DVR解剖型桡骨掌侧锁定接骨板置入内固定治疗桡骨远端C型骨折：与普通掌侧接骨板的比较★

背景：纵观目前治疗粉碎及不稳定桡骨远端骨折的各种方法，金属材料桡骨掌侧锁定接骨板的优点日益突出。 目的：观察DVR解剖型桡骨掌侧锁定接骨板置入内固定治疗桡骨远端AO分型C型骨折的效果。 方法：纳入AO分型桡骨远端C型骨折患者51例，根据其意愿及经济状况非随机分为2组，实验组27例应用DVR解剖型桡骨掌侧锁定接骨板，对照组24例应用普通掌侧接骨板。对比两组患者在手术时间、术中C臂透视次数，术中接骨板安装次数，正中神经炎发生、术后腱鞘炎发生、腕关节功能恢复时间6个方面的差异。 结果与结论：实验组X射线片显示骨折全部Ⅰ期愈合，均无感染、骨不连、钢板松动、正中神经炎等并发症。和同期普通掌侧接骨板治疗方法相比，具有明显的优势，Mcbride腕关节功能恢复优良率明显高于对照组(P < 0.001)。提示使用DVR解剖型桡骨掌侧锁定接骨板置入内固定治疗桡骨远端C型骨折具有操作更加便捷，安全可靠，完全解剖复位，固定坚强，可早期进行功能锻炼，关节功能恢复优良等优点。     

带变向锁钉掌侧钢板DVRTM在不稳定桡骨远端骨折中的应用

背景：用锁定钉的最终固定依赖于钢板的放置,为避免螺钉锁入关节,要求在放入螺钉前反复确认骨折块的复位及钢板位置的放置,无疑增加了操作繁琐及螺钉进入关节的风险。 目的：观察新型带变向螺钉的解剖型掌侧锁定钢板DVRTM治疗不稳定桡骨远端骨折的疗效。 方法：21例不稳定桡骨远端骨折患者,AO分型A3型3例,B2型3例,B3型2例,C1型3例,C2型5例,C3型5例。受伤后0~12 d采用带变向螺钉的解剖型掌侧锁定钢板DVRTM治疗。 结果与结论：随访至24周时,所有患者均获得骨性愈合,无软组织并发症,无螺钉移位及钢板断裂,影像学及功能评估满意。据此得出,对于不稳定桡骨远端骨折,这种固定方式能提供解剖复位、固定确切、并发症发生率低,钉板之间能更灵活、弹性的搭配。     

动力髋螺钉与锁定加压接骨板置入内固定治疗高龄老年股骨转子间骨折的效果比较

背景：治疗股骨转子间骨折的内固定有动力髋螺钉、Gamma钉、股骨近端交锁髓内钉等,究竟使用何种内固定目前仍存在争议。 目的：比较传统动力髋螺钉与锁定加压接骨板治疗老年股骨转子间骨折临床疗效的差异。 方法：2007-06/2010-03收治老年股骨转子间骨折96例,分别采用动力髋螺钉与锁定加压接骨板治疗各48例,两组患者性别、年龄、骨折类型、致伤原因等情况匹配。股骨近端锁定加压接骨板采用00Cr18Ni14Mo3不锈钢、Ti6Al4V钛合金或纯钛,部分钛合金或纯钛产品表面经阳极化处理,非灭菌包装。动力髋螺钉内固定弹性模量接近人体骨,耐体液电解,耐腐蚀强,性质稳定。比较两组患者手术时间、术中出血量、伤口引流量、骨折愈合时间及内固定后髋关节功能恢复情况。 结果与结论：与动力髋螺钉组相比,锁定加压接骨板组的手术时间及骨折愈合时间均明显缩短,术中出血量明显减少(P < 0.01)。锁定加压接骨板组髋关节功能恢复优良率显著高于动力髋螺钉组(94.6%,87.9%,P < 0.01)。提示与传统动力髋螺钉相比,锁定加压接骨板内固定治疗高龄股骨转子间骨折生物力学更合理,操作简便、微创、固定稳固、骨折易愈合,尤其适用于骨质疏松或老年患者。     

