Early electrical field stimulation prevents the loss of spinal cord anterior horn motoneurons and muscle atrophy following spinal cord injury

Our previous study revealed that early application of electrical field stimulation（EFS） with the anode at the lesion and the cathode distal to the lesion reduced injury potential, inhibited secondary injury and was neuroprotective in the dorsal corticospinal tract after spinal cord injury（SCI）. The objective of this study was to further evaluate the effect of EFS on protection of anterior horn motoneurons and their target musculature after SCI and its mechanism. Rats were randomized into three equal groups. The EFS group received EFS for 30 minutes immediately after injury at T_（10）. SCI group rats were only subjected to SCI and sham group rats were only subjected to laminectomy. Luxol fast blue staining demonstrated that spinal cord tissue in the injury center was better protected; cross-sectional area and perimeter of injured tissue were significantly smaller in the EFS group than in the SCI group. Immunofluorescence and transmission electron microscopy showed that the number of spinal cord anterior horn motoneurons was greater and the number of abnormal neurons reduced in the EFS group compared with the SCI group. Wet weight and cross-sectional area of vastus lateralis muscles were smaller in the SCI group to in the sham group. However, EFS improved muscle atrophy and behavioral examination showed that EFS significantly increased the angle in the inclined plane test and Tarlov＇s motor grading score. The above results confirm that early EFS can effectively impede spinal cord anterior horn motoneuron loss, promote motor function recovery and reduce muscle atrophy in rats after SCI.

Sciatic nerve injury alters the spatial arrangement of neurons and glial cells in the anterior horn of the spinal cord

The spatial arrangement of the cell is important and considered as underlying mechanism for mathematical modeling of cell to cell interaction.The ability of cells to take on the characteristics of other cells in an organism,it is important to understand the dynamical behavior of the cells.This method implements experimental parameters of the cell-cell interaction into the mathematical simulation of cell arrangement.The purpose of this research was to explore the three-dimensional spatial distribution of anterior horn cells in the rat spinal cord to examine differences after sciatic nerve injury.Sixteen Sprague-Dawley male rats were assigned to control and axotomy groups.Twelve weeks after surgery,the anterior horn was removed for first-and second-order stereological studies.Second-order stereological techniques were applied to estimate the pair correlation and cross-correlation functions using a dipole probe superimposed onto the spinal cord sections.The findings revealed 7% and 36% reductions in the mean volume and total number of motoneurons,respectively,and a25% increase in the neuroglial cell number in the axotomized rats compared to the control rats.In contrast,the anterior horn volume remained unchanged.The results also indicated a broader gap in the pair correlation curve for the motoneurons and neuroglial cells in the axotomized rats compared to the control rats.This finding shows a negative correlation for the distribution of motoneurons and neuroglial cells in the axotomized rats.The cross-correlation curve shows a negative correlation between the motoneurons and neuroglial cells in the axotomized rats.These findings suggest that cellular structural and functional changes after sciatic nerve injury lead to the alterations in the spatial arrangement of motoneurons and neuroglial cells,finally affecting the normal function of the central nervous system.The experimental protocol was reviewed and approved by the Animal Ethics Committee of Shahid Beheshti University of Medical Sciences(approval No.IR.SBMU.MSP.REC1395.375) on October 17,2016.

p75 neurotrophin receptor signal pathway influence on apoptosis in anterior horn neurons of the spinal cord in a rat model of cauda equina compression injury

