Publications (16) View all
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Article: Chronological changes and effects of AMP-activated kinase in the hippocampal CA1 region after transient forebrain ischemia in gerbils.
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ABSTRACT: Adenosine monophosphate-activated kinase (AMPK) is an energy-specific sensor within the central nervous system. In this study, we observed AMPK and its phosphorylated form (pAMPK) in the hippocampal CA1 region after 5 minutes of transient forebrain ischemia. In addition, we also investigated the effects of Compound C, an AMPK inhibitor, against ischemic damage in gerbils. Adenosine monophosphate-activated kinase and pAMPK immunoreactivity was observed in the hippocampal CA1 region at various time points after ischemia and Compound C was intraperitoneally administered to gerbils immediately after reperfusion and the animals were sacrificed at 5 days after ischemia/reperfusion. Adenosine monophosphate-activated kinase immunoreactivity was transiently increased in the hippocampal CA1 region 1-2 days after ischemia/reperfusion, while AMPK immunoreactivity was almost undetectable in the stratum pyramidale of the CA1 region 4-7 days after ischemia/reperfusion. The administration of Compound C caused a dose-dependent decrease in the ischemia-induced hyperactive behavior, the depletion of ATP, and lactate accumulation in the hippocampal CA1 region within 24 hours after ischemia/reperfusion. In addition, the administration of Compound C decreased reactive gliosis (astrocytes and microglia) and increased the number of cresyl violet-positive neurons when compared to the vehicle-treated group at 5 days post-ischemia/reperfusion. These results suggest that AMPK is transiently phosphorylated following forebrain ischemia in the hippocampal CA1 region and inhibition of AMPK has neuroprotective effects against ischemic damage through the reduction of ATP depletion and lactate accumulation in the hippocampal CA1 region.Neurological Research 05/2013; 35(4):395-405. · 1.52 Impact Factor -
Article: Radiological and pathological evaluation of the spinal cord in a rat model of electrical injury-induced myelopathy.
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ABSTRACT: No study has reported an animal-based experimental model of electrical injury to the spinal cord. This paper presents the first systematic establishment of an animal model of electrical injury to the spinal cord with subsequent pathophysiologic analysis. The voltage required for the electrical shock was generated by an electroconvulsive therapy apparatus (57800ECT unit; UGO BASILE, Italy). We used one side ear as the entry site and the contralateral hind limb as the exit site. Seven electrical shock (frequency, 120Hz; pulse width, 0.9ms; duration, 3s; current, 99mA) was applied to each rat and used rat showing hind limb weakness. Radiologic and histologic evaluations were performed at one day, one, two and four weeks after injury. Twelve rats showed the hind limb weakness among the total 18 rats. Manganese-enhanced magnetic resonance imaging showed interruption of spinal cord enhancement in the thoracic area. Histological examination showed a greater decrease in the number of neurons in the ventral horn versus the dorsal horn. This study demonstrates a novel design and analysis of an animal-based experimental model of spinal cord injury by electrical etiology. This model is useful for experimental studies of injuries to the spinal cord.Burns: journal of the International Society for Burn Injuries 06/2012; 38(7):1066-71. · 1.95 Impact Factor -
Article: Neuroprotective effects of adipose-derived stem cells against ischemic neuronal damage in the rabbit spinal cord.
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ABSTRACT: Transplantation of adipose-derived stem cells (ASCs) is one of the possible therapeutic tools for ischemic damage. In this study, we observed the effects of ASCs against ischemic damage in the ventral horn of L(5-6) levels in the rabbit spinal cord. ASCs were isolated from rabbits, and cell type was confirmed by flow cytometry analysis, labeling with CM-DiI dye and differentiation into adipocytes in adipogenesis differentiation medium. ASCs were administered intrathecally into recipient rabbits (2 × 10⁵) immediately after reperfusion following a 15-min aortic artery occlusion in the subrenal region. Transplantation of ASCs significantly improved functions of the hindlimb and morphology of the ventral horn of spinal cord although CM-DiI-labeled ASCs were not observed in the spinal cord parenchyma. In addition, transplantation of ASCs significantly increased brain-derived neurotrophic factor (BDNF) levels at 72h after ischemia/reperfusion. These results suggest that transplantation of ASCs prevents motor neurons from spinal ischemic damage and reactive gliosis by increasing neurotrophic factors such as BDNF in the spinal cord.Journal of the neurological sciences 04/2012; 317(1-2):40-6. · 2.32 Impact Factor -
Article: Clinical outcome of posterior fixation of the C1 lateral mass and C2 pedicle by polyaxial screw and rod.
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ABSTRACT: Because of atlantoaxial complex has a unique and complicated anatomy and instability of this complex is very dangerous. We investigated the clinical results of posterior C1-C2 fixation with a polyaxial screw-rod system. Between July 2001 and December 2007, the authors treated 17 patients suffering from atlantoaxial deformity and instability. Atlantoaxial fusion was employed in 9 patients with upper cervical fracture and dislocation, in 6 patients with atlantoaxial subluxation, in 1 patient with pure transverse ligament injury, and in 1 patient with basilar invagination. The mean age at the time of surgery was 40.4 years (range, 15-68 years). Operative times ranged from 165 to 420 min (average 306 min), and the postoperative mean VAS score was 2.4. The mean follow-up period was 26 months. Solid fusion was achieved in 15 patients at the last follow up; no injury of the vertebral artery or spinal cord and no operative mortality occurred in these cases. We suggest that posterior atlantoaxial fixation using the polyaxial screw-rod system is an effective and relatively safe technique. The navigation guidance system employed during the surgical procedure was helpful methods. Future studies of the feasibility of navigation system-guided surgical procedures will be required.Clinical neurology and neurosurgery 11/2011; 114(6):539-44. · 1.30 Impact Factor -
Article: Neuroprotective effects of PEP-1-Cu,Zn-SOD against ischemic neuronal damage in the rabbit spinal cord.
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ABSTRACT: A rabbit model of spinal cord ischemia has been introduced as a good model to investigate the pathophysiology of ischemia-reperfusion (I-R)-induced paraplegia. In the present study, we observed the effects of Cu,Zn-superoxide dismutase (SOD1) against ischemic damage in the ventral horn of L(5-6) levels in the rabbit spinal cord. For this study, the expression vector PEP-1 was constructed, and this vector was fused with SOD1 to create a PEP-1-SOD1 fusion protein that easily penetrated the blood-brain barrier. Spinal cord ischemia was induced by transient occlusion of the abdominal aorta for 15 min. PEP-1-SOD1 (0.5 mg/kg) was intraperitoneally administered to rabbits 30 min before ischemic surgery. The administration of PEP-1-SOD1 significantly improved neurological scores compared to those in the PEP-1 (vehicle)-treated ischemia group. Also, in this group, the number of cresyl violet-positive cells at 72 h after I-R was much higher than that in the vehicle-treated ischemia group. Malondialdehyde levels were significantly decreased in the ischemic spinal cord of the PEP-1-SOD1-treated ischemia group compared to those in the vehicle-treated ischemia group. In contrast, the administration of PEP-1-SOD1 significantly ameliorated the ischemia-induced reduction of SOD and catalase levels in the ischemic spinal cord. These results suggest that PEP-1-SOD1 protects neurons from spinal ischemic damage by decreasing lipid peroxidation and maintaining SOD and catalase levels in the ischemic rabbit spinal cord.Neurochemical Research 10/2011; 37(2):307-13. · 2.24 Impact Factor