AO钩型接骨板置入治疗NeerⅡ型锁骨远端骨析

背景：既往锁骨远端骨折常采用克氏针张力带或普通钢板螺钉固定,易出现张力带钢丝的松弛、螺钉松动及钢板断裂、针道感染,甚至内固定失败等现象。近年来,AO钩板内固定治疗该类骨折取得良好疗效,但是由于钩型接骨板中板钩的存在,理论上仍然影响肩关节功能,在这一点不同学者有不同的观点。 目的：观察AO钩型接骨板并喙锁韧带修复或重建治疗NeerⅡ型锁骨远端骨折的效果。 方法：北京大学人民医院创伤骨科2002-09/2008-03使用AO钩型接骨板置入治疗NeerⅡ型不稳定性锁骨远端骨折27例,并在术中采用了直接修复或肌腱移植方法重建喙锁韧带,术后2周开始康复训练。X射线检查判断骨折愈合情况,采用Constant-Murley评分系统评价肩关节功能。 结果与结论：27例患者得到6个月以上随访,置入后3个月骨折愈合,置入后平均8.2个月取出内固定,肩关节功能恢复满意,Constant-Murley评分平均87分。结果表明AO钩型接骨板内固定是治疗锁骨远端NeerⅡ型骨折较理想的方法,但在内固定的同时必须注意喙锁韧带的修复或重建。     

以AO原则置入解剖接骨板固定治疗肱骨髁间骨折37例：一所市级医院骨科5年病例回顾

背景：保守治疗肱骨髁间骨折效果差，关节功能恢复相对于其他部位骨折有较大的差别，主要因为固定时间过长所致。而早期的功能锻炼必须要以坚强的内固定为基础。 目的：观察利用AO原则行解剖接骨板内固定治疗肱骨髁间骨折的效果。 方法：纳入2000-06/2005-11来宾市人民医院骨科收治的肱骨髁间骨折患者37例，行三维CT重建检查后按AO/ASIF分类分型标准：C1型11例，C2型21例，C3型5例。均采用后路鹰嘴截骨入路切开复位后用双侧解剖接骨板内固定，应用常州市康辉医疗器械有限公司的解剖型接骨板。内固定后第1天开始指导患者行手指和腕关节的屈伸活动。拔除引流后1 d开始物理治疗，早期进行肘关节主动功能锻炼。根据骨折的影像资料以及临床随访结果，结合骨折愈合的进展情况，内固定后4周左右逐渐进行轻微的抗力练习，以恢复肌肉的力量。8~12周后可开始逐渐负重。 结果与结论：37例患者中36例获得随访，随访时间为13~26个月，平均19.5个月，骨折均愈合，优良率为91.7%。内固定复位越早功能锻炼越早，则肘关节功能恢复越快越好。提示根据AO原则应用双解剖接骨板治疗肱骨髁间骨折可提供牢固的内固定，有利于早期功能锻炼和功能恢复。     

老年踝关节旋后外旋型骨折金属植入物内固定方式及内固定物选择

背景：为了恢复关节的功能,移位的旋后外旋型踝关节骨折常常需要切开复位内固定。老年人由于存在骨质疏松,实施内固定存在一定困难,而且容易出现伤口并发症。 目的：探讨老年移位的踝关节旋后外旋骨折手术治疗方式及内固定物的选择。 方法：选择北京大学第一医院骨科收治的移位踝关节旋后外旋型骨折患者128例,其中单纯外踝骨折29例,双踝骨折52例,三踝骨折47例。外踝选用前外侧切口98例,后外侧切口30例;后侧防滑接骨板固定6例,加压螺钉与中和接骨板固定122例(其中1/3管状接骨板98例,锁定接骨板24例);内踝骨折均使用空心加压螺钉固定;后踝骨折通过后外侧切口复位固定24例。术后根据骨折稳定情况,选择是否使用石膏外固定。随访时,根据X射线平片评估骨折愈合情况,采用Olerud and Molander评分系统进行评定。 结果与结论：128例患者均获得随访,随访时间12~25个月,骨折均愈合。外踝伤口延迟愈合5例(4%),其中锁定接骨板固定者3例、1/3管状板2例,两者间差异无显著性意义(P > 0.05)。无深部感染发生。骨折愈合后关节功能评分优55例,良61例,可10例,差2例,优良率91%。骨折愈合后,因局部不适取出内固定物31例,其中管状接骨板19例,锁定接骨板12例,两者相比,差异有显著性意义(P < 0.05)。在取出的12例锁定接骨板中,2例(17%)发生螺钉与接骨板间的“冷焊接”。1例防滑接骨板固定后出现腓骨肌腱炎,保守治疗后疼痛缓解。提示针对老年人移位的踝关节旋后外旋型骨折,合理选用手术入路和内固定物有利于减少伤口的并发症,解剖复位和良好的内固定有利于骨折恢复。     