BACKGROUND： Studies have demonstrated that cauda equina compression results in apoptosis of motor neurons in the spinal cord. The combination of p75 neurotrophin receptor （p75NTR） and precursor of nerve growth factor （pro-NGF） expression initiates the apoptotic pathway and induces neuronal apoptosis. However, few reports have focused on the p75-mediated mechanism of neuronal apoptosis following cauda equine compression injury OBJECTIVE： To determine apoptosis of spinal cord neurons and activation of the pro-NGF-p75NTR-JNK（c-Jun N-terminal kinase） signal pathway in rats following cauda equina compression, and to verify experimental outcomes. DESIGN, TIME AND SETTING： A randomized, controlled, in vivo experiment was performed at the Medical Experimental Center of Xi＇an Jiaotong University between April and November in 2008. MATERIALS： Streptavidin-perosidase kit was purchased from Wuhan Boster, China; in situ end labeling detection kit was provided by Promega, USA; type AEG-220G electron microscope was purchased from Hitachi, Japan. METHODS： A total of 48 healthy, adult, female, Sprague Dawley rats were randomly assigned to three groups： normal （n = 6）, sham-surgery （n = 6）, and compression （n = 36）. The compression group was randomly assigned to six subsets at 1,3, 5, 7, 14, and 28 days, respectively, with 6 rats in each subset. A cylindrical silica gel stick was implanted into the rats to compress 75% of the vertebral canal in the compression group; in the sham-surgery group, only vertebral resection was performed; and no procedures were performed in the normal group. MAIN OUTCOME MEASURES： At 1,3, 5, 7, 14, and 28 days following compression, L2-3 spinal cord segments were processed for immunohistochemistry, in situ cell apoptosis detection, and transmission electron microscopy observation. Nissl staining was used to observe neuronal survival in the L2 spinal cord segment. Immunohistochemistry was applied to detect expressions of pro-NGF, p75NTR, and JNK in the L2 segment. TUNEL fluorometric method was used to observe apoptosis of neurons in the L2 segment. RESULTS： In the normal and sham-surgery groups, little neuronal apoptosis was observed in the L2-3 spinal cord segment. At 3 days after compression injury, pro-NGF, p75NTR and JNK expression was observed in the spinal cord. Expression levels reached a peak at 7 days, and then gradually decreased. In the compression and sham-surgery groups, neurons primarily expressed pro-NGF and p75NTR. The number of JNK-positive neurons in the compression group was dramatically increased compared with the sham-surgery group （P〈 0.05）. A few neurons were apoptotic in the spinal cord 1 day after compression injury. The number of apoptotic neurons gradually increased and reached a peak at 7 days, and subsequently decreased. Apoptosis was still detectable at 28 days. There was a positive correlation between p75NTR expression and neuronal apoptosis （r= 0.75, P〈 0.05）. CONCLUSION： Following cauda equina compression injury, apoptosis of spinal cord neurons was observed. The compression-induced neuronal apoptosis was associated with p75NTR expression in the L2-3 spinal cord segment.

Effects of Epidural Spinal Cord Stimulation and Treadmill Training on Locomotion Function and Ultrastructure of Spinal Cord Anterior Horn after Moderate Spinal Cord Injury in Rats

Objective:To investigate the effects of epidural spinal cord stimulation(ESCS) and treadmill training on the locomotion function and ultrastructure of spinal cord anterior horn after moderate spinal cord injury in rats.Method:Nine adult female Sprague-Dawley rats were randomly distributed into three groups:①spinal cord injury group(SI,n=3).②spinal cord injury plus ESCS group(SE,n=3).③spinal cord injury plus treadmill training group(TT,n=3).All rats received a moderate spinal cord injury surgery.Four weeks after surgery,rats in SE group received an electrode implantation procedure,with the electrode field covering spinal cord segments L2-S1.Four weeks after electrode implantation,rats received subthreshold ESCS for 30 min/d.Rats in TT group received 4cm/s treadmill training for 30min/d.Rats in SI group received no intervention,as a control group.All procedures in these three groups lasted four weeks.The open field Basso,Beattie and Bresnahan(BBB) scale was used before and after intervention to evaluate rats' hindlimb motor function.Result:After four weeks intervention,rats in TT group improved their open field locomotion scores to 20.In contrast,no significant improvement was observed in groups SI and SE.The morphology of synapses and neurons were similar regardless of whether rats had undergone ESCS,treadmill training or not.Conclusion:ESCS alone was not sufficient to improve the walking ability of spinal cord injured rats.ESCS or treadmill training alone might not contribute to the changes of ultrastructure in anterior horn of spinal cord that underlie the recovery of walking ability.Further research is needed to understand the contributions of combination of ESCS and treadmill training to the rehabilitation of spinal cord injured rats.

