目的:对同侧胫腓骨骨折、髋关节骨折后脱位合并膝后交叉韧带损伤的创伤机制及诊断进行分析探讨。方法:对2007年1月至2008年6月收治的7例同侧胫腓骨骨折、髋关节骨折后脱位合并膝后交叉韧带损伤患者的临床资料、诊治经过和随访结果进行总结分析。结果: 胫腓骨开放性骨折3例(42.9%),闭合性骨折4例(57.1%);髋关节均有后脱位,其中伴有髋部骨折5例(71.4%)。膝后交叉韧带实质部断裂4例(57.1%),胫骨止点撕脱骨折3例(42.9%)。7例患者获平均14.7个月(12～18个月)随访。Lysholm膝关节功能评分术后6月95.8±3.71,术后12月97.6±2.7。结论:明确同侧胫腓骨骨折、髋关节骨折后脱位合并膝后交叉韧带损伤的创伤机制,全面、准确、系统的问诊查体和完善的辅助检查是早期确诊、提高疗效的关键。
Objective To explore the influence factors for the functional improvement after the fetal olfactory ensheathing cell (OEC) transplantation for chronic spinal cord injury(SCI). Methods The olfactory bulbs were harvested and trypsinized down to single fetal OEC. They were cultured for 12-17 days prepared for use. From November 2001 to December 2003, a total of 300 patients volunteered for the fetal OEC transplantation, among whom 222 suffered from complete chronicSCI and 78 suffered from incomplete chronic SCI. The procedures were performed on the patients with a disease course ranging from 6 months to 31 years (average 3.1 years) after their injuries. The fetal OEC was transplanted by the form of injections into the spinal cord at the upper and lower ends of the injury site. All the patients were assessed by the ASIA standard before the transplantation and 2-8 weeks after the transplantation. The influence factors including age, sex, duration after the injury, and injury degreesand levels were compared with those in the functional improvement after fetal OEC transplantation. Results The partially-improved neurological functions assessed by the ASIA standard were indicated by the motor scores increasing from 39.1±20.6 to 45.9±20.3 (Plt;0.001), the light touch scores from 51.7±24.9 to 63.4±23.0 (Plt;0.001), and the pin prick scores from 53.0±24.2 to 65.3±22.7(Plt;0.001). There was no significant difference in the functional improvement of the motor, light touch, and pin brick when compared with the age, sex, duration after theinjury, and the injury degrees and levels. The motor scores and light touch scores at the cervical level were higher than the scores at the thoracic level. Conclusion The fetal OEC transplantation can partially improve the neurological functions quickly in treatment of the chronic spinal cord injury. All the influence factors except the motor scores and light touch scores, which were higher at the cervical level than at thoracic level, have no impact on the functional improvement after the fetal OEC transplantation.
Objective Targeted adenoviral gene delivery from peripheral nerves was used to integrally analyse the characterization and time course of LacZ gene (AdLacZ) retrograde transfer to spinal cord and transgene product anterograde labeling ofperipheral nerve. Methods Recombinant replication-defective adenovirus containing AdLacZ was administrated to the cut proximal stumps of median and tibial nerves in Wister rats. Then the transected nerve was repaired with 10-0 nylon sutures. At different time point postinfection the spinal cords of C5 to T1 attached with DRGs and brachial plexuses, or L2 to L6 attached with DRGs and lumbosacralplexuses were removed. The removed spinal cord and DRGs were cut into 50 μm serialcoronal sections and processed for X-gal staining and immunohistochemical staining. The whole specimens of brachial or lumbosacral plexuses attaching with theirperipheral nerves were processed for X-gal staining. The number of X-gal stained neurons was counted and the initial detected time of retrograde labeling, peaktime and persisting period of gene expression in DRG sensory neurons, spinal cord motor neurons and peripheral nerves were studied. Results The gene transfer was specifically targeted to the particular segments of spinal cord andDRGs, and transgene expression was strictly unilaterally corresponding to the infected nerves. Within the same nerve models, the initial detected time of gene expression was earliest in DRG neurons, then in the motor neurons and latest in peripheral nerves. The persisting duration of β-gal staining was shortest in motor neurons, then in sensory neurons and longest in peripheral nerves. The initial detected time of β-gal staining in median nerve models was earlier in mediannerve models compared with that in the tibial nerve models. Although the initial detected time and the beginning of peak duration of β-gal staining were not same, the decreasing time of β-gal staining in motor and sensory neurons of thetwo nerve models were started at about the same day 8 post-infection. The labeled neurons were more in tibial nerve-models than that in median nerve models. Within the same models, the labeled sensory neurons of DRGs were morethan labeled motor neurons of ventral horn. The β-gal staining was tenser in median nerves than that in tibial nerves. However the persisting time of β-gal staining was longer in tibial nerve models. Conclusion The b gene expression in neurons and PNS renders this system particularly attractive for neuroanatomical tracing studies. Furthermore this gene delivery method allowing specific targeting of motor and sensory neurons without damaging the spinal cord might offer potentialities for the gene therapy of peripheral nerve injury.
