Deformation and Fracture Failure of a High-Speed Long Rod Intercepted by Linear Explosively Formed Penetrators Sequence

The fracture failure of a high-speed long rod has historically been a challenge. Since the flying plate and flying rod have a relatively low velocity, it is challenging to achieve a multi-stage fracture of the high-speed long rod within the range of existing technology. In this paper, the linear explosively formed penetrators (LEFPs) sequence with a stable flight velocity of 850 m/s were used to cut a high-speed long rod. We investigated the deformation and fracture of Φ10 mm tungsten alloy long rods having different length-diameter ratios (20, 26, 35) and different speeds (1200, 1400, 1600 m/s) by employing the LEFPs sequence with different spacings (0–40 mm) and different interception angles (30°, 60°). In the meantime, the fractured rods movement pattern was recorded with a high-speed camera to elucidate the change law of the length, speed, linear momentum, and angular momentum of fractured rods. It was found that the length loss rate of the fractured rods is as high as 27%. The fractured rods rotated around the center of mass, and the vertical speed change could reach up to 18% of the muzzle velocity of the long rod, and the greatest reduction of horizontal speed and momentum could reach 37%. The longer the interaction time between LEFPs sequence and the long rod, the more beneficial the failure of the long rod. The application of LEFPs sequence solved the difficult problem of disabling the high-speed long rod, and the quantitative analysis of the fracture failure of the long rod had an important sense for studying the terminal penetration effect of the fractured rods.     

Quadrant可扩张通道显微镜下手术治疗腰椎间盘突出症的研究

目的探讨腰椎间盘突出症应用Quadrant可扩张通道系统显微镜下不同手术方法治疗的临床效果。方法选择2017年3月～2018年4月腰椎间盘突出症患者40例为研究对象,按随机数表法分为单侧组和双侧组各20例,患者均应用Quadrant可扩张通道系统显微镜下手术,对单侧组实施单侧钉棒系统固定治疗,对双侧组实施双侧钉棒系统固定治疗,分析患者手术指标、术后并发症、JOA评分变化、疗效。结果单侧组患者术中出血量、手术时间、手术切口长度、术后住院时间、单病种总医疗费用低于双侧组,差异有统计学意义(P0.05)。患者术后脊柱稳定性均良好,术后1年植骨融合。单侧组术后并发症发生率、术后1年恢复优良率与双侧组比较,差异无统计学意义(P0.05)。单侧组术后1周JOA评分高于双侧组,差异有统计学意义(P0.05)。结论应用Quadrant可扩张通道系统显微镜下手术治疗腰椎间盘突出症效果良好,并发症少,且实施单侧钉棒系统固定时比双侧固定创伤更小,早期恢复效果更好。     

Edwards套棒方法治疗胸腰段脊柱不稳定损伤的生物力学实验研究

本文报告Edwards套棒装置及单纯Harrington分离棒治疗胸腰椎不稳定损伤的力学实验研究结果。取成年猪新鲜胸腰椎脊柱6具,切断前纵韧带、椎间盘纤维环、后纵韧带,造成前中柱不稳定损伤15处。测力传感器固定于椎体前缘并骑跨损伤处,使之检测纵向复位力。单侧内固定装置固定。实验结果表明:单侧Edwards套棒装置产生纵向复位力量89N,较Harrington分离棒48.7N提高82.7％(P<0.0005);二种内固定装置分别用于胸、腰椎时,纵向复位力均无显著差异(P<0.05),表明胸段肋骨对纵向复位力无影响。生物力学分析,纵向复位力与横向前推力成正比例关系,增大内固定装置对伤椎的横向前推力,可提高纵向复位力量。同时其它学者也报告Edwards套棒装置具有良好的脊柱三维稳定作用。所以,作者认为Edwards套棒装置集对脊柱骨折复位与稳定于一体,是理想的内固定装置。     

表面改性TiNi记忆合金棒的回复力学实验研究

采用直径为6~7 mm钛铌涂层T iN i记忆合金棒与未经表面改性的T iN i记忆合金棒,相变温度平均为33.0℃,低温下在三点弯卡具上进行预弯,挠度分别为5.0、10.0、15.0和20.0 mm,保持位移恒定,分别在37℃及50℃的生理盐水溶液恒温水浴箱中测量其三点弯回复力变化特性。结果表明,T iN i记忆合金棒的回复力随回复温度、棒直径、变形量增加而增加;经钛铌表面喷涂后6 mm及6.5 mm棒的回复力有一定降低,但7 mm棒回复力没有显著性差异。依照以上数据可以为临床设计脊柱侧弯矫形棒提供参考。     

Retrieval and clinical analysis of distraction-based dual growing rod constructs for early-onset scoliosis

Background Context

Growing rod constructs are an important contribution for treating patients with early-onset scoliosis. These devices experience high failure rates, including rod fractures.