Visualizing Wallerian degeneration in the corticospinal tract after sensorimotor cortex ischemia in mice

Stroke can cause Wallerian degeneration in regions outside of the brain,particularly in the corticospinal tract.To investigate the fate of major glial cells and axons within affected areas of the corticospinal tract following stroke,we induced photochemical infarction of the sensorimotor cortex leading to Wallerian degeneration along the full extent of the corticospinal tract.We first used a routine,sensitive marker of axonal injury,amyloid precursor protein,to examine Wallerian degeneration of the corticospinal tract.An antibody to amyloid precursor protein mapped exclusively to proximal axonal segments within the ischemic cortex,with no positive signal in distal parts of the corticospinal tract,at all time points.To improve visualization of Wallerian degeneration,we next utilized an orthograde virus that expresses green fluorescent protein to label the corticospinal tract and then quantitatively evaluated green fluorescent protein-expressing axons.Using this approach,we found that axonal degeneration began on day 3 post-stroke and was almost complete by 7 days after stroke.In addition,microglia mobilized and activated early,from day 7 after stroke,but did not maintain a phagocytic state over time.Meanwhile,astrocytes showed relatively delayed mobilization and a moderate response to Wallerian degeneration.Moreover,no anterograde degeneration of spinal anterior horn cells was observed in response to Wallerian degeneration of the corticospinal tract.In conclusion,our data provide evidence for dynamic,pathogenic spatiotemporal changes in major cellular components of the corticospinal tract during Wallerian degeneration.

宫颈前角、宫颈长度及剪切波速度在宫颈机能不全自发性早产风险中的预测价值研究

目的分析宫颈前角(Anterior uterocervical angle,ACA)、宫颈长度(Cervical length,CL)及剪切波速度(Shear wave velocity,SWV)在宫颈机能不全自发性早产风险中的联合预测价值。方法以2023年2月-6月在南京医科大学第二附属医院妇产科建档的376例宫颈机能不全孕妇为研究对象,分析不同孕周(19~23 w+6 d、24~27 w+6 d、28~33 w+6 d、34~36 w+6 d)时ACA、CL、SWV与孕周的相关性。对所有孕妇随访至完成分娩,根据孕妇是否早产分为早产组与非早产组,比较2组孕妇的一般资料。经Logistic回归分析宫颈机能不全孕妇早产的风险因素,根据危险因素构建预测模型,采用受试者工作特征(Receiver operating characteristic curve,ROC)曲线分析ACA、CL、SWV对宫颈机能不全孕妇自发性早产风险的单独及联合预测效能,采取Pearson相关性分析ACA、CL及SWV与宫颈机能不全孕妇孕周的相关性。结果不同孕周的宫颈机能不全孕妇SWV、CL间,差异有统计学意义(P<0.05),且随着孕周增加SWV、CL呈下降趋势(P<0.05),不同孕周的宫颈机能不全孕妇比较,ACA差异无统计学意义(P>0.05)。Pearson相关性分析结果表明,SWV、CL与宫颈机能不全孕妇的孕周呈负相关关系(r=-0.628、-0.867,P<0.05)。ACA与宫颈机能不全孕妇的孕周无相关性(r=0.109,P=0.081)。376例孕妇中自发性早产79例,自发性早产率为21.01%(79/376),足月产297例,足月产率为78.99%(297/376)。将79例自发性早产孕妇纳入早产组,其余297例足月产孕妇分为非早产组,经单因素分析表明,两组年龄、BMI、流产次数、辅助生殖技术妊娠情况、孕周,差异无统计学意义(P>0.05),与非早产组比较,早产组ACA升高,CL、SWV降低(P<0.05)。Logistic回归分析表明ACA、CL、SWV均是导致宫颈机能不全孕妇自发性早产的重要风险因素(P<0.05),建立早产联合预测模型:Logistic(P)=-48.126+6.059×SWV+0.206×CL+0.295×ACA;ROC曲线分析表明,ACA、CL、SWV对宫颈机能不全孕妇自发性早产的单独预测灵敏度分别为82.90%、68.30%、80.50%,ACA+CL+SWV联合预测灵敏度为93.90%。结论ACA、CL、SWV在宫颈机能不全孕妇自发性早产风险中具有一定预测价值,3个指标联合预测的敏感度与准确度较高。