目的:总结经鼻内窥镜下手术治疗管内段视神经损伤的疗效。方法:回顾性分析11例视神经损伤住院患者的临床资料。结果:行视神经减压术的11例患者中1例失访，7例有效，其中4例视力有较明显的提高。结论:经鼻内镜视神经减压术损伤小，并发症少，手术时间短，疗效满意。
ObjectiveTo observe the early ultrastructural changes of the optic nerves after the brain impact injury.MethodsEighteen 15-week-old Wistar rats were used in the air-pressure brain impact injury examination. All of the rats underwent the procedures of right-parietal-bone fenestration after abdominal cavity anesthesia with 1% sodium pentolbarbital (45 mg/kg), and then they were divided randomly into 3 groups, i.e., mild injury group (8 rats) underwent with 7 kg of air pressure in distance of 11 cm; severe injury group (8 rats) with 7 kg of airpressure in distance of 8 cm; and control group (2 rats) underwent with the parietalbone fenestration but without impact injury.The ultrastructural changes of the optic nerves were observed 1, 6, 24, and 72 hours after the injury by electron microscopy.ResultsThe difference of ultrastructural changes of optic nerve was not obvious in wild injury group and the control group, and the lanthanum nitrate was only found in the blood vessels in optic nerve. The lanthanum nitrate entered the nerve stroma 1 hour after severe and increased as time goes on. Simultaneously, displayed dilatation of endoplasmic reticulum, cavitation and tumefaction of mitochondrion, vacuolation of nerve stroma, and vacuolation of some axis-cylinder were seen in the glial cells.ConclusionThe brain impact injury may cause ultrastructural changes of the optic nerve and increase of permeability of blood vessels. (Chin J Ocul Fundus Dis, 2005,21:41-43)
Objective To investigate the relationship between the expression of hypoxia inducible factor 1α (HIF-1α) and the neuron apoptosis during a hypoxia ischemia brain damage and explore the role of HIF1α in regulating the neuron apoptosis and repairing the brain damaged by hypoxia and ischemia. Methods Forty SD rats aged 10 days were randomly divided into the experiment group and the control group, with 20 rats in each group. In the experimental group, the rats were anesthetized with ethylether. The right common carotid artery was exposed and ligated. Then, they were exposed to hypoxia ina normobaric chamber filled with 8% oxygen and 92% nitrogen for 2.5 hours. In the control group, the right common carotid artery was exposed but was not ligated or exposed to hypoxia. The brain tissues were harvested from the rats in the both groups at 4, 8, 24, 48 and 72 hours after the hypoxia and ischemia, and fromthe rats in the control group at the same time points. The HIF-1α protein expression and the cleaved caspase 3 (CC3) protein expression were detected with the immunohistochemistry method. The apoptosis cells were detected with the TUNEL staining method. Results In the experimental group, the HIF-1α expression was significantly increased at 4 hours after operation, at the peak level at 8 hours, and began to decrease at 24 hours. The CC3 protein was expressed at 4 hours after operation, and was slightly expressed at 8 hours, but was significantly increased at 24 hours; the higher levels were maintained at 48 and 72 hours. However, in the control group, both the expression levels of HIF-1α and the CC3 protein were extremely low. So, the expression levels of HIF-1α andthe CC3 protein were significantly higher in the experimental group than in the control group (P＜0.01). The TUNEL staining showed that in the experimentalgroup the positive cells were significantly increased after the hypoxia and ischemia, with a peak level at 72 hours after the hypoxia and ischemia; however, in the control group there were few positive cells.TUNEL positive cells in the experimental group were significantly more than that in the control group(P＜0.01).ConclusionThe expression tendency of HIF-1α is completely different from that of CC3.HIF-1α may have a protective role in regulating the neuron apoptosis in the neonatal hypoxia-ischemia brain damage and may promote the repairing and rebuilding process in the brain that was damaged by hypoxia and ischemia.
Objective To study the mRNA expressions of protein kinase C(PKC) and nerve growth factor (NGF) in rat sciatic nerve and the number ofaxons after phorbol-12-myristate-13-acetate (PMA) was injected into silicone chamber. Methods Forty-two SD adult rats were divided into six groups depending on the time of injury (1 day, 3 days, 1 week, 2 weeks, 3 weeks and 4 weeks). A 0.5 cm nerve was cut in doublerat sciatic nerves and “T” type silicone chamber was sutured. PMA at the concentration of 1×10-9mol/L was injected discontinuously into the right side of Ttype silicone chamber(PMA group) and saline was injected into the left side(control group). Nucleic acid in situ hybridization histochemistry technique and thecomputer imagine analysis were employed to detect dynamic changes of PKC mRNA and NGF mRNA in rat sciatic nerves. The number of axons was measured. Results The expressions of PKC mRNA and NGF mRNA increased after injury, and the expressions of PKC mRNA and NGF mRNA reached the peak 2 weeks and3 weeks after injury respectively in control group. The expressions of PKC mRNA and NGF mRNA in PMA group were significantly increased than those in control group 2,3 and 4 weeks after injury(Plt;0.01).The number of axons in PMA group significantly increased than that in control group(Plt;0.01). Conclusion PKC involved inthe expression of NGF mRNA and nerve regeneration after injury. During the regenerated course, PMA can promote the expression of NGF mRNA and the number of axons after injury.