周期蛋白依赖性蛋白激酶抑制物1A相互作用锌指蛋白1在临床相关疾病中的研究进展

周期蛋白依赖性蛋白激酶抑制物1A相互作用锌指蛋白1(Ciz1)作为细胞周期蛋白依赖性激酶抑制剂p21^(Cip1/Waf1)的互相作用蛋白,不仅参与哺乳动物DNA复制,还参与细胞周期、细胞凋亡等生物学活动的调节。Ciz1在常见肿瘤(如肺癌、尤因肉瘤、结肠癌、胆囊癌、前列腺癌、乳腺癌)中过表达,表明Ciz1可能是肿瘤生长的驱动因素。Ciz1还与阿尔茨海默病、肌张力障碍等疾病发生相关。深入研究Ciz1与临床相关疾病的关系,可能为多种疾病的治疗提供新靶点。

肌肉功能定位水针注射治疗脑性瘫痪下肢肌张力障碍疗效观察

目的探讨肌肉功能定位水针注射治疗脑性瘫痪患儿下肢肌张力障碍的准确性和安全性。方法将60例脑瘫下肢肌张力障碍患儿随机分为治疗组和对照组各30例,前者采用综合康复加肌肉功能定位注射治疗,后者采用综合康复治疗。按修订Ashworth量表评价疗效。结果2组治疗后Ashworth评分有显著性差异(P<0.05),治疗组疗效明显优于对照组。结论肌肉功能定位水针注射治疗脑瘫患儿下肢肌张力障碍疗效好,且针对性强,适宜脑瘫患儿多动的特点。

A型肉毒毒素治疗儿童痉挛型肌张力障碍的护理

局部肌内注射A型肉毒毒素治疗儿童痉挛型肌张力障碍是一种新的治疗方法。报道260例患儿接受A型肉毒毒素治疗前后的观察和护理。(1)治疗前对患儿关节活动度、肌张力进行评估,有针对性地做好心理护理,减少因心理紧张而导致的过度肌肉痉挛;注射前准备好抢救药品及物品,做好操作过程中的应急措施。(2)注射时根据解剖知识触摸动脉走向,避开大血管,注射过程中不断与患儿交谈,安抚患儿,注意观察患儿有无呼吸异常、突然停止哭闹、大汗、反应迟钝、不应答、面色苍白、四肢冰凉等不良反应。(3)注射后注意观察患儿的生命体征及药物不良反应,如咀嚼无力、吞咽困难、呼吸异常等;评估异常姿势、步态及关节活动度,进行康复训练指导;做好出院指导,告知家长及患儿在出院回家2～4周时为药物不良反应高峰期,可能出现注射肌群过度无力,要求家长注意观察患儿走路是否易摔跤,有无明显双腿发软、无力等情况。260例患儿经治疗后提高了关节活动范围,运动功能均得到不同程度的改善,有效率95%。所有患儿生命体征平稳,无吞咽困难、咀嚼无力、呼吸异常等现象。

A型肉毒毒素治疗偏侧面肌痉挛和头颈部肌张力障碍的疗效观察

为评估Ａ型肉毒毒素治疗偏侧面肌痉挛和头颈部肌张力障碍的疗效，本文对４２例偏侧面肌痉挛及３４例头颈部肌张力障碍（后者包括１８例眼睑痉挛，１２例Ｍｅｉｇｅ氏病、４例痉挛性斜颈）病人进行Ａ型肉毒毒素肌肉多点注射治疗，并治疗前后的病情分级对比。结果表明，Ａ型肉毒毒素治疗有效率为１００％，疗效持续８～２６周，可重复注射，并再次取得疗效。部分病人局部出现轻度肌无力，数周后均可恢复，无全身毒副作用。结论认为Ａ型肉毒毒素能治疗偏侧面肌痉挛和头颈部局限性肌张力障碍，不失为一种有效安全简便易行的治疗手段。

