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Treatment with sodium orthovanadate reduces blood-brain barrier disruption via phosphatase and tensin homolog deleted on chromosome 10 (PTEN) phosphorylation in experimental subarachnoid hemorrhage.

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Attenuation of blood-brain barrier (BBB) disruption is one of the therapeutic candidates for treatment of subarachnoid hemorrhage (SAH). In this study, the protective effect of sodium orthovanadate (SOV) on BBB disruption was investigated in SAH using the endovascular perforation model. Fifty-five

Liver metabolomic changes identify biochemical pathways in hemorrhagic shock.

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BACKGROUND Despite ongoing advances in treatment, thousands of patients still die annually from complications due to hemorrhagic shock, a condition causing dramatic physiologic and metabolic changes as cells switch to anaerobic metabolism in response to oxygen deprivation. As the shift from aerobic

Cannabinoid receptor type 2 agonist attenuates apoptosis by activation of phosphorylated CREB-Bcl-2 pathway after subarachnoid hemorrhage in rats.

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Early brain injury (EBI) which comprises of vasogenic edema and apoptotic cell death is an important component of subarachnoid hemorrhage (SAH) pathophysiology. This study evaluated whether cannabinoid receptor type 2 (CB2R) agonist, JWH133, attenuates EBI after SAH and whether CB2R stimulation

Effects of low-dose unfractionated heparin on early brain injury after subarachnoid hemorrhage in mice.

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Sphingosine kinase (SphK) 1 has been reported as an important signaling node in anti-apoptotic signaling. Heparin is a pleiotropic drug that antagonizes many pathophysiological mechanisms. In this study, we evaluated if heparin prevents early brain injury (EBI) after subarachnoid

Purification and biophysical properties of acute haemorrhagic conjunctivitis virus.

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The buoyant density of acute haemorrhagic conjunctivitis virions labeled with either [(3)H]uridine or [(3)H]leucine was 1.34 g/ml in CsCl and 1.25 g/ml in sucrose. RNA extracted from the virions gave a sedimentation coefficient of approximately 34S in sucrose, and was found to be sensitive to RNase.

Progranulin Reduced Neuronal Cell Death by Activation of Sortilin 1 Signaling Pathways After Subarachnoid Hemorrhage in Rats.

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OBJECTIVE Progranulin has been reported to have neuroprotective actions in cultured neurons. This study investigated the effect of recombinant rat progranulin on early brain injury after subarachnoid hemorrhage. METHODS Controlled in vivo laboratory study. METHODS Animal research

Early changes in rabbit cerebral artery reactivity after subarachnoid hemorrhage.

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OBJECTIVE Subarachnoid hemorrhage frequently leads to long-term cerebral artery narrowing called vasospasm. Very early changes in cerebral arteries have not been studied extensively and may be critical for the later pathological developments. We therefore determined what changes in the reactivity of

Increased influence of calcium and nicardipine on rabbit basilar artery reactivity after brief subarachnoid hemorrhage.

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We studied the changes in reactivity of basilar arteries immediately after a subarachnoid hemorrhage (SAH) in response to serotonin (5-HT), uridine 5'-triphosphate (UTP), and extracellular Ca2+. Although much evidence suggests that an early phase of vasoconstriction occurs after SAH, no direct data

Alterations of mechanical properties in canine basilar arteries after subarachnoid hemorrhage.

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The purpose of this study was to examine the hypotheses that structural stiffening of the arterial wall contributes to chronic cerebral vasospasm, and that alteration in properties of smooth muscle takes place after subarachnoid hemorrhage (SAH). Subarachnoid hemorrhage and subsequent chronic

Preservation of tropomyosin-related kinase B (TrkB) signaling by sodium orthovanadate attenuates early brain injury after subarachnoid hemorrhage in rats.

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OBJECTIVE Recent studies reported that apoptosis was involved in the pathogenesis of early brain injury after subarachnoid hemorrhage (SAH). The aim of this study was to examine whether sodium orthovanadate (SOV) prevents post-SAH apoptosis by modulating growth factors and its downstream receptor

Effects of tenascin-C on early brain injury after subarachnoid hemorrhage in rats.

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OBJECTIVE We previously reported that tenascin-C (TNC), a matricellular protein, was involved in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH), but the role of TNC in early brain injury (EBI) is unknown. This study assessed whether inhibition of TNC upregulation in brain

Tyrosine phosphatase inhibition attenuates early brain injury after subarachnoid hemorrhage in rats.

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OBJECTIVE Sodium orthovanadate (SOV) is a representative tyrosine phosphatase inhibitor and has been shown to ameliorate neuronal injury in cerebral ischemia. We hypothesized that tyrosine phosphatase inhibition by SOV might attenuate early brain injury after subarachnoid hemorrhage (SAH) in this

Alterations in endothelium-dependent responsiveness of the canine basilar artery subarachnoid hemorrhage.

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To investigate the alteration of endothelium-dependent responses in chronic vasospasm after subarachnoid hemorrhage (SAH), experiments were carried out in the double-hemorrhage canine model. After the presence of vasospasm was confirmed by cerebral angiography on Days 0 and 7, pharmacological

Metabolic networks in a porcine model of trauma and hemorrhagic shock demonstrate different control mechanism with carbohydrate pre-feed.

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BACKGROUND Treatment with oral carbohydrate prior to trauma and hemorrhage confers a survival benefit in small animal models. The impact of fed states on survival in traumatically injured humans is unknown. This work uses regulatory networks to examine the effect of carbohydrate pre-feeding on

Fisetin alleviates early brain injury following experimental subarachnoid hemorrhage in rats possibly by suppressing TLR 4/NF-κB signaling pathway.

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Early brain injury (EBI) determines the unfavorable outcomes after subarachnoid hemorrhage (SAH). Fisetin, a natural flavonoid, has anti-inflammatory and neuroprotection properties in several brain injury models, but the role of fisetin on EBI following SAH remains unknown. Our study aimed to

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