Journal ArticleDOI
Pathophysiologic mechanisms of acute ischemic stroke: An overview with emphasis on therapeutic significance beyond thrombolysis
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TLDR
The objective of this review is to critically evaluate the major mechanisms underlying stroke pathophysiology, with emphasis on potential novel targets for designing newer therapeutic modalities.About:
This article is published in Pathophysiology.The article was published on 2010-06-01. It has received 492 citations till now. The article focuses on the topics: Ischemic cascade & Stroke.read more
Citations
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Journal ArticleDOI
Imbalance between IL-17A-producing cells and regulatory T cells during ischemic stroke.
TL;DR: The proportion of peripheral Tregs and the levels of IL-10 and TGF-β were reduced in patients with IS compared with controls using flow cytometry, real-time PCR, and ELISA assays, but the proportions of Th17 and γ δ T cells, the primary IL-17A-secreting cells, increased dramatically, and these effects were accompanied by increases in the levels in IS patients.
Journal ArticleDOI
Patterns in neurosurgical adverse events: open cerebrovascular neurosurgery.
Judith M. Wong,John E. Ziewacz,Allen L Ho,Jaykar R. Panchmatia,Albert H. Kim,Angela M. Bader,B. Gregory Thompson,Rose Du,Atul A. Gawande,Atul A. Gawande +9 more
TL;DR: A significant proportion of these complications may be avoidable through development and testing of standardized protocols to incorporate monitoring technologies and specific technical practices, teamwork and communication, and concentrated volume and specialization.
Journal ArticleDOI
Targeting the Immune System for Ischemic Stroke.
TL;DR: It is argued that safe and effective therapies will need to balance pro- and anti-inflammatory mechanisms in a time-sensitive manner, to maximize the likelihood of an improved long-term outcome.
Journal ArticleDOI
Glibenclamide ameliorates ischemia-reperfusion injury via modulating oxidative stress and inflammatory mediators in the rat hippocampus.
TL;DR: Glibenclamide reversed all the former alterations in the hippocampus of rats exposed to IR brain injury via modulating oxidative stress and inflammatory mediators, thus highlighting a potential therapeutic utility for this sulphonyl urea in IR brain injuries.
Journal ArticleDOI
Signaling pathways involved in ischemic stroke: molecular mechanisms and therapeutic interventions
Chuan Qin,Sheng Yang,Yunjie Chu,Hang-xiang Zhang,Xiaoyi Pang,Lian Chen,Luoqi Zhou,Man Chen,Dai-Shi Tian,Wei Wang +9 more
TL;DR: In this paper , the authors describe the signaling pathways involved in ischemic stroke and categorize them based on the pathophysiological processes they participate in, and summarize the therapeutic approaches targeted various pathophysiology.
References
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Journal ArticleDOI
Atherosclerosis — An Inflammatory Disease
TL;DR: Atherosclerosis is an inflammatory disease as discussed by the authors, and it is a major cause of death in the United States, Europe, and much of Asia, despite changes in lifestyle and use of new pharmacologic approaches to lower plasma cholesterol concentrations.
Journal ArticleDOI
Direct Proinflammatory Effect of C-Reactive Protein on Human Endothelial Cells
TL;DR: The hypothesis that CRP may play a direct role in promoting the inflammatory component of atherosclerosis and present a potential target for the treatment of Atherosclerosis is supported.
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p53 Has a Direct Apoptogenic Role at the Mitochondria
Motohiro Mihara,Susan Erster,Alex Zaika,Oleksi Petrenko,Thomas Chittenden,Petr Pancoska,Ute M. Moll +6 more
TL;DR: Evidence that p53 translocation to the mitochondria occurs in vivo in irradiated thymocytes is provided and it is shown that the p53 protein can directly induce permeabilization of the outer mitochondrial membrane by forming complexes with the protective BclXL and Bcl2 proteins, resulting in cytochrome c release.
Journal ArticleDOI
Glutamate-mediated astrocyte-neuron signalling.
Vladimir Parpura,Trent A. Basarsky,Fang Liu,Ksenija Jeftinija,Srdija Jeftinija,Philip G. Haydon +5 more
TL;DR: Astrocytes regulate neuronal calcium levels through the calcium-dependent release of glutamate, and an NMDA (N-methyl-d-aspartate) receptor-mediated increase in neuronal calcium is demonstrated.
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