Acrylamide inhibits nerve sprouting induced by botulinum toxin type A

Botulinum toxin type A is a potent muscle relaxant that blocks the transmission and release of acetylcholine at the neuromuscular junction. Intramuscular injection of botulinum toxin type A has served as an effective and safe therapy for strabismus and focal dystonia. However, muscular weakness is temporary and after 3-4 months, muscle strength usually recovers because function- al recovery is mediated by nerve sprouting and reconstruction of the neuromuscular junction. Acrylamide may produce neurotoxic substances that cause retrograde necrotizing neuropathy and inhibit nerve sprouting caused by botulinum toxin type A. This study investigated whether acrylamide inhibits nerve sprouting after intramuscular injection of botulinum toxin type A. A tibial nerve sprouting model was established through local injection of botulinum toxin type A into the right gastrocnemius muscle of Sprague-Dawley rats. Following intramuscular injection, rats were given intraperitoneal injection of 3% acrylamide every 3 days for 21 days. Nerve sprout- ing appeared 2 weeks after intramuscular injection of botulinum toxin type A and single-fiber electromyography revealed abnormal conduction at the neuromuscular junction I week after intra- muscular injection of botulinum toxin type A. Following intraperitoneal injection of acrylamide, the peak muscle fiber density decreased. Electromyography jitter value were restored to normal levels 6 weeks after injection. This indicates that the maximal decrease in fiber density and the time at which functional conduction of neuromuscular junction was restored were delayed. Addition- ally, the increase in tibial nerve fibers was reduced. Acrylamide inhibits nerve sprouting caused by botulinum toxin type A and may be used to prolong the clinical dosage of botulinum toxin type A.

等速肌张力测试系统的开发

针对帕金森病患者的肌张力障碍,该文设计了一种新型等速肌张力测试系统。该系统包括机械装置、数据采集单元和上位机数据处理分析软件。其中机械装置包括手臂支撑装置、安全限位装置、高度调节装置等;数据采集单元由力矩传感器模块、电机控制模块、数据通信模块等组成,用于控制手臂进行等速运动并将传感器的模拟信号转换成数字信号实时传输到上位机;上位机数据处理分析软件采用USB接口传输数据,基于VC++程序开发,完成数据处理、显示、存储及报表生成等功能。实验结果表明:设计的等速肌张力测试系统安全可靠,不仅能够较好地评估帕金森患者的肌张力异常程度,还能应用于辅助肌张力患者的康复训练,具有较强的可扩展性。

脑深部电刺激在神经系统疾病治疗中的研究进展

脑深部电刺激(DBS)是通过脑立体定位仪在特定神经核团植入电极,给予低频或高频电刺激来抑制神经元的异常电活动,治疗各种神经精神疾病。与传统手术相比,DBS具有选择性好、靶点明确、无损伤、可调、可逆、手术安全、并发症少等优点。且在神经调节方面具有广阔的应用前景,同时其可辅助传统手术发挥更广泛的作用。近年来,DBS在帕金森病、癫痫、肌张力障碍等各种神经系统疾病的治疗中应用越来越广泛,但其作用机制尚未完全清楚,未来需进一步研究。

