THE EFFECT OF ACUPUNCTURE ON PREVENTION AND TREATMENT OF ISCHEMIC ARRHYTHMIA AND THE RELATION BETWEEN EFFECT OF ACUPUNCTURE AND CHOLINERGIC MUSCARINE-LIKE RECEPTORS

For investigating the effect of acupuncture on ischemic arrhythmia and its mech-anism, adult albino rats with ligated anterior descending branch of coronary artery as experimentalmodel were treated with