腓骨长肌腱前半部作为自体移植材料的临床研究

 目的 探讨腓骨长肌腱前半部（anterior half of the peroneus longus tendon,AHPLT）作为自体肌腱移植材料重建膝关节韧带的可行性及疗效。方法 2007年7月至2008年1月采用AHPLT作为自体肌腱移植材料的膝关节韧带损伤患者100例,男33例,女67例;年龄16~62岁,平均32.3岁。关节镜下内侧髌股韧带重建49例、多条韧带重建19例、后十字韧带双束重建18例和前十字韧带双束重建14例。切取AHPLT作为全部（49例）或部分（51例）重建材料,采用单切口或双切口技术,重建韧带用螺钉挤压固定。术后评估膝关节Kujala评分、Lysholm评分、Marx评分、国际膝关节文献委员会（International Knee Documentation Committee,IKDC）膝关节主观评估表和客观等级评定、踝关节足踝功能障碍指数（Foot and Ankle Disability Index,FADI）及美国足踝外科学会（American Orthopedic Foot and Ankle Society,AOFAS）评分。结果 92例获得2年以上随访。术后2年,不同韧带重建组患者膝关节IKDC主观评分、Kujala评分、Lysholm评分及Marx评分均高于重建术前。多条韧带重建、后十字韧带双束重建和前十字韧带双束重建术后IKDC客观等级评定结果达到正常及接近正常者分别为17例、15例和12例,优良率分别为89.5%（17/19）、93.7%（15/16）和100%（12/12）。全部患者手术前后AOFAS评分分别为（97.4±2.0）分和（97.2±1.6）分,FADI评分分别为（96.8±2.2）分和（96.9±2.5）分,差异均无统计学意义。患者均未出现腓神经损伤、腓骨长肌腱断裂等并发症。结论 AHPLT作为自体肌腱移植材料重建膝关节韧带具有操作可行性,近期临床疗效好,切取肌腱后对踝关节功能影响小。     

NMDA receptor antagonist MK-801 reduces neuronal damage and preserves learning and memory in a rat model of traumatic brain injury

Objective

NMDA receptor channel plays an important role in the pathophysiological process of traumatic brain injury (TBI). The present study aims to study the pathological mechanism of TBI and the impairment of learning and memory after TBI, and to investigate the mechanism of the protective effect of NMDA receptor antagonist MK-801 on learning and memory disorder after TBI.

Methods

Forty Sprague-Dawley rats (weighing approximately 200 g) were randomized into 5 groups (n = 8 in each group): control group, model group, low-dose group (MK-801 0.5 mg/kg), middle-dose group (MK-801 2 mg/kg), and high-dose group (MK-801 10 mg/kg). TBI model was established using a weight-drop head injury mode. After 2-month drug treatment, learning and memory ability was evaluated by using Morris water maze test. Then the animals were sacrificed, and brain tissues were taken out for morphological and immunohistochemical assays.

Results

The ability of learning and memory was significantly impaired in the TBI model animals. Besides, the neuronal caspase-3 expression, neuronal nitric oxide synthase (nNOS)-positive neurons and OX-42-positive microglia were all increased in TBI animals. Meanwhile, the number of neuron synapses was decreased, and vacuoles degeneration could be observed in mitochondria. After MK-801 treatment at 3 different dosages, the ability of learning and memory was markedly improved, as compared to that of the TBI model animals. Moreover, neuronal caspase-3 expression, OX-42-positive microglia and nNOS-positive neurons were all significantly decreased. Meanwhile, the mitochondria degeneration was greatly inhibited.

Conclusion

MK-801 could significantly inhibit the degeneration and apoptosis of neurons in damaged brain areas. It could also inhibit TBI-induced increase in nNOS-positive neurons and OX-42-positive microglia. Impairment in learning and memory in TBI animals could be repaired by treatment with MK-801.