In vivo imaging of the neuronal response to spinal cord injury:a narrative review

Deciphering the neuronal response to injury in the spinal cord is essential for exploring treatment strategies for spinal cord injury(SCI).However,this subject has been neglected in part because appropriate tools are lacking.Emerging in vivo imaging and labeling methods offer great potential for observing dynamic neural processes in the central nervous system in conditions of health and disease.This review first discusses in vivo imaging of the mouse spinal cord with a focus on the latest imaging techniques,and then analyzes the dynamic biological response of spinal cord sensory and motor neurons to SCI.We then summarize and compare the techniques behind these studies and clarify the advantages of in vivo imaging compared with traditional neuroscience examinations.Finally,we identify the challenges and possible solutions for spinal cord neuron imaging.

前列腺前角穿刺活检在前列腺癌诊断中的价值

目的·探讨前角穿刺活检在前列腺癌诊断中的临床价值。方法·回顾性分析1 679 例在上海交通大学医学院附属仁济医院行超声引导下经会阴12 点初次前列腺穿刺活检患者的临床及病理资料,分析比较12 点(包括前角)穿刺活检方案和10 点(除外前角)穿刺活检方案在总体及不同亚组间前列腺癌检出率的差异。结果· 1 679 例患者经穿刺诊断为前列腺癌者678 例(40.4%),仅前角阳性59 例(8.7%)。排除前角穿刺点后,穿刺阳性率为36.9%(619/1 679),低于包含前角穿刺点的总体阳性率(40.4% vs 36.9%,P=0.046)。在对前列腺特异性抗原(prostate specific antigen,PSA)及前列腺体积分组比较中,对PSA>10 ng/mL 或前列腺体积≥ 30 mL的患者,采用前角穿刺后可提高穿刺阳性率(P<0.05)。在临床特征比较中,仅前角穿刺阳性患者的前列腺体积显著高于除前角穿刺阳性患者(P=0.006),Gleason 评分显著低于除前角穿刺阳性患者(P=0.000)。结论·增加前角穿刺能提高穿刺阳性率,推荐在初次经会阴前列腺穿刺活检中常规应用。

实验性马尾神经综合征家兔骶髓前角细胞凋亡的观察

目的 :观察马尾神经综合征 (CES)个体骶髓前角细胞的病理改变 ,以探讨其可能的发生机制。 方法 :选用纯种健康雄性新西兰兔 80只 ,将压迫装置置于其 S2 ～ S3棘突之间压迫马尾神经制备 CES模型。取出现 CES后不同时期 (发病后 1/ 4、1/ 2、3、7、30 d)的动物麻醉后 ,用生理盐水和 4 %多聚甲醛心脏灌注固定 ,取脊髓圆锥包埋 ,以 5μm厚度连续切片 ,进行 H- E染色和 DNA片段原位末端标记 (TUNEL)法检测 ,结合其形态学改变进行凋亡细胞计数 ,并作对比研究。结果 :出现 CES后1/ 4 d,TUNEL 法检测示骶髓前角细胞发生凋亡改变 ;至 1/ 2 d时 ,凋亡细胞明显增多 ,且以早期凋亡细胞为主 ,与对照组比较有显著差异 ,H- E染色示骶髓前角细胞形态发生改变 ;以后凋亡细胞逐渐减少 ,但仍高于对照组水平。结论 :CES时骶髓前角细胞病理改变的主要方式是细胞凋亡 ;随着病情的发展 ,大部分凋亡细胞由凋亡早期进入死亡期 (不可逆期 ) 。

