Neurological research
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Neurological research · Jun 2012
Glycerol accumulation in edema formation following diffuse traumatic brain injury.
Traumatic brain injury (TBI) induces brain edema via water and glycerol transport channels, called aquaporins (AQPs). The passage of glycerol across brain cellular compartments has been shown during edema. Using a modified impact/head acceleration rodent model of diffuse TBI, we assessed the role of hypoxia inducible factor (HIF)-1alpha in regulating AQP9 expression and glycerol accumulation during the edema formation. ⋯ This reduction was temporally associated with significant (P<0.05) decreases in both edema and glycerol accumulation. The data suggested an associated induction of HIF-1alpha, AQP9, and extracellular glycerol accumulation in edema formation following diffuse TBI. The implication of HIF-1alpha and AQP9 underlying TBI-induced edema formation offers possibilities for novel TBI therapies.
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Neurological research · May 2012
Activation of Akt/GSK-3beta/beta-catenin signaling pathway is involved in survival of neurons after traumatic brain injury in rats.
Apoptotic cell death is an important factor influencing the prognosis after traumatic brain injury (TBI). Akt/GSK-3beta/beta-catenin signaling plays a critical role in the apoptosis of neurons in several models of neurodegeneration. The goal of this study was to determine if the mechanism of cell survival mediated by the Akt/GSK-3beta/beta-catenin pathway is involved in a rat model of TBI. ⋯ Phosphorylation of Akt (Ser473) and GSK3beta (Ser9) was accelerated in the injured cortex, and involved in the neuronal survival after TBI. Moreover, neuroprotection of beta-catenin against ischemia was partly mediated by enhanced and persistent activation of the Akt/GSK3beta signaling pathway.
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Neurological research · May 2012
ReviewNeuroprotection targeting ischemic penumbra and beyond for the treatment of ischemic stroke.
Neuroprotection to attenuate or block the ischemic cascade and salvage neuronal damage has been extensively explored for the treatment of ischemic stroke. In the last two decades, neuroprotective strategy has been evolving from targeting a signal pathway in neurons to protecting all neurovascular components and improving cell-cell and cell-extracellular matrix interaction that ultimately benefits the brain recovery after ischemic stroke. The progression from potentially reversible to irreversible injury in the ischemic penumbra has provided the opportunity to develop therapies to attenuate the ischemic stroke damage. ⋯ In addition, increasing evidence has indicated ischemic stroke could induce long-lasing cellular and hemodynamic changes beyond the ischemic territory. It is unclear whether and how the global responses induced by the ischemic cascade contribute to the progression of cognitive impairment after ischemic stroke. The prolonged pathophysiological cascades induced by ischemic stroke beyond the ischemic penumbra might provide novel therapeutic opportunities for the neuroprotective intervention, which could prevent or slow down the progression of vascular dementia after ischemic stroke.
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Neurological research · May 2012
Changes in spinal cord met-enkephalin levels and mechanical threshold values of pain after pulsed radio frequency in a spared nerve injury rat model.
The present study investigated changes in the met-enkephalin (M-ENK) levels in the spinal cord. We also determined the mechanical threshold value of pain in spared nerve injury (SNI) rats after applying pulsed radiofrequency (PRF) on L5 dorsal root ganglion (DRG). ⋯ This study demonstrates that applying PRF on the DRG can improve hyperalgesia and increase M-ENK levels in the spinal cord of SNI rats within 24 hours. These findings indicate that the endogenous M-ENK in the spinal cord is involved in the mechanism of PRF on the therapy of neuropathic pain.
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Neurological research · Apr 2012
Microneurosurgical management of anterior choroidal artery aneurysms: a 16-year institutional experience of 102 patients.
Surgical treatment of anterior choroidal artery aneurysms (AChAAs) continues to be challenging and technically demanding for vascular neurosurgeons. Ischemic stroke is the most common complication after surgical clipping of AChAAs. We retrospectively studied a series of 102 consecutive patients with AChAAs to evaluate the clinical outcomes and ischemic complications after surgical clipping. ⋯ The surgery of AChAAs is not easy, surgical management of AChAAs carries with it a high risk of postoperative ischemic complications, especially for those aneurysms originating entirely or partially from the AChA itself.