双生长棒固定治疗重度早发型脊柱侧凸的疗效分析

目的:分析应用双生长棒固定治疗重度早发型脊柱侧凸患者的临床效果,评估其临床应用的临床疗效及安全性。方法:2007年1月~2015年6月我科收治的重度早发型脊柱侧凸并行双生长棒矫形术治疗的患者25例(男12例,女13例),初次术前主弯Cobb角均大于80°且Risser征≤Ⅰ级。测量初次手术前、手术后以及末次随访时冠状面主弯Cobb角、T1~S1高度、矢状面最大后凸角,分析患者的矫形效果及脊柱高度变化。同时收集患者初次术前、初次术后6月及末次随访的肺功能指标及胸部CT,测量患者初次术前、初次术后及末次随访时的肺容积,分析患者肺功能变化情况。结果:入组患者初次术前年龄7.8±1.4岁(5~9岁),随访时间40.3±13.1个月(22~54个月),撑开手术次数平均3.2次(3~7次)。冠状面主弯Cobb角初次术前为96.7°±15.5°,初次术后改善为50.7°±16.1°,至末次随访时改善为40.3°±10.9°;T1~S1高度由初次术前23.2±3.5cm增至初次术后31.1±3.8cm,而末次随访时增至36.5±4.2cm,矢状面最大后凸角初次术前为73.2°±18.9°,初次术后改善为47.7°±15.8°,末次随访时改善为41.2°±11.6°。患者末次随访时肺功能指标及胸廓容积较初次术前明显改善。入组患者共9例出现并发症,其中内固定相关并发症7例(8次),近端交界性后凸4例。结论:双生长棒应用于重度早发型脊柱侧凸患者的治疗可以获得良好的矫形效果,有助于改善和维持患者肺功能,但仍存在一定的手术并发症风险。     

应用Smiley face rod固定系统治疗L5椎弓峡部裂的疗效分析

目的 :探讨应用Smiley face rod固定系统治疗L5椎弓峡部裂的临床疗效。方法:2016年1月~2017年6月,我科采用Smiley face rod固定系统节段内固定植骨融合治疗腰椎峡部裂患者18例,男13例,女5例,年龄28.2±3.2岁(25~32岁),术前平均病程为16.3±5.7个月(7~24个月)。峡部裂节段均位于L5。术后3个月、1年时进行随访,对患者进行疼痛视觉模拟评分(visual analogue scale,VAS)及Oswestry功能障碍指数(Oswestry disability index,ODI)评定,评价其临床治疗效果。行X线、CT等检查,分析术前和术后L5/S1椎间活动度变化及椎间不稳发生率变化情况,并评价患者术后植骨融合情况。结果:手术时间平均90.0±24.1min,术中出血量平均140±15ml。平均随访18.5±5.0个月(12~24个月)。术前VAS评分为7.3±2.5分,ODI为(67.0±15.1)%;术后3个月时分别为3.0±1.2分和(17.2±4.5)%,较术前明显改善(P0.05);术后1年时分别为1.0±0.6分和(9.1±5.3)%,较术后3个月时进一步改善(P0.05)。术前L5/S1间隙活动度为13.1°±2.1°,存在腰椎不稳或小于Ⅰ度滑脱者共15例(83.3%,15/18);术后1年时分别为9.3°±1.6°和2例(11.1%,2/18),两者之间存在统计学差异(P0.05)。术后1年时随访患者峡部裂均获得骨性愈合。结论 :应用Smiley face rod固定系统治疗L5椎弓峡部裂具有创伤小、对神经干扰少、恢复正常的解剖结构、提高椎间稳定性的优点。     