Etiological characteristics and treatment of tardive dyskinesia

OBJECTIVE ： The pathogenesis of tardive dyskinesia （TD） is complicated and uncertain, Thus, there is not any effective treatment for it. The psychiatrists pay more and more attention to TD, which lasts for a long time and is difficult to treat. DATA SOURCES： A computer-based online search of Medline database was undertaken to identify articles about the feature of etiology and the progression of treatment for TD published in English by using the keywords of ＂rD, etiology, pathogenesis＂ and ＂TD, therapy, drug treatment＂. Meanwhile, Chinese articles about the feature of etiology and the progression of treatment for TD were searched in Wanfang database and China journal full-text database, and the keywords were ＂TD, etiology, pathogenesis＂ and ＂TD, therapy, drug Treatment＂ in Chinese. STUDY SELECTION： Articles met the following inclusion criteria were selected in this paper. Inclusion criteria： （1） Researches of randomized blind control design, before and after control design and retrospective. （2） Researches of the feature of etiology and the progression of treatment for TD. Exclusion criteria： the repetitive researches and individual reports. DATA EXTRACTION ： Totally 65 articles related the feature of etiology and the progression of treatment for TD of randomized blind control design, before and after control design and retrospective studies were collected, and 53 of them were accorded with the inclusion criteria. Of the 12 excluded ones, 8 were concerning with genetics, 4 were repetitive researches. DATA SYNTHESIS ： The feature of etiology for TD includes：（1） Hypothesis of dopamine receptor super-sensitivity： The dopamine receptor is persistently blocked, so it will result in functional disorder in CNS, and then TD may take place. （2）） Hypothesis of neuronal degeneration： The concentration of aminosuccinic acid and glutamic acid will increase after the antipsychotic used for a long time and this will result in neuronal degeneration through glutamic acid receptor in the postsynaptic membrane; meanwhile with free radical, the nerve cells of corpus striatum may degenerate and become necrosis. （3） Sex and age： The females and gerontal patients are liability to the TD disease. It is may related to the lower estrogen. （4） Molecule heredity： TD may association with the dopamine and 5-HT receptor gene polymorphism. （5） Other theories： Hypofunction of γ-amino-butyri acid （GABA）, hypothesis of noradrenaline 5-serotonin and nutrition metabolism can cause TD disease. Treatlent for TD： （1） Dopamine receptor agonist： The therapeutic effect is not satisfactory, especially for gerontism females. （2） Oxygen free radical scavenger： As represent of vitamin E, it can clear out free radicals and reduce the potential cytotoxic effect of free radicals. （3） Calcium channel blocker： This maybe related to block calcium ions releasing from muscle cells and inhibit muscle convulsion; therefore, it can be used for symptomatic treatment. （4） GABA receptor agonist： It is more effective for the prominent dysmyotonia than dancing slowly symptom. （5） Antipsychotic： There is some therapeutic effect with ciozapine, but the effect will reduce because of the age growing up and the symptom exacerbating. （6） Other therapies： Valproate sodium, cyproheptadine, melatonin, branched chain amino acid, ahalysantinfarctasum, electric acupuncture and injection ad acumen, traditional Chinese drug have a certain effects on TD. Prevention of TD： The serum creatine phosphokinase （CPK） combined with symptoms should be checked regularly so as to early discovery TD. CONCLUSION ： （1） Etiology of TD： The hypothesis of dopamine receptor super-sensitivity is denyed; the hypothesis of neuronal degeneration is approved in academic circles; the sex and age is a finding of generally received; but the dopamine and 5-HT receptor gene polymorphism, hypofunction of GABA, noradrenaline, 5-serotonin and nutrition metabolism cannot explain the pathogenesis of TD. （2） Treatment for TD： The therapeutic effect of dopamine receptor agonist is not satisfactory; the oxygen free radical scavenger maybe effective; calcium channel blocker maybe used for symptomatic treatment; GABA receptor agonist maybe more effective for the prominent dysmyotonia than dancing slowly symptom; the consequence of antipsychotic is discrepancy; other therapies maybe use to adjunctive therapies. （3） As far as prevention of TD is concerned, and the serum CPK combined with symptoms should be checked regularly so as to early discovery TD.

山豆根对大鼠神经行为的影响

目的观察山豆根对大鼠神经行为的影响及神经病理的改变，建立一种新的肌张力障碍动物模型。方法雌性SD大鼠24只，按照随机数字表法分为实验组和对照组，每组各12只。实验组大鼠通过灌胃给药法给予中药山豆根煎剂1．5mL，对照组则给予等量的生理盐水，1次／d，连续10d。观察2组大鼠的神经行为变化，并用Noldus动物行为分析系统、转棒实验仪对大鼠运动行为和协调能力进行量化分析，行为实验结束后完整取脑，观察纹状体、中脑和海马的病理形态学变化。结果实验组大鼠在灌注中药山豆根汤剂后3～7d开始出现程度不同的神经行为学症状．主要表现为运动减少，平衡能力下降，颈部及躯干扭转。运动行为轨迹分析显示实验组大鼠运动距离、平均运动速度、直立次数、活动性指标数值均明显小于对照组，运动协调能力明显下降，在转棒上停留的时间较对照组明显缩短，差异均有统计学意义（P〈0．05）。病理学检查显示实验组大鼠纹状体、海马及中脑神经元细胞数与对照组相比有减少趋势，其中以海马部位变化为著。结论中药山豆根对大鼠神经行为的影响与该药中毒造成的人体肌张力障碍表现极为相似，表现为运动障碍，运动协调性差，推测与肌张力障碍有关。病理学上的改变显示这些神经行为的改变有神经病理改变的基础．可作为一种新的肌张力障碍的动物模型。