Subarachnoid Hemorrhage Induces Gliosis and Increased Expression of the Pro-inflammatory Cytokine High Mobility Group Box 1 Protein. - Wikidata - wikimedia - TriplyDB

Subarachnoid Hemorrhage Induces Gliosis and Increased Expression of the Pro-inflammatory Cytokine High Mobility Group Box 1 Protein.

Subarachnoid Hemorrhage Induces Gliosis and Increased Expression of the Pro-inflammatory Cytokine High Mobility Group Box 1 Protein.

http://www.wikidata.org/entity/Q34769364

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Early brain injury, an evolving frontier in subarachnoid hemorrhage research Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca2+-activated K+ (BK) channels.Anti-high mobility group box-1 (HMGB1) antibody attenuates delayed cerebral vasospasm and brain injury after subarachnoid hemorrhage in rats High-Throughput Sequencing and Co-Expression Network Analysis of lncRNAs and mRNAs in Early Brain Injury Following Experimental Subarachnoid Haemorrhage A novel technique for morphometric quantification of subarachnoid hemorrhage-induced microglia activation.Resolving the negative data publication dilemma in translational stroke research.Early release of high-mobility group box 1 (HMGB1) from neurons in experimental subarachnoid hemorrhage in vivo and in vitro.Release of neuronal HMGB1 by ethanol through decreased HDAC activity activates brain neuroimmune signaling.Cardiac reactive oxygen species after traumatic brain injury.Heparin reduces neuroinflammation and transsynaptic neuronal apoptosis in a model of subarachnoid hemorrhage.Astrocyte Ca2+ Signaling Drives Inversion of Neurovascular Coupling after Subarachnoid Hemorrhage Relationship between plasma high mobility group box-1 protein levels and clinical outcomes of aneurysmal subarachnoid hemorrhage.Experimental animal models and inflammatory cellular changes in cerebral ischemic and hemorrhagic stroke.Toll-like receptor 4 signaling in intracerebral hemorrhage-induced inflammation and injury.Subarachnoid hemorrhage, spreading depolarizations and impaired neurovascular coupling.The rodent endovascular puncture model of subarachnoid hemorrhage: mechanisms of brain damage and therapeutic strategies.Smooth muscle phenotype switching in blast traumatic brain injury-induced cerebral vasospasm.Inhibiting HMGB1 with Glycyrrhizic Acid Protects Brain Injury after DAI via Its Anti-Inflammatory Effect.Heparin and Heparin-Derivatives in Post-Subarachnoid Hemorrhage Brain Injury: A Multimodal Therapy for a Multimodal Disease.Prostaglandin E2 EP4 Receptor Activation Attenuates Neuroinflammation and Early Brain Injury Induced by Subarachnoid Hemorrhage in Rats.Activation of TRPV4 channels does not mediate inversion of neurovascular coupling after SAH.Subarachnoid blood converts neurally evoked vasodilation to vasoconstriction in rat brain cortex.Detection of Neuroinflammation in a Rat Model of Subarachnoid Hemorrhage Using [18F]DPA-714 PET Imaging.P2X7R/cryopyrin inflammasome axis inhibition reduces neuroinflammation after SAH.Glycyrrhizin attenuates Toll like receptor-2, -4 and experimental vasospasm in a rat model.Activated microglia mediate synapse loss and short-term memory deficits in a mouse model of transthyretin-related oculoleptomeningeal amyloidosis.SAH-induced suppression of voltage-gated K(+) (K (V)) channel currents in parenchymal arteriolar myocytes involves activation of the HB-EGF/EGFR pathway.Aneurysmal subarachnoid hemorrhage--status quo and perspective.Cerebrospinal fluid high mobility group box 1 is associated with neuronal death in subarachnoid hemorrhage.Melatonin alleviates secondary brain damage and neurobehavioral dysfunction after experimental subarachnoid hemorrhage: possible involvement of TLR4-mediated inflammatory pathway.AG490 ameliorates early brain injury via inhibition of JAK2/STAT3-mediated regulation of HMGB1 in subarachnoid hemorrhage.Glycyrrhizic acid exerts anti-inflammatory effect to improve cerebral vasospasm secondary to subarachnoid hemorrhage in a rat model.Characterization of spinal subarachnoid bleeding associated to graded traumatic spinal cord injury in the rat.

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Subarachnoid Hemorrhage Induces Gliosis and Increased Expression of the Pro-inflammatory Cytokine High Mobility Group Box 1 Protein.

http://www.wikidata.org/entity/Q34769364

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2011 nî lūn-bûn

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2011 թվականի մարտին հրատարակված գիտական հոդված

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2011年の論文

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Translational stroke research

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Bruce I Tranmer

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George C Wellman

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Kentaro Murakami

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Masayo Koide

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Sheila R Russell

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Travis M Dumont

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P2860

The nuclear protein HMGB1 is secreted by monocytes via a non-classical, vesicle-mediated secretory pathway

Glibenclamide reduces inflammation, vasogenic edema, and caspase-3 activation after subarachnoid hemorrhage

S100: a multigenic family of calcium-modulated proteins of the EF-hand type with intracellular and extracellular functional roles

Cerebral vasospasm after subarachnoid hemorrhage: putative role of inflammation.

Inflammation in the brain after experimental subarachnoid hemorrhage.

Glial fibrillary acidic protein: GFAP-thirty-one years (1969-2000).

Astrocyte activation and reactive gliosis.

Case-fatality rates and functional outcome after subarachnoid hemorrhage: a systematic review.

Reactive astrocytes in neural repair and protection.

Elucidating novel mechanisms of brain injury following subarachnoid hemorrhage: an emerging role for neuroproteomics

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