用乳腺Ⅰ号治疗乳腺囊性增生病400例疗效观察

目的：观察蒙药乳腺Ⅰ号治疗乳腺囊性增生病的疗效．方法：将400例乳腺囊性增生病病人分为两组，治疗组300例用蒙药治疗，对照组100例用中药乳癖消治疗．结果：蒙药有效率为98％，中药有效率为70％，两组间具有显著性差异．结论：蒙药乳腺Ⅰ号治疗乳腺囊性增生病疗效显著．     

蒙药配合玻璃酸钠治疗膝关节骨性关节炎56例观察

目的:探讨蒙药配合玻璃酸钠治疗膝关节骨性关节炎的疗效.方法:对56例膝关节骨性关节炎采用蒙药珍宝丸、风湿二十五味丸、嘎迪五味丸治疗的基础上配合玻璃酸钠关节腔内注射治疗.结果:56例中,临床治愈5例(8.93%),显效45例(80.35%),有效5例(8.93%),无效1例(1.78%),总有效率98.21%.结论:蒙药口服配合玻璃酸钠关节腔内注射治疗膝关节骨性关节炎能起到标本兼治的作用,疗效显著.     

两种方法治疗瘢痕疙瘩114例疗效观察

本文随机分组，对１１４例瘢痕疙瘩患者采用损害内注射确炎舒松－Ａ及皮损冷冻后注射确炎舒松－Ａ的治疗．结果表明．冷冻＋局部注射确炎舒松－Ａ治愈率比单纯局部注射确炎舒松－Ａ高，其总有效率两者无明显差异．     

凿岩机器人钻臂的运动学研究

为实现凿岩机器人钻臂在凿岩过程中的自动定位,建立了多关节钻臂的运动学方程;根据钻臂的实际工作特点和工作范围提出了一种求逆解的方法．运算结果表明,该方法可以成功地实现快速、精确求解,具有较高的实用价值．     

蒙西医对腰椎间盘突出症的认识和蒙西医药物治疗措施

综述了蒙西医对腰椎间盘突出症病因的认识以及蒙药和西药对腰椎间盘突出症的药物治疗措施．     

盐酸消旋山茛菪碱联合补骨脂酊治疗白癜风

目的观察盐酸消旋山莨菪碱联合补骨脂酊治疗白癜风的疗效。方法选择局限性或散发性白癜风患者118例,随机分为试验组和对照组,试验组采用盐酸消旋山莨菪碱局部皮损内注射,联系补骨脂酊外搽的治疗方法;对照组外搽0．025％醋酸氟氢松软膏。结果试验组总有效率95．6％,对照组总有效率34．0％,两组有显著性差异（P〈0．01）。结论盐酸消旋山莨菪碱局部注射联合补骨脂酊外搽的方法可有效治疗白癜风。     

苦参的有效成分及蒙医复方制剂药理作用研究现状

苦参为蒙药中的常用药,它具有发汗、抗风湿、抗粘病、抗炎镇痛、治疗皮肤病等作用．苦参蒙药复方制剂已被广泛开发应用于临床．现就苦参有效成份及蒙医复方制剂药理作用研究现状做一综述．     

蒙药吉祥安坤丸的药效学研究

目的：研究蒙药吉祥安坤丸对动物子宫功能的影响及抗炎作用．方法：观察药物对大鼠在体子宫收缩的影响；采用二甲苯致小鼠耳廓炎症的动物模型，观察吉祥安坤丸的抗炎作用．结果：蒙药吉祥安坤丸能使大鼠在体子宫平滑肌松弛，对小鼠具有明显抗炎作用．结论：蒙药吉祥安坤丸对子宫平滑肌的影响及抗炎作用是用于治疗月经不调、产后发烧、乳腺炎等的重要药理学基础．     

蒙药苏龙嘎-4汤加减治疗藏獒犬细小病毒感染初探

蒙药苏龙嘎-4汤加减治疗犬细小病毒感染尚属新的尝试,初步临床治疗结果显示,蒙西医结合治疗可明显缩短疗程,提高治疗效果．     

慢性前列腺炎的注射治疗

从局部注射抗菌素治疗慢性前列腺炎３０例的疗效看出前列腺局部注射药物比肌肉注射药物效果好。因为前者的药物浓度高，且作用持久，１个疗程治愈者１４例，２个疗程愈者１２例，有效３例，无效１例，总有效率为９６．６％。     