神经根撕脱后脊髓运动神经元的病理表现

目的 :观察神经根撕脱后脊髓前角运动神经元的病理表现 ,探讨在该条件下运动神经元死亡的神经生物学机制。方法 :选择成年SD雌性大鼠 2 0只 ,体重 2 0 0 - 30 0g ,撕脱右侧臂丛C5-T8神经根 ,术后动物存活 3d、5d、1周后取C5-C8节段脊髓 ,对冰冻切片行NADPH -d组化、c -jun免疫组化、中性红和HE染色。观察神经元的形态 ,计数脊髓前角NOS阳性运动神经元及存活运动神经元数目 ,以非损伤侧的前角运动神经元数目为 10 0 % ,计算百分比。结果 :神经根撕脱 3d、5d、1周后 ,损伤侧脊髓前角NOS运动神经元平均阳性率分别为 :0 74%± 0 5 9%、2 4 83%± 6 73%、5 1 16 %± 8 6 7%。神经元平均存活率分别为 93 0 0 %± 4 32 %、93 6 7%± 5 2 7%、89 83%±2 6 5 % ;c -Jun从撕脱术后 3d就有表达 ,5d后表达开始减少。运动神经元形态变化不明显。 1周时偶见前角运动神经元的胞核偏位 ,但核膜清晰 ,核仁尚存 ,染色体固缩。结论 :脊神经根撕脱 1周内 ,脊髓前角运动神经元NOS表达递增 ,c-Jun表达递减 ,运动神经元开始死亡。NO/NOS可能通过抑制神经元损伤后的再生反应 ,促进脊髓前角运动神经元的死亡。

针刺对实验性脊髓损伤前角运动神经元酶学的影响

目的:探讨针刺对大鼠脊髓损伤前角运动神经元酶学的影响。方法:采用酶组织化学染色方法定性分析针刺治疗前后脊髓前角运动神经元乙酰胆碱酯酶(ACHE)、琥珀酸脱氢酶(SDH)、酸性磷酸酶(ACP)的含量变化;同时,运用全自动图像分析仪系统进行定量分析。结果:脊髓损伤后ACHE和SDH含量减少(P<001);ACP含量增加(P<001)。而针刺组针刺后均较对照组同时段点ACHE、SDH酶含量高;ACP酶含量低(P<005,P<001)。结论:针刺能调节脊髓损伤后前角运动神经元酶含量,具有抑制或延缓神经元变性程度并能促进其恢复。

不同强度训练后大鼠脊髓前角细胞线粒体的定量研究

目的 :研究不同强度耐力训练对大鼠脊髓前角细胞线粒体超微结构的不同影响 ,探讨适合神经系统发展的最佳训练强度。方法 :2 4只雄性SD大鼠随机分为 4组 ,即对照组、小强度运动组、大强度运动组、大强度运动力竭组各 6只。训练后对各组大鼠脊髓前角细胞线粒体进行电镜观测并用体视学方法做定量分析。结果 :各训练组脊髓前角细胞线粒体数量增多 ,嵴多而致密 ,基质电子密度增高。但大强度运动力竭组出现线粒体嵴断裂、空泡变 ,甚至线粒体裂解现象。体视学测量结果表明 ,各训练组与对照组之间以及各训练组之间线粒体Vv、Sv、Nv、δ均发生不同程度的改变。结论 :不同强度耐力训练可引起大鼠脊髓前角细胞线粒体形态结构的不同改变 ,小强度运动训练通过线粒体形状改变和膜面积增加即可达到能量代谢的需求 ;大强度运动可引起线粒体的总体积、数量及膜面积等形态结构发生适应性代偿 ,为有效的训练强度 ;大强度力竭运动则可引起线粒体形态结构的不可逆损害 ,不利于机体健康。

