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Free Radical Damage in Ischemia-Reperfusion Injury: An Obstacle in Acute Ischemic Stroke after Revascularization Therapy
by
Zhang, Fu-Liang
, Huang, Shuo
, Sun, Xin
, Sun, Ming-Shuo
, Guo, Zhen-Ni
, Jin, Hang
, Yang, Yi
in
Apoptosis
/ Brain research
/ Cell death
/ Deoxyribonucleic acid
/ DNA
/ DNA damage
/ Free Radical Scavengers - pharmacology
/ Free Radical Scavengers - therapeutic use
/ Free radicals
/ Free Radicals - chemistry
/ Free Radicals - metabolism
/ Free Radicals - toxicity
/ Health aspects
/ Humans
/ Ischemia
/ Lipid peroxidation
/ Morbidity
/ Mortality
/ Myocardial Revascularization - adverse effects
/ NADPH Oxidases - metabolism
/ Neurology
/ Neurons
/ Neuroprotective Agents - therapeutic use
/ Neurosciences
/ Oxidative stress
/ Oxidative Stress - drug effects
/ Patients
/ Physiology
/ Proteins
/ Reperfusion injury
/ Reperfusion Injury - metabolism
/ Reperfusion Injury - pathology
/ Review
/ Rodents
/ Stroke
/ Stroke (Disease)
/ Stroke - etiology
/ Stroke - prevention & control
/ Therapy
/ Tissue plasminogen activator
/ Zonula Occludens-1 Protein - metabolism
2018
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Free Radical Damage in Ischemia-Reperfusion Injury: An Obstacle in Acute Ischemic Stroke after Revascularization Therapy
by
Zhang, Fu-Liang
, Huang, Shuo
, Sun, Xin
, Sun, Ming-Shuo
, Guo, Zhen-Ni
, Jin, Hang
, Yang, Yi
in
Apoptosis
/ Brain research
/ Cell death
/ Deoxyribonucleic acid
/ DNA
/ DNA damage
/ Free Radical Scavengers - pharmacology
/ Free Radical Scavengers - therapeutic use
/ Free radicals
/ Free Radicals - chemistry
/ Free Radicals - metabolism
/ Free Radicals - toxicity
/ Health aspects
/ Humans
/ Ischemia
/ Lipid peroxidation
/ Morbidity
/ Mortality
/ Myocardial Revascularization - adverse effects
/ NADPH Oxidases - metabolism
/ Neurology
/ Neurons
/ Neuroprotective Agents - therapeutic use
/ Neurosciences
/ Oxidative stress
/ Oxidative Stress - drug effects
/ Patients
/ Physiology
/ Proteins
/ Reperfusion injury
/ Reperfusion Injury - metabolism
/ Reperfusion Injury - pathology
/ Review
/ Rodents
/ Stroke
/ Stroke (Disease)
/ Stroke - etiology
/ Stroke - prevention & control
/ Therapy
/ Tissue plasminogen activator
/ Zonula Occludens-1 Protein - metabolism
2018
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Free Radical Damage in Ischemia-Reperfusion Injury: An Obstacle in Acute Ischemic Stroke after Revascularization Therapy
by
Zhang, Fu-Liang
, Huang, Shuo
, Sun, Xin
, Sun, Ming-Shuo
, Guo, Zhen-Ni
, Jin, Hang
, Yang, Yi
in
Apoptosis
/ Brain research
/ Cell death
/ Deoxyribonucleic acid
/ DNA
/ DNA damage
/ Free Radical Scavengers - pharmacology
/ Free Radical Scavengers - therapeutic use
/ Free radicals
/ Free Radicals - chemistry
/ Free Radicals - metabolism
/ Free Radicals - toxicity
/ Health aspects
/ Humans
/ Ischemia
/ Lipid peroxidation
/ Morbidity
/ Mortality
/ Myocardial Revascularization - adverse effects
/ NADPH Oxidases - metabolism
/ Neurology
/ Neurons
/ Neuroprotective Agents - therapeutic use
/ Neurosciences
/ Oxidative stress
/ Oxidative Stress - drug effects
/ Patients
/ Physiology
/ Proteins
/ Reperfusion injury
/ Reperfusion Injury - metabolism
/ Reperfusion Injury - pathology
/ Review
/ Rodents
/ Stroke
/ Stroke (Disease)
/ Stroke - etiology
/ Stroke - prevention & control
/ Therapy
/ Tissue plasminogen activator
/ Zonula Occludens-1 Protein - metabolism
2018
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Free Radical Damage in Ischemia-Reperfusion Injury: An Obstacle in Acute Ischemic Stroke after Revascularization Therapy
Journal Article
Free Radical Damage in Ischemia-Reperfusion Injury: An Obstacle in Acute Ischemic Stroke after Revascularization Therapy
2018
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Overview
Acute ischemic stroke is a common cause of morbidity and mortality worldwide. Thrombolysis with recombinant tissue plasminogen activator and endovascular thrombectomy are the main revascularization therapies for acute ischemic stroke. However, ischemia-reperfusion injury after revascularization therapy can result in worsening outcomes. Among all possible pathological mechanisms of ischemia-reperfusion injury, free radical damage (mainly oxidative/nitrosative stress injury) has been found to play a key role in the process. Free radicals lead to protein dysfunction, DNA damage, and lipid peroxidation, resulting in cell death. Additionally, free radical damage has a strong connection with inducing hemorrhagic transformation and cerebral edema, which are the major complications of revascularization therapy, and mainly influencing neurological outcomes due to the disruption of the blood-brain barrier. In order to get a better clinical prognosis, more and more studies focus on the pharmaceutical and nonpharmaceutical neuroprotective therapies against free radical damage. This review discusses the pathological mechanisms of free radicals in ischemia-reperfusion injury and adjunctive neuroprotective therapies combined with revascularization therapy against free radical damage.
Publisher
Hindawi Publishing Corporation,Hindawi,John Wiley & Sons, Inc
Subject
/ DNA
/ Free Radical Scavengers - pharmacology
/ Free Radical Scavengers - therapeutic use
/ Humans
/ Ischemia
/ Myocardial Revascularization - adverse effects
/ Neurons
/ Neuroprotective Agents - therapeutic use
/ Oxidative Stress - drug effects
/ Patients
/ Proteins
/ Reperfusion Injury - metabolism
/ Reperfusion Injury - pathology
/ Review
/ Rodents
/ Stroke
/ Stroke - prevention & control
/ Therapy
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