桡神经前臂段浅层肌支的定位观察

目的：为给前臂部创伤修复及肌瓣移植提供形态学依据。方法：采用解剖剥离测量方法，对25具（共50例）成人上肢标本的桡神经浅层肌支进行自身比例定位研究。结果：①桡神经发出的各肌支主要以2支型出现率最多；②桡神经发出的各肌支主要集中于上肢的Ⅵ段；③桡神经发出的各肌支进入各肌门的区位，均有倾向于以神经干为轴心近距离分布的规律。结论：确定了桡神经肌支的危险区段和危险区位，有利于开展带神经血管蒂肌瓣移植的肌支类型。     

BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain

Neuropathic pain that occurs after peripheral nerve injury depends on the hyperexcitability of neurons in the dorsal horn of the spinal cord. Spinal microglia stimulated by ATP contribute to tactile allodynia, a highly debilitating symptom of pain induced by nerve injury. Signalling between microglia and neurons is therefore an essential link in neuropathic pain transmission, but how this signalling occurs is unknown. Here we show that ATP-stimulated microglia cause a depolarizing shift in the anion reversal potential (E(anion)) in spinal lamina I neurons. This shift inverts the polarity of currents activated by GABA (gamma-amino butyric acid), as has been shown to occur after peripheral nerve injury. Applying brain-derived neurotrophic factor (BDNF) mimics the alteration in E(anion). Blocking signalling between BDNF and the receptor TrkB reverses the allodynia and the E(anion) shift that follows both nerve injury and administration of ATP-stimulated microglia. ATP stimulation evokes the release of BDNF from microglia. Preventing BDNF release from microglia by pretreating them with interfering RNA directed against BDNF before ATP stimulation also inhibits the effects of these cells on the withdrawal threshold and E(anion). Our results show that ATP-stimulated microglia signal to lamina I neurons, causing a collapse of their transmembrane anion gradient, and that BDNF is a crucial signalling molecule between microglia and neurons. Blocking this microglia-neuron signalling pathway may represent a therapeutic strategy for treating neuropathic pain.     

P2X4 receptors induced in spinal microglia gate tactile allodynia after nerve injury

Pain after nerve damage is an expression of pathological operation of the nervous system, one hallmark of which is tactile allodynia-pain hypersensitivity evoked by innocuous stimuli. Effective therapy for this pain is lacking, and the underlying mechanisms are poorly understood. Here we report that pharmacological blockade of spinal P2X4 receptors (P2X4Rs), a subtype of ionotropic ATP receptor, reversed tactile allodynia caused by peripheral nerve injury without affecting acute pain behaviours in naive animals. After nerve injury, P2X4R expression increased strikingly in the ipsilateral spinal cord, and P2X4Rs were induced in hyperactive microglia but not in neurons or astrocytes. Intraspinal administration of P2X4R antisense oligodeoxynucleotide decreased the induction of P2X4Rs and suppressed tactile allodynia after nerve injury. Conversely, intraspinal administration of microglia in which P2X4Rs had been induced and stimulated, produced tactile allodynia in naive rats. Taken together, our results demonstrate that activation of P2X4Rs in hyperactive microglia is necessary for tactile allodynia after nerve injury and is sufficient to produce tactile allodynia in normal animals. Thus, blocking P2X4Rs in microglia might be a new therapeutic strategy for pain induced by nerve injury.     

Noradrenaline hyperalgesia is mediated through interaction with sympathetic postganglionic neurone terminals rather than activation of primary afferent nociceptors

In hyperalgesic states, observed commonly as a major symptom of tissue inflammation or after central or peripheral nerve injury, non-noxious stimuli produce pain and noxious stimuli are perceived as more painful than usual. The mechanisms underlying the generation of hyperalgesia are not known. In patients with causalgia (burning pain and severe hyperalgesia after a nerve injury) activation of sympathetic post-ganglionic neurones or application of noradrenaline to painful skin exacerbates pain and hyperalgesia while sympathectomy may afford complete relief. One suggestion is that noradrenaline released from sympathetic post-ganglionic neurons increases the discharge of damaged small-diameter afferents by a direct action on the primary afferents. Here we present a new model for noradrenaline-sensitive hyperalgesia and demonstrate that the site of action of noradrenaline is not on the primary afferents but rather is presynaptic on the sympathetic post-ganglionic terminals.     