LISS-DF钢板近端螺钉不同固定方式的力学分析

背景：近年来LISS-DF钢板在临床上得到了广泛应用,随访过程出现了近端螺钉松动、退出的现象,这种现象与近端螺钉的单皮质固定是否存在着相关性尚无定论。 目的：探讨LISS-DF钢板近端螺钉单双皮质不同组合方式固定的力学特性。 方法：用185根新鲜羊股骨,造成股骨远端AO33-A3型骨折模型,均采用5孔LISS-DF钢板通过骨折近端螺钉单双皮质不同组合方式固定,分别作拔出、扭转力学实验,寻找理想的固定方式。 结果与结论：骨折远、近端螺钉常规固定4孔,拔出实验显示：骨折近端螺钉第1、3双皮质、2、4双皮质及1、4双皮质固定时,骨折两端的抗拔出力无显著性差异(P > 0.05)。扭转实验显示：第1、3孔、2、4孔和1、4孔双皮质固定时的抗扭矩值大比较接近,其中1、3孔、2、4孔比较,无显著性差异(P > 0.05),其余各组之间比较差异显著(P < 0.05)。提示,采用相同规格的LISS-DF钢板治疗股骨远端骨折时,骨折近端螺钉第1、3孔或2、4孔双皮质组合方式固定时,骨折两端的钢板螺钉固定强度的平衡性好,同时在对抗扭转和抗拔出方面明显优于其他组合固定方式。     

数字散斑法测量加载100 N与400 N肱骨干骨折钢板固定下的位移

背景：将光学测量技术数字散斑相关方法应用到生物医学领域中,能更精确地分析螺钉断裂的特点。 目的：以数字散斑法测量肱骨钢板螺钉的位移。 方法：取4根肱骨制造肱骨中段骨折模型。将骨折标本进行复位,用8孔钢板固定,骨折线两端各使用4枚螺钉固定。分别在100及400 N拉力下,将模型设计成骨折前后的5种状态,即状态a是未骨折加压钢板坚强内固定组(模拟骨折愈合,未锯断);状态b是骨折后近端去1枚螺钉;状态c是在状态b的基础上远端去1枚螺钉;状态d是在状态c的基础上近端去1枚螺钉;状态e是在状态d的基础上远端去1枚螺钉。分别测量骨折线两端两枚螺钉的位移,通过相关软件计算位移。 结果与结论：在100 N及400 N拉力下,骨折线旁对称分布的两枚螺钉随着其他螺钉的减少,所产生的位移差异存在显著性意义(P < 0.01);骨折线旁成对称分布的两枚螺钉所承受的应力差异无显著性意义(P > 0.05)。提示骨折线两端的2枚螺钉是承受较多应力的部位(应力集中),易于发生断裂,应选用比现有螺钉的直径增大1.0~2.5 mm的螺钉,增加骨折线旁的固定螺钉稳定性以避免断钉等后遗症。     

计算机辅助设计-快速成型在股骨转子间骨折修复中的应用：与常规手术修复效果比较**

背景：计算机辅助设计-快速成型技术的发展,实现了从二维图像到三维实物的飞跃,为临床医生对疾病的诊断、病变点的定位、手术方案的确定提供了重要的依据,使得手术的安全性和手术的质量有了明显的提高。 目的：评估计算机辅助设计-快速成型技术应用于股骨转子间骨折手术治疗的临床疗效。 方法：选择2008年解放军广州军区广州总医院骨科收治的股骨转子间骨折患者30例,年龄18~55岁,随机分成常规手术组及计算机辅助组,常规手术组仅行术前胫骨结节牵引,计算机辅助组行胫骨结节牵引后提取二维CT数据,计算机辅助设计股骨转子间骨折模型,并模拟骨折复位手术,逆向设计与股骨大转子相吻合的组件,计算机精确设计手术钉道。两组均采用动力髋螺钉内固定,均记录手术时间,术中出血量,术后随访1年并采用Harris评分标准对手术效果进行评估。 结果与结论：快速成型建立股骨转子间骨折的1∶1实体模型及置钉导向模版,精确地指导手术快速精确实施。快速成型技术做好的模型应用于手术,提高了手术的安全性,与常规手术组比较缩短了手术时间,减少了手术出血量,术后复查X射线见骨折端复位良好,内固定位置良好,应用Harris髋关节评分患者恢复良好,无髋内翻畸形及患肢短缩畸形,显著提高了手术的有效性,均达到了术前的预期效果。相比传统手术存在精确性不足、创伤较大、术中医生和患者需要反复受到射线照射等缺点,计算机辅助骨科-快速成型技术应用于手术具有安全,准确等优点,术前采集图像可术中反复使用,并减少术中医患的放射性损伤。 关键词：计算机辅助设计;快速成型;骨折;个性化手术;数字化骨科技术     