不同手术路径对脑室-腹腔分流手术效果的影响

目的探讨脑室-腹腔分流的手术路径的改进方法。方法对56例脑积水患者行脑室-腹腔分流术。根据手术路径不同,分成两组。实验组22例,采用经侧脑室额角穿刺、经耳前路径的方法。对照组34例,采用传统的侧脑室枕角穿刺、耳后路径。分析比较两组手术的治疗结果和并发症发生情况。结果术后早期CT检查,发现实验组脑室明显缩小者占86.4%,脑室内导管位置满意者占94.4%,均明显高于对照组(P<0.05)。随访期内发现,实验组导管阻塞1例(4.5%),对照组导管阻塞9例(26.5%),两组比较有显著性差异(P<0.05)。结论经侧脑室额角穿刺、经耳前路径的手术方法可能优于传统分流手术,值得临床推广应用。

大鼠坐骨神经损伤后脊髓前角神经元死亡数量的研究

目的 :研究周围神经损伤后 ,脊髓前角运动神经元胞体的死亡数量变化。方法 :选择 10只正常SD大鼠 ,先计算两侧的脊髓前角运动神经元胞体数量是否对称 ;再选择 3 5只SD大鼠 ,切断并原位吻合其右侧坐骨神经 ,左侧不作任何处理、作为对照 ,于术后不同时间取L4～ 6节段脊髓作HE染色 ,计算脊髓前角运动神经元胞体数量的变化。结果 :正常SD大鼠两侧的脊髓前角运动神经元胞体数量呈对称分布 ;右侧坐骨神经损伤后 ,其脊髓前角运动神经元胞体数量较左侧减少。结论 :大鼠坐骨神经损伤后 ,脊髓前角运动神经元的胞体有死亡 ,其死亡具有一定的时间特征。

运动对小鼠寿命和脊髓前角神经元形态和数量的影响

用C_(57)BL/3J小鼠29只,分成运动组(12只),对照组(12只)和青年组(5只)三组.运动组从第6个月起隔天跑转笼2小时,对照组不跑转笼.当这两组小鼠死亡总数达50%时(经过16个月零8天),将两组余下的小鼠(22月龄)全部杀死,取出脊髓腰膨大(L_2)与青年组(6月龄)的相比较.结果表明:运动组与对照组的存活率无显著性差异,P>0.05;老年的小鼠脊髓前角神经元总数比青年组的少,但运动组神经元减少较轻,P<0.05,减少的主要的是小神经元,大、中神经元并没有减少;而对照组神经元减少明显,P<0.01,减少的主要是大、中神经元.在三组随机抽出的大神经元胞体切面面积中,运动组最大,青年组居中,对照组最小,两两比较P均<0.01.实验结果提示:长期适量的运动对小鼠的寿命影响不大,但可能会减轻脊髓前角神经元在衰老过程中的死亡程度,最明显的影响是将运动神经元保存下来.