Faulty splicing and cytoskeleton abnormalities in Huntington's disease

Huntington's disease (HD) is caused by a CAG‐repeat encoding a polyglutamine (polyQ) tract in the huntingtin protein. There is plenty of evidence of polyQ‐driven toxicity. However, CAG repeat RNA‐driven alteration of splicing has recently been proposed in analogy to CUG‐repeat diseases. Here we review the reported alteration of the CAG‐repeat associated splicing factor SRSF6 in brains of HD patients and mouse models and how this correlates with altered splicing of, at least, two microtubule‐associated proteins in HD, namely MAPT (tau) and MAP2. Regarding tau, altered splicing of exon 10 has been reported, along with increased levels and 4R/3R‐tau ratio and detection of tau in a new nuclear rod‐shaped histopathological hallmark termed tau nuclear rod (TNR) or tau nuclear indentation (TNI). These findings, together with an attenuation of HD phenotype in R6/1 mice with tau deficiency and subsequent studies showing increased phosphorylation in mouse models and increased levels in CSF of patients, has led to proposing HD as a tauopathy. Regarding MAP2, an increase in its juvenile form and a decrease in total MAP2 together with redistribution from dendrites to soma is observed in HD patients, which may contribute to the dendritic atrophy in HD. Furthermore, MAP2 positive structures filling nuclear indentations have occasionally been found and co‐localized with tau. Therefore, altered MAP function with imbalance in tau/MAP2 content could contribute to HD striatal atrophy and dysfunction. Besides, TNIs might be indicative of such MAP abnormalities. TNIs are also found in early pathology Alzheimer's disease and in tauopathy mice over‐expressing mutant 4R‐tau. This indicates that tau alteration is sufficient for TNI detection, which becomes a marker of increased total tau and/or altered 4R/3R‐tau ratio and reporter of pathology‐associated nuclear indentations. Altogether, these recent studies suggest that correcting the SRSF6‐driven missplicing and/or microtubule‐associated imbalance might be of therapeutic value in HD.     

Noncompaction cardiomyopathy is caused by a novel in‐frame desmin (DES) deletion mutation within the 1A coiled‐coil rod segment leading to a severe filament assembly defect

Mutations in DES, encoding desmin protein, are associated with different kinds of skeletal and/or cardiac myopathies. However, it is unknown, whether DES mutations are associated with left ventricular hypertrabeculation (LVHT). Here, we performed a clinical examination and subsequent genetic analysis in a family, with two individuals presenting LVHT with conduction disease and skeletal myopathy. The genetic analysis revealed a novel small in‐frame deletion within the DES gene, p.Q113_L115del, affecting the α‐helical rod domain. Immunohistochemistry analysis of explanted myocardial tissue from the index patient revealed an abnormal cytoplasmic accumulation of desmin and a degraded sarcomeric structure. Cell transfection experiments with wild‐type and mutant desmin verified the cytoplasmic aggregation and accumulation of mutant desmin. Cotransfection experiments were performed to model the heterozygous state of the patients and revealed a dominant negative effect of the mutant desmin on filament assembly. DES:p.Q113_L115del is classified as a pathogenic mutation associated with dilated cardiomyopathy with prominent LVHT.     

Novel ACTN1 variants in cases of thrombocytopenia

The ACTN1 gene has been implicated in inherited macrothrombocytopenia. To decipher the spectrum of variants and phenotype of ACTN1‐related thrombocytopenia, we sequenced the ACTN1 gene in 272 cases of unexplained chronic or familial thrombocytopenia. We identified 15 rare, monoallelic, nonsynonymous and likely pathogenic ACTN1 variants in 20 index cases from 20 unrelated families. Thirty‐one family members exhibited thrombocytopenia. Targeted sequencing was carried out on 12 affected relatives, which confirmed presence of the variant. Twenty‐eight of 32 cases with monoallelic ACTN1 variants had mild to no bleeding complications. Eleven cases harbored 11 different unreported ACTN1 variants that were monoallelic and likely pathogenic. Nine variants were located in the α‐actinin‐1 (ACTN1) rod domain and were predicted to hinder dimer formation. These variants displayed a smaller increase in platelet size compared with variants located outside the rod domain. In vitro expression of the new ACTN1 variants induced actin network disorganization and led to increased thickness of actin fibers. These findings expand the repertoire of ACTN1 variants associated with thrombocytopenia and highlight the high frequency of ACTN1‐related thrombocytopenia cases. The rod domain, like other ACTN1 functional domains, may be mutated resulting in actin disorganization in vitro and thrombocytopenia with normal platelet size in most cases.