个体化股骨假体的计算机辅助设计实践及模拟力学实验

背景：由于人体的绝对个性化特点，标准人工假体与患者骨骼之间的误差使二者难以很好匹配，不能确保人工关节的长期稳定。 目的：利用已开发的计算机辅助设计和制造程序，建立个体化股骨假体的三维模型。并通过模拟对比力学实验，验证个体化股骨假体是否优于普通型股骨假体。 设计、时间及地点：开放性实验，于2006-09/2007-05在吉林大学第一临床医院骨科研究所和吉林大学生物力学研究所完成。 材料：成人新鲜股骨尸体骨。 方法：取成人尸体股骨做全长CT扫描，得到CT二维图像。将其输入计算机。利用开发的边缘识别和三维轮廓提取软件对二维图像进行处理，识别髓腔内外轮廓，提取髓腔内外轮廓及假体轮廓数据，建立股骨和个体化股骨假体的三维模型。利用SolidWorks软件建立普通生物型和骨水泥型假体三维模型，在此平台上模拟临床手术置换骨水泥型、生物型和个体化定制型3类股骨假体。 主要观察指标：分别模拟单足和双足站立状态，测量3种股骨假体的应力分布、界面应力和初始微动情况。 结果：对最初设计的软件中边缘提取算法进行了改进，采用Canny算子，得到了更好的边缘检测结果。改进后的软件运行稳定，计算结果可信，符合预期要求。设计的个体化股骨假体的假体应力、股骨上应力、界面应力及初始微动均显著低于生物型和骨水泥型股骨假体（P < 0.01）。 结论：开发的计算机辅助设计程序运行准确可靠，可完成假体的计算机辅助设计，在此平台上设计的个体化股骨假体具有优于普通股骨假体的生物力学特性。     

Tau-induced neurodegeneration: mechanisms and targets

The accumulation of hyperphosphorylated tau is a common feature of several dementias. Tau is one of the brain microtubule-associated proteins. Here we discuss tau’s functions in microtubule assembly and stabilization and with regard to its interactions with other proteins. We describe and analyze important post-translational modifications: hyperphosphorylation, ubiquitination, glycation, glycosylation, nitration, polyamination, proteolysis, acetylation, and methylation. We discuss how these post-translational modifications can alter tau’s biological function. We analyze the role of mitochondrial health in neurodegeneration. We propose that microtubules could be a therapeutic target and review different approaches. Finally, we consider whether tau accumulation or its conformational change is related to tau-induced neurodegeneration, and propose a mechanism of neurodegeneration.     