改良无切口针孔式外内多针缝合术在半月板前体部损伤中的应用

目的探讨改良无切口针孔式外内多针缝合技术治疗膝关节半月板前体部损伤的临床疗效。方法 38例膝关节半月板前体部损伤患者,均于关节镜下使用MM-Ⅱ缝合器进行改良无切口针孔式外内多针缝合,术后随访1~2年。比较术前及末次随访时患者膝关节活动度、Lysholm评分及国际膝关节评分委员会(IKDC)膝关节主观功能评分。结果所有患者在末次随访时均无关节交锁及失稳症状,膝关节活动度、Lysholm及IKDC评分均高于术前(P<0.05)。结论使用MM-Ⅱ进行改良无切口针孔式外内多针缝合术治疗膝关节半月板前体部损伤,切口更美观,缝合的灵活性更大,安全性好,近期疗效满意。

猫脊髓前角运动神经元区的P物质样及胆碱乙酰化酶样免疫反应

用ABC法对猫脊髓前角运动神经元区(Ⅸ层)的P物质样及胆碱乙酰化酶样免疫反应(SP-LI和ChAT-LI)的分布作了观察与比较。结果发现:(1)Ⅸ层的大、中型神经元几乎均为ChAT-LI阳性,部分ChAT-LI神经元胞体及近端树突表面有少量ChAT-LI终扣。(2)SP-LI出现于Ⅸ层多数大、中型神经元的胞体和突起根部,约半数以上SP-LI神经元显示较强呈色反应。较多SP-LI串珠状终末纤维散在于Ⅸ层,SP-LI神经元表面可见SP-LI终扣。以上提示:(1)P物质(SP)和乙酰胆碱(ACh)共存于前角运动神经元,SP可能参与调制神经肌接头的胆碱能传递。(2)前角运动神经元尚接受SP能及胆碱能神经支配。

神经生长因子对兔坐骨神经损伤后脊髓前角运动神经元乙酰胆碱酯酶的影响

钳夹损伤兔右坐骨神经，于损伤处注射蛇毒ＮＧＦ４００Ｂｕ／ｋｇ／日，损伤术后１，３，７天和２，３，４，６，８周动态观察脊髓腰段伤侧第Ⅸ板层外侧群的大型运动神经元的ＡＣｈＥ活性改变。结果表明术后１，３天实验组（指损伤给药组）和对照组（指损伤对照组）ＡＣｈＥ活性均下降（Ｐ＞００５）；术后１，２，３周对照组ＡＣｈＥ活性明显下降，而实验组ＡＣｈＥ活性逐渐趋于恢复（Ｐ＜００１）；术后６周实验组ＡＣｈＥ活性恢复至正常水平（Ｐ＜００１）。本研究显示蛇毒ＮＧＦ对坐骨神经损伤后脊髓前角运动神经元ＡＣｈＥ活性恢复有促进作用。

龟龄集对大鼠小脑皮质和脊髓前角内突触小泡蛋白变化的影响

目的研究龟龄集对大鼠小脑皮质和脊髓前角内突触小泡蛋白表达的影响,探讨龟龄集抵抗中枢神经系统衰老的机制。方法采用神经行为结合免疫组织化学和图像分析的方法,检测了小脑皮质和脊髓颈膨大、腰膨大前角内突触小泡蛋白的含量及其意义。结果喂药组小脑皮质和脊髓颈、腰膨大前角内突触小泡蛋白的含量均明显高于对照组（P〈0.01~P〈0.001）。结论龟龄集可延缓神经元的衰老,防止中枢神经系统内突触小泡蛋白的丢失,维持动物正常的运动及其运动的灵活性。

关节镜下外侧半月板前角缝合34例临床观察

目的探讨关节镜下应用半月板缝合技术治疗外侧半月板前角损伤的临床效果。方法选取沈阳军区总医院骨科2015年3—12月应用半月板过线缝合系统治疗外侧半月板前角损伤患者34例,其中,16例应用半月板缝合钩,18例应用MM-Ⅱ半月板缝合器。所有患者术后均采用Lysholm评分系统进行疗效评价。结果本组34例患者术后均获随访3~8个月,平均(6.1±1.3)个月。所有患者术后疼痛及屈伸活动均较术前明显改善;但两组间比较,差异无统计学意义(P>0.05)。结论两种半月板缝合方法治疗外侧半月板前角损伤均疗效确切,可早期修复外侧半月板前角损伤。