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Jickling, G.C., Liu, D., Stamova, B., Ander, B.P., Zhan, X., Lu, A., et al. (2014) Hemorrhagic Transformation after Ischemic Stroke in Animals and Humans. Journal of Cerebral Blood Flow & Metabolism, 34, 185-199.
https://doi.org/10.1038/jcbfm.2013.203

has been cited by the following article:

• TITLE: Pathophysiology of Cerebral Ischemia: Role of Oxidative/Nitrosative Stress

  AUTHORS: Hiba A. Awooda

  KEYWORDS: Reactive Oxygen Species, Reactive Nitrogen Species, Cerebral Ischemia, Oxidative Stress

  JOURNAL NAME: Journal of Biosciences and Medicines, Vol.7 No.3, March 6, 2019

  ABSTRACT: Stroke is a devastating disease with a complex pathophysiology; it ranks second to ischemic heart disease as a cause of death and long-term disability. Tissue damage results from diverse mechanisms with central involvement of free radicals’ overproduction that results in oxidative stress and hence contributes to brain damage. Free radicals [Reactive oxygen species/Reactive nitrogen species] play central a role in the diverse normal physiological processes and as defense mechanisms against harmful substances. When the rate of their production exceeds the anti-oxidant capacity of the body, oxidative stress occurs. Oxidative stress is implicated in the pathogenesis of various diseases including hypertension, atherosclerosis, diabetes mellitus and cancer; they mediate damage to cell structures, lipid peroxidation, protein denaturation, nucleic acid and DNA damage.