电热药物治疗带治疗神经病合并疼痛100例疗效观察

目的：研究电热药物治疗带,对某些神经病合并疼痛的治疗效果。方法：通过对各种神经病合并疼痛病人的治疗前后临床观察,解决了慢性疼痛单纯药物治疗效果较差的问题。结果：电热药物治疗带对退行性骨关节病变、慢性肌肉损害所致疼痛疗效较好。而对枕神经、耳大神经等单神经痛疗效较差。结论：电热药物治疗带,在热疗基础上辅以活血化瘀止痛的消痛散（中药）,加强其治疗效果,改善局部血液循环,疗效达93％,此治疗带适用于各种慢性损伤,尤以运动系统各组织、骨骼、关节、肌肉、肌腱等慢性损害疗效较为满意。     

Mechanism for chronic pain generation

Neuropathic pain and the other abnormalities of sensation induced by axon injury or by peripheral nerve inflammation should result from functional compensations of the injured neurons during their regeneration. Ectopic distribution of proteins related to Na⁺, K⁺ and Ca²⁺ channels as well as of receptors on both membranes of injured axon and its cell body becomes a main pacemaker from which spontaneous ectopic afferent of primary sensatory neurons and crosstalk between neurons occur. Abnormal ectopic afferent activities lead to disorders of the sensation, such as hyperalgesia, allodynia, spontaneous pain and paraesthesia. Administration of some ion channel agents and/or α2-adrenergic blockers has shown efficiency in preventing neuropathic pain development and in relieving neuropathic pain.     

大鼠SNL神经性疼痛模型的建立

摘要:目的　建立大鼠L5和L6脊神经结扎(Spinal nerve ligation,SNL)疼痛模型并进行评价, 方法　根据大鼠痛阈值测定结果,选择90只符合要求的SD雄性大鼠进行手术操作,术后每隔1d测定大鼠后足的机械痛阈值,比较术前和术后大鼠对疼痛刺激的反应变化。 结果　术后大鼠左足的痛阈值逐渐降低,至10d 后趋于稳定,与术前有明显差异(P≤0.01);右足的痛阈值微有升高,保持在稳定的水平内。 结论　本研究建立的大鼠SNL模型机械痛阈变化明显,稳定性好,可靠性高,可以作为大鼠一种神经病理性疼痛的模型。     

Reversing pathological neural activity using targeted plasticity

Brain changes in response to nerve damage or cochlear trauma can generate pathological neural activity that is believed to be responsible for many types of chronic pain and tinnitus. Several studies have reported that the severity of chronic pain and tinnitus is correlated with the degree of map reorganization in somatosensory and auditory cortex, respectively. Direct electrical or transcranial magnetic stimulation of sensory cortex can temporarily disrupt these phantom sensations. However, there is as yet no direct evidence for a causal role of plasticity in the generation of pain or tinnitus. Here we report evidence that reversing the brain changes responsible can eliminate the perceptual impairment in an animal model of noise-induced tinnitus. Exposure to intense noise degrades the frequency tuning of auditory cortex neurons and increases cortical synchronization. Repeatedly pairing tones with brief pulses of vagus nerve stimulation completely eliminated the physiological and behavioural correlates of tinnitus in noise-exposed rats. These improvements persisted for weeks after the end of therapy. This method for restoring neural activity to normal may be applicable to a variety of neurological disorders.     

基于Optistruct脱模约束函数的悬架控制臂拓扑设计

以麦弗逊悬架下控制臂为研究对象,将Adams/car提供的悬架参数为基础在CATIA中建立控制臂原始几何模型并在Hyperworks中建立有限元模型。进行了转向及制动工况中控制臂的受载分析,并在此基础上进行了以最小加权应变能为目标基于脱模方向约束的拓扑优化。根据对优化结果的解读对控制臂进行了重新建模,并进行了模态分析验证。结果表明,该结构能有效地减少控制臂材料,保证刚度,并避免了悬架系统的共振,为控制臂设计提供了一套新的系统化设计方法,具有一定工程指导意义。     

基于C空间的双臂机器人无碰撞运动规划

研究了双臂机器人无碰撞运动规划问题,将C空间法成功地应用于双臂机器人的无碰撞运动规划,并提出了从臂从碰撞状态数据库（CSDB）概念,在本算法中,双臂机器人无碰撞运动规划问题被归结为对从臂无碰撞状态数据库的搜索,运用该算法可以找到一条最优的无碰撞运动轨迹,并已在双臂CARATES型机器人上通过试验论证。结果表明,该算法可行且效率较高。