross. Vol Pages ii-xiii, () Download full volume. Previous volume select article Chapter 13 Nitrone-Based Free Radical Traps as Neuroprotective Agents in Cerebral Ischaemia and Other Pathologies.
Goodreads helps you keep track of books you want to read. Start by marking “International Review of Neurobiology, Volume Neuroprotective Agents and Cerebral Ischaemia” as Want to Read: Want to Read saving Pages: Neuroprotective Agents and Cerebral Ischaemia (ISSN Book 40) 1st Edition, Kindle Edition "In balance, I recommend this book as a superior volume, whose high 'power-to-weight ratio,' readability, and availability in paperback make it attractive for personal use."Manufacturer: Academic Press.
Get this from a library. International review of neurobiology. Vol Neuroprotective agents and cerebral ischaemia. [A Richard Green; Alan J Cross;] -- General Description of Series SinceInternational Review of Neurobiology has been a well-known series appealing to neuroscientists, clinicians, psychologists, physiologists, and.
This compact book (Vol. 40 in the International Review of Neurobiology series edited by R.J. Bradley, R.A. Harris and P. Jenner) brings together an impressive panel of experts to discuss emerging strategies for reducing the brain's vulnerability to ischemic injury.
L.P. Kotra, J. Park, in Comprehensive Medicinal Chemistry III, Donepezil. Neuroprotective agents with multiple mechanisms of action are used for the treatment of AD, and donepezil mechanism of action is related to the neuroprotective effects of this compound.
Donepezil is a potent, noncompetitive, and reversible acetylcholine esterase (AChE) inhibitor (Table 2). In an.
Volume Neuroprotective Agents and Cerebral Ischaemia. Neuroprotective Agents and Cerebral Ischaemia presents an up-to-date review of current research and developing therapies.
This book is essential reading for all clinicians and researchers searching for neuroprotective bes the mechanisms involved in cell death and the.
and sometimes complete recanalization of major cerebral arteries to restore reper - fusion in acute ischemic brain injury by salvaging potentially viable neurons in the penumbra that surrounds the infarct core.
Over neuroprotective agents have been studied in preclinical stroke research, many with promising results . Cerebral ischemia is still one of the most important topics in neurosciences. Our study aimed to investigate the neuroprotective and anti-oxidant effects of glycyrrhizic acid on focal cerebral ischemia in rats.
Twenty-four rats were divided equally into three groups. A middle cerebral artery occlusion model was performed in this study where sham and glycyrrhizic acid were administered.
Neuroprotective strategies that limit secondary tissue loss and/or improve functional outcomes have been identified in multiple animal models of ischemic, hemorrhagic, traumatic and nontraumatic cerebral lesions.
However, use of these potential interventions in human randomized controlled studies has generally given disappointing results. In this paper, we summarize the current.
Neuroprotective agents refer to substances that are capable of preserving brain function and structure. When the brain is exposed to high levels of oxidative stress, mitochondrial dysfunction, inflammation, various forms of neurotoxicity (e.g.
excitotoxicity), and protein deficiencies - neurodegeneration can occur. To prevent or mitigate the effects of any neurodegeneration, strategic. The role of neuroprotection in the management of acute cerebrovascular disease is reviewed.
Neuroprotection is a valuable adjunct to thrombolytic therapy in acute cerebral ischaemia. Studies were included if focal cerebral ischemia model was performed in mammals and including a control group that has been compared with a minocycline group.
Written in languages other than English; duplicate data; in vitro studies and combination of minocycline with other neuroprotective agents were excluded. Neurological function of patients.
Ischemic stroke is a leading cause of death worldwide, bringing about serious long-lasting disability and considerable social burden. Stroke patients suffer from various disabilities, including. Neuroprotective agents and cerebral ischaemia. [A Richard Green; Alan J Cross;] Responsibility: editors A.
Richard Green and Alan J. Cross. Reviews. Editorial reviews. Publisher Synopsis "In balance, I recommend this book as a superior volume, whose high 'power-to-weight ratio,' readability, and availability in paperback make it.
We treated rats intraperitoneally with osthole (40 mg/kg) or vehicle 30 min before cerebral ischemia. We harvested the brains for infarct volume, brain water content, histological changes and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) staining as well as cleaved caspase-3, bax, and bcl Neuroprotective agents in Acute Ischemic Stroke—A Reality Check Article (PDF Available) in Biomedicine & Pharmacotherapy January with 54 Reads How we measure 'reads'.
Several studies have shown that cerebral ischemia increases VEGF expression (5, 6, 38 – 40), so it may be puzzling that administration of exogenous VEGF should be able to modify infarct size, neurogenesis, or angiogenesis in the ischemic brain.
This apparent paradox may be explained by differences in concentration, distribution, or timing of. Introduction. Cerebral ischemia is a common refractory brain disease that seriously endangers human health.
There are 15 million new stroke patients worldwide each year, and six million people die from the disease, among which ischemic stroke accounts for 80% [1,2].Cerebral ischemia-reperfusion (I/R) injury is the damage caused by the recovery of blood supply after a certain period of brain.
of those neuroprotective agents have shown beneficial effects in animal models of cerebral ischemia, but none has proven to reduce tissue damage and improve the neurological out-come in human stroke patients when given at patient’s arrival to emergency departments.
Translation from animal studies.We show here that FK is a powerful neuroprotective agent in an in vivo model of focal cerebral ischaemia when administered up to 60 min post-occlusion. The minimum effective neuroprotective.Neuroprotection refers to the relative preservation of neuronal structure and/or function.
In the case of an ongoing insult (a neurodegenerative insult) the relative preservation of neuronal integrity implies a reduction in the rate of neuronal loss over time, which can be expressed as a differential equation.
It is a widely explored treatment option for many central nervous system (CNS.