Vascular Mechanisms in CNS Trauma: 5 (Springer Series in Translational Stroke Research)

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Contents

  1. Vascular Mechanisms in CNS Trauma
  2. Vascular Mechanisms in CNS Trauma
  3. Bestselling Series
  4. Introduction
  5. Vascular mechanisms in CNS trauma in SearchWorks catalog

Lara V. Philip N. Pia Mellody.

Vascular Mechanisms in CNS Trauma

Anne Unkenstein. Helen Thomson. Adolfo Bronstein. Max Lugavere. Jean-Marie Saudubray. Dr Gary Small. Hans H. Jean-Michel Vallat.

Vascular Mechanisms in CNS Trauma

Paul A. Jeffrey M. Eng H. Weijian Jiang. Li-Ru Zhao. Jun Chen. Bestselling Series. Harry Potter.

The ischemic cascade in stroke - Circulatory System and Disease - NCLEX-RN - Khan Academy

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Free delivery worldwide. Description This book provides a comprehensive overview of the latest research in the role of non-neuronal cells - astrocytes, oligodendrocytes, endothelial cells, pericytes, microglia, and other immune cells in ischemic brain injury and long-term recovery. In these cases, neurodegeneration and brain repair are controlled in a sophisticated system, incorporating interactions between different cell types and cellular systems.

Also explored are the therapeutic strategies that target non-neuronal responses after stroke and their translational potentials.

Bestselling Series

Product details Format Hardback pages Dimensions x x Add to basket. Into the Magic Shop Dr. Why We Sleep Matthew Walker. Awakenings Oliver Sacks. Brain on Fire Susannah Cahalan. Hallucinations Oliver Sacks. Common Pitfalls in Epilepsy Dieter Schmidt.

Introduction

Deep Medicine Eric Topol. Introducing Mind and Brain Angus Gellatly. Keep Clear Tom Cutler. Principles of Neural Science Eric R. The Autistic Brain Temple Grandin. An Anthropologist on Mars Oliver Sacks. The New Codependency Melody Beattie. The Antidepressant Solution Joseph Glenmullen. Springer titles to be cut. Collections update 9 January Library cost reduction strategy update National Journal Usage survey Additional individual journal and database titles being cancelled. Collections update 7 December Library cost reduction strategy update. Collections update 6 October Library cost reduction strategy update.

Collections update 5 September Library cost reduction strategy update Summary report on collections survey Collections cost reduction strategy briefing. Collections update 4 June Library cost reduction strategy update. The miRa mimic significantly promoted OGD-driven cell death and caspase-3 activity, while the miRa inhibitor produced the opposite effects. Treatment with the scrambled-sequence microRNA negative control produced no significant effect.

As miRa is upregulated in cerebrovascular endothelial cells in response to ischemia, we hypothesized that miRa may serve a pro-apoptotic function in these cells under ischemic conditions. To test this hypothesis, gain-of-miRa function or loss-of-miRa function was produced in cerebrovascular endothelial cells through transfection of a miRa mimic or a miRa inhibitor, respectively.

These findings show that miRa induces cerebrovascular endothelial cell death under OGD conditions. On the basis of this previous evidence, we hypothesized that miRa may be a potential downstream target of pioglitazone suppression. These findings indicate that miRa is a downstream target of pioglitazone suppression in cerebrovascular endothelial cells under OGD conditions. GFP group. Real-time PCR on the total RNA content from these cerebral microvessels revealed that cerebral ischemia-induced miRa upregulation was reversed by pioglitazone.

As miRa shows evidence of being a downstream target of pioglitazone suppression, we hypothesized that the promoter region of miRa may possess a PPRE site. We transfected cerebrovascular endothelial cells with a luciferase reporter vector containing a miRa promoter segment with either the wild-type PPRE site or a mutated PPRE site.


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We also found that silencing of IRF6 expression promotes pioglitazone-driven cytoprotection in murine cerebrovascular endothelial cells under ischemic conditions. Recently, Yin et al. Our current findings support those of Yin et al. As Yin et al. Previous research reveals that miRa is upregulated in animal models of retinal and renal ischemia 20 , 21 , and the miRa promoter has been shown to be enriched for IRF6 binding sites On this basis, we hypothesized that miRa may serve a pro-apoptotic function under ischemic conditions and may be a potential downstream target of pioglitazone suppression in murine cerebrovascular endothelial cells.


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  6. Consistent with our hypothesis, in vitro OGD and in vivo MCA occlusion produced significant miRa upregulation in cerebrovascular endothelial cells and the cerebral microvasculature, respectively. Moreover, application of a miRa mimic induces cerebrovascular endothelial cell death under OGD conditions. The favorable results of thiazolidinedione use in animal models of stroke suggest that these drugs may be useful therapeutic tools for stroke patients Indeed, clinical trials have revealed that pioglitazone reduces recurrent stroke risk in stroke patients 27 , On this basis, Yin et al.

    Feigin, V. Global and regional burden of stroke during — findings from the Global Burden of Disease Study The Lancet , —, doi: Neuroprotection in acute stroke: targeting excitotoxicity, oxidative and nitrosative stress, and inflammation. The Lancet Neurology 15 , —, doi: Mukohda, M. Jin, H. Arteriosclerosis, thrombosis, and vascular biology 35 , —, doi: Zhao, X.

    The Journal of Neuroscience 29 , —, doi: Guo, Q. Fenofibrate improves cerebral blood flow after middle cerebral artery occlusion in mice.

    Vascular mechanisms in CNS trauma in SearchWorks catalog

    Liu, J. Ketsawatsomkron, P.


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    3. Vascular Mechanisms in CNS Trauma | Eng H. Lo | Springer.
    4. Molecular mechanisms regulating vascular tone by peroxisome proliferator activated receptor gamma. Current opinion in nephrology and hypertension 24 , —, doi: Yin, K. Brain , —, doi: Mangold, E. Breakthroughs in the genetics of orofacial clefting. Trends in molecular medicine 17 , —, doi: Kondo, S.

      Nature genetics 32 , —, doi: Ingraham, C.