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@# Tethered cord syndrome (TCS) is a progressive neurodevelopmental disorder. The TCS model was established mainly using physical and chemical Methods and surgery, but remained problems in failing to fully reflect the progressive course of the human TCS. In the future, it may select a single etiological factor to analyze, and gradually add other factors until we have deeper understanding of this disease.
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@#Twophoton microscopy is a new technique which combines laser scanning con-focal microscopy and two-photon excitation technique. Two-photon fluorescence microscopy has the advantages of little light damage, small bleaching area, strong penetrability, high resolution, high fluorescence collection efficiency, and high image contrast. It is suitable for dark field imaging and multi-labeled compound measurement, and has been widely used in small animals in vivo optical imaging, such as research for tumour, gene therapy, stem cells, drug development, spinal cord injury, etc.
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@# Objective To explore the related factors of common postoperative complications after cranioplasty. Methods From November, 2009 to June, 2013, a total of 211 patients after cranioplasty were reviewed. The conventional two-dimensional titanium alloy was used. The incidence of scalp effusion, seizure and spontaneous intracerebral hemorrhage were recorded, and the related factors including gender, age, primary disease, skull defect site, attack time, concomitant hydrocephalus and intraoperative dural damage were analyzed. Results The incidence of these complications was 4.7% (10/211) in total. There were four cases with scalp effusion, five cases with seizures and one case with spontaneous intracerebral hemorrhage. The scalp effusion was related to hydrocephalus (χ2=4.804, P=0.028) and intraoperative dural damage (χ2=7.510, P=0.006). Seizure and spontaneous intracerebral hemorrhage were not related with any factors above (P>0.05). Conclusion The occurrence of postoperative scalp effusion can be reduced by repairing intraoperative dural damage, and dealing with extreme hydrocephalus timely.
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Objective To observe the effects of myelotomy on autophagy activation after traumatic spinal cord injury (SCI) in rats. Methods 54 adult female Sprague-Dawley rats were randomly assigned to sham-operated group (SG, n=18), contusion group (CG, n=18) or myelotomy group (MTG, n=18). The T10 SCI model in rats was induced with a New York University (NYU) impactor and myelotomy was performed 24 hours after SCI. They were evaluated with the BBB score 1, 7, 14 days after injury. The expression of mRNA of Beclin-1 and Bcl-2 were detected with real-time quantitative reverse transcriptase polymerase chain reaction (RT-PCR). The formation of autophagosome was investigated under electronic microscope (EM) 3 days after injury. Results BBB score was more in the MTG than in the CG 7 and 14 days after injury (P<0.05), while the expression of Beclin-1 mRNA was less (P<0.05). The expression of Bcl-2 mRNA was more in the MTG than in the CG 3 and 7 days after injury (P<0.05). The expression of Beclin-1 mRNA was negatively correlated with BBB scores (P<0.05). The formation of autophagosome was less in the MTG than in the CG. Conclusion Myelotomy can improve the recovery of motor function in rats after acute traumatic SCI, which may associate with neuroprotection mediated by inhibition of autophagy through the Bcl-2 signaling pathway.
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@#Objective To observe the effects of myelotomy on autophagy activation after traumatic spinal cord injury (SCI) in rats. Methods 54 adult female Sprague-Dawley rats were randomly assigned to sham-operated group (SG, n=18), contusion group (CG, n=18) or myelotomy group (MTG, n=18). The T10 SCI model in rats was induced with a New York University (NYU) impactor and myelotomy was performed 24 hours after SCI. They were evaluated with the BBB score 1, 7, 14 days after injury. The expression of mRNA of Beclin-1 and Bcl-2 were detected with real-time quantitative reverse transcriptase polymerase chain reaction (RT-PCR). The formation of autophagosome was investigated under electronic microscope (EM) 3 days after injury. Results BBB score was more in the MTG than in the CG 7 and 14 days after injury (P<0.05), while the expression of Beclin-1 mRNA was less (P<0.05). The expression of Bcl-2 mRNA was more in the MTG than in the CG 3 and 7 days after injury (P<0.05). The expression of Beclin-1 mRNA was negatively correlated with BBB scores (P< 0.05). The formation of autophagosome was less in the MTG than in the CG. Conclusion Myelotomy can improve the recovery of motor function in rats after acute traumatic SCI, which may associate with neuroprotection mediated by inhibition of autophagy through the Bcl-2 signaling pathway.
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Although previous studies have shown functional efficacy of myelotomy for the treatment of spinal cord injury (SCI), the underlying mechanism remained unknown. This study aimed to determine the relationship between myelotomy-mediated neuroprotection and autophagy following SCI by evaluating the expression of microtubule-associated protein light chain 3 (LC3-II) and mammalian target of rapamycin complex 1 (mTORC1). Ninety-nine adult female rats were randomly assigned to either sham-operated group (SG), model group (MG), or 24 h-myelotomy group (MTG). SCI at T10 was induced with a New York University impactor, and myelotomy was performed 24 h after SCI. Functional recovery was evaluated via the open-field test. The protein expression of LC3-II was analyzed by Western blot, and the mRNA expression of LC3-II and mTORC1 were detected by real-time quantitative reverse transcriptase polymerase chain reaction. Rats in the MTG exhibited significantly better performance in the hind limbs compared to those in the MG on day seven and fourteen post-injury. Myelotomy suppressed the protein and mRNA expression of LC3-II on day three, seven and fourteen post-injury and increased the mRNA expression of mTORC1 in the MTG on day three and seven post-injury. The LC3-II protein expression was significantly and negatively correlated with BBB scores at day seven and fourteen post-injury. These results showed that myelotomy-induced neuroprotection in a rat model of SCI was likely mediated by inhibition of autophagy by activation of the mTORC1 signaling pathway