星形胶质细胞对天冬氨酸特异性半胱氨酸蛋白酶介导β淀粉样蛋白早期突触毒性作用的影响

目的探讨星形胶质细胞(astrocyte,AS)对天冬氨酸特异性半胱氨酸蛋白酶(cysteinyl aspartate specific proteinase,caspase)介导β淀粉样蛋白(β-amyloid,Aβ)早期突触毒性作用的影响,以期为进一步研究与血管性痴呆(vascular dementia,Va D)的发病机制奠定基础。方法以原代培养大鼠海马纯神经元体系(NE-S)及混合培养体系(MIX-S,主要包含神经元及AS)为研究对象,各体系分为6组:对照组、caspase-8抑制剂组、caspase-9抑制剂组、Aβ处理组、caspase-8抑制剂预处理加Aβ组和caspase-9抑制剂预处理加Aβ组。免疫荧光检测各组近胞体10μm段树突中突触后密度蛋白(postsynaptic density-95,PSD95)表达量的变化。结果 1在NE-S与MIX-S中,与对照组相比,caspase-8抑制剂组、caspase-9抑制剂组PSD95的表达量均无明显差异,Aβ处理组PSD95的表达量均显著降低(P均0.001)。2在NE-S中,与Aβ处理组相比,caspase-9抑制剂预处理加Aβ组PSD95的表达量显著回升至对照组水平,caspase-8抑制剂预处理加Aβ组则无显著改变;在MIX-S中的结果则相反,即caspase-8抑制剂预处理加Aβ组PSD95的表达量显著回升至对照组水平,而caspase-9抑制剂预处理加Aβ组则无显著改变。3MIX-S与NE-S两种培养系统间相比较,对照组间及Aβ处理组间PSD95的表达量均无显著差异,而caspase-8抑制剂预处理加Aβ组间及caspase-9抑制剂预处理加Aβ组间PSD95的表达量差异有显著性。结论在Aβ早期突触毒性作用中,AS参与caspase-8介导的死亡受体通路激活过程,且参与抑制神经元的线粒体通路。     

Ultrastructure of non-myelinated neurons during energy deprivation

Summary This paper examines the neuropathology of oxygen-glucose deprivation uncomplicated by stagnant conditions. Rabbit vagus nerves were pulled into asmulti-compartment perfusion chamber, stimulated five times per second and deprived of energy by substituting nitrogen and deoxyglucose for oxygen and glucose in the Locke's perfusate. After incubation the compartments were perfused with gluteraldehyde solution, and the nerves were prepared for electron microscopy. Fixation in the compartments ensured precise cross and longitudinal sections which permitted quantitative comparisons. Although the action potentials ceased in 45 min, 1 h of energy deprivation did not significantly affect the ultrastructure. After 2 h of deprivation the axons were smaller and flattened and microtubules appeared packed together. In the smallest axons the microtubules were gone, the neurofilaments were compacted and the few mitochondria had a dense, homogenous appearance. By 4 h the shrinking was extreme, yet 8% were swollen much larger than any of the controls. Longitudinal views showed these balloned areas were greatly expanded regions of the smallest axons. Both tiny and huge regions were devoid of microtubules and the swollen axons contained expanded mitochondria.Calcium is indirectly implicated in the pathogenesis by the concurrence of mitochondrial alteration as the microtubules disappear coupled with the known role of mitochondria in calcium regulation and the reported effect of high calcium on microtubual dissociation. In is suggested that axons first shrink as osmotially active molecules are used or washed out. After a time without energy the mitochondria can no longer regulate the intracellular calcium, microtubules dissociate, and calcium-activated phospholipases create osmotically active molecules. Finally, high-amplitude, disruptive swelling occurs.Supported, in part, by a Grant-in-aid from the American Heart Association with funds contributed by the American Heart Association, Kansas Affiliate and by the University of Kansas Biomedical Sciences Support Grant RR0737     

Norharman-induced motoric impairment in mice: neurodegeneration and glial activation in substantia nigra

Summary. The β-carboline norharman is present in cooked food and tobacco smoke and show structural resemblance to the neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. C57BL/6 mice were injected subcutaneously with norharman (3 and 10 mg/kg) twice per day for five consecutive days. Eighteen hours after the last dose an increased expression of glial fibrillary acidic protein and fluoro-jade staining were demonstrated whereas the number of tyrosine hydroxylase positive cells were unchanged in the substantia nigra. Two weeks after the last treatment a decreased motor activity was observed whereas cognitive functions remained intact. In cultured PC12 cells norharman treatment induced mitochondrial dysfunction and increased the number of caspase-3 and TUNEL-positive cells. The results demonstrate that norharman induced apoptosis in cultured cells as well as early neurodegeneration, glial activation and sustained motor deficits in mice and suggest that exposure to norharman may contribute to idiopathic Parkinson’s disease.     

The effect of risperidone on reward‐related brain activity is robust to drug‐induced vascular changes

Dopamine (DA) mediated brain activity is intimately linked to reward‐driven cerebral responses, while aberrant reward processing has been implicated in several psychiatric disorders. fMRI has been a valuable tool in understanding the mechanism by which DA modulators alter reward‐driven responses and how they may exert their therapeutic effect. However, the potential effects of a pharmacological compound on aspects of neurovascular coupling may cloud the interpretability of the BOLD contrast. Here, we assess the effects of risperidone on reward driven BOLD signals produced by reward anticipation and outcome, while attempting to control for potential drug effects on regional cerebral blood flow (CBF) and cerebrovascular reactivity (CVR). Healthy male volunteers (n = 21) each received a single oral dose of either 0.5 mg, 2 mg of risperidone or placebo in a double‐blind, placebo‐controlled, randomised, three‐period cross‐over study design. Participants underwent fMRI scanning while performing the widely used Monetary Incentive Delay (MID) task to assess drug impact on reward function. Measures of CBF (Arterial Spin Labelling) and breath‐hold challenge induced BOLD signal changes (as a proxy for CVR) were also acquired and included as covariates. Risperidone produced divergent, dose‐dependent effects on separate phases of reward processing, even after controlling for potential nonneuronal influences on the BOLD signal. These data suggest the D2 antagonist risperidone has a wide‐ranging influence on DA‐mediated reward function independent of nonneuronal factors. We also illustrate that assessment of potential vascular confounds on the BOLD signal may be advantageous when investigating CNS drug action and advocate for the inclusion of these additional measures into future study designs.     

Development of 18F-labeled radiotracers for neuroreceptor imaging with positron emission tomography

Positron emission tomography (PET) is an in vivo molecular imaging tool which is widely used in nuclear medicine for early diagnosis and treatment follow-up of many brain diseases. PET uses biomolecules as probes which are labeled with radionuclides of short half-lives, synthesized prior to the imaging studies. These probes are called radiotracers. Fluorine-18 is a radionuclide routinely used in the radiolabeling of neuroreceptor ligands for PET because of its favorable half-life of 109.8 min. The delivery of such radiotracers into the brain provides images of transport, metabolic, and neurotransmission processes on the molecular level. After a short introduction into the principles of PET, this review mainly focuses on the strategy of radiotracer development bridging from basic science to biomedical application. Successful radiotracer design as described here provides molecular probes which not only are useful for imaging of human brain diseases, but also allow molecular neuroreceptor imaging studies in various small-animal models of disease, including genetically-engineered animals. Furthermore, they provide a powerful tool for in vivo pharmacology during the process of pre-clinical drug development to identify new drug targets, to investigate pathophysiology, to discover potential drug candidates, and to evaluate the pharmacokinetics and pharmacodynamics of drugs in vivo.     

The ENIGMA‐Epilepsy working group: Mapping disease from large data sets

Epilepsy is a common and serious neurological disorder, with many different constituent conditions characterized by their electro clinical, imaging, and genetic features. MRI has been fundamental in advancing our understanding of brain processes in the epilepsies. Smaller‐scale studies have identified many interesting imaging phenomena, with implications both for understanding pathophysiology and improving clinical care. Through the infrastructure and concepts now well‐established by the ENIGMA Consortium, ENIGMA‐Epilepsy was established to strengthen epilepsy neuroscience by greatly increasing sample sizes, leveraging ideas and methods established in other ENIGMA projects, and generating a body of collaborating scientists and clinicians to drive forward robust research. Here we review published, current, and future projects, that include structural MRI, diffusion tensor imaging (DTI), and resting state functional MRI (rsfMRI), and that employ advanced methods including structural covariance, and event‐based modeling analysis. We explore age of onset‐ and duration‐related features, as well as phenomena‐specific work focusing on particular epilepsy syndromes or phenotypes, multimodal analyses focused on understanding the biology of disease progression, and deep learning approaches. We encourage groups who may be interested in participating to make contact to further grow and develop ENIGMA‐Epilepsy.     

缺血性卒中并发2型糖尿病患者颈动脉斑块内新生血管分布特点的超声造影研究

目的 应用超声造影观察缺血性卒中并发2型糖尿病患者颈动脉斑块内新生血管分布情况,明确其 斑块内新生血管分布特征。 方法 病例组选取因急性缺血性卒中住院的糖尿病患者40例（入组前未服用降糖药）,卒中同侧颈 动脉斑块形成;对照组为同期门诊就诊的颈动脉斑块形成患者,无卒中病史,性别及年龄匹配的非 糖尿病患者32例。两组患者行弓上计算机断层扫描血管造影（computed tomography angiography,CTA） 检查排除主动脉弓斑块及颅内动脉病变,排除卵圆孔未闭及心房颤动等。对所有患者均行常规超声 及超声造影检查。常规超声观察斑块厚度及内部回声,超声造影观察斑块增强情况,横切面多角度 观察,将超声造影结果分为近内膜处有增强（代表新生血管）及近内膜处无增强两种。 结果 两组患者颈动脉斑块厚度及回声情况差异无统计学意义。超声造影结果显示病例组颈动脉 斑块近内膜处增强者34例（85%）,对照组近内膜处增强12例（37.5%）,差异有统计学意义（χ 2=17.38, P＜0.01）。 结论 未服用降糖药的2型糖尿病并发急性缺血性卒中的患者颈动脉粥样硬化斑块内近内膜处新生 血管增生多于无糖尿病患者,提示血糖升高与颈动脉斑块内血管新生有关。     

轻型缺血性卒中静脉溶栓后双重抗血小板疗效观察

目的 观察rt-PA静脉溶栓联合双重抗血小板治疗轻型缺血性卒中的有效性及安全性。 方法 以2013年12月-2016年12月在石家庄市第一医院连续住院治疗的轻型缺血性卒中患者为研究 对象,将其随机分为对照组、溶栓+单抗组和溶栓+双抗组。对照组不进行静脉溶栓,长期口服阿 司匹林（100 mg/d）抗血小板治疗;溶栓+单抗组在rt-PA静脉溶栓（0.9 mg/kg,最大剂量90 mg）基 础上长期单用阿司匹林（100 mg/d）抗血小板治疗;溶栓+双抗组在溶栓后单抗基础上加用氯吡格雷 （75 mg/d）双重抗血小板治疗,双抗治疗21 d后改为阿司匹林长期单抗治疗。随访3个月,有效性指标 为3个月时NIHSS 0～1分、Barthel指数（Barthel index,BI）95～100分和mRS 0～1分的比例,3个月时缺 血性卒中的复发率;安全性指标为治疗24 h出血转化和症状性出血转化的发生率。另外比较三组间 基线和3个月时血清hs-CRP和IL-6的水平差异。 结果 研究共纳入85例患者,对照组28例,溶栓+单抗组28例,溶栓+双抗组29例,全部患者均完 成3个月随访,无死亡患者。对照组、溶栓+单抗组和溶栓+双抗组3个月随访时NIHSS 0～1分比例分 别为46.43%、78.57%和93.10%,BI 95～100分比例分别为53.57%、82.14%和89.66%,mRS 0～1分 的比例分别为50.00%、82.14%和93.10%,三组上述有效性指标差异均有统计学意义,两两比较显 示,溶栓+双抗组高于溶栓+单抗组和对照组,溶栓+单抗组高于对照组,差异均有统计学意义;对 照组、溶栓+单抗组和溶栓+双抗组3个月时缺血性卒中复发率分别为32.14%、7.14%和3.45%,差异 有统计学意义。安全性指标方面,三组均无出血转化事件。对照组、溶栓+单抗组和溶栓+双抗组3 个月时的hs-CRP水平分别为11.92±3.58 mg/L、9.04±2.85 mg/L和6.04±2.65 mg/L,IL-6水平分别为 26.18±4.65 ng/L、16.11±6.93 ng/L和12.84±2.57 ng/L,三组上述炎症因子水平差异均有统计学意 义,其中溶栓+双抗组低于溶栓+单抗组和对照组,溶栓+单抗组低于对照组。 结论 对于急性轻型缺血性卒中患者,rt-PA静脉溶栓治疗后短期双重抗血小板治疗可显著改善患 者神经功能,降低炎症因子水平,降低复发率,且不增加出血风险。     

The role of post-translational modifications of huntingtin in the pathogenesis of Huntington’s disease

Post-translational modifications are rapid, effective and reversible ways to regulate protein stability, localization, function, and their interactions with other molecules. Post-translational modifications usually occur as chemical modifications at amino acid residues, including SUMOylation, phosphorylation, palmitoylation, acetylation, etc. These complex biochemical modifications tightly regulate and control a variety of cellular processes. Several forms of post-translational modifications of huntingtin (Htt) have been described. These modifications affect Htt metabolism, protein-protein interactions and cellular toxicity. Cleavage and clearance of mutant Htt, and the interactions between mutant Htt and other cellular proteins are important biochemical events leading to Huntington’s disease (HD). Therefore, identifying signaling pathways of Htt modification and evaluating the significance of Htt modifications would lead to a better understanding of the normal function of wild-type Htt and the pathogenic mechanisms of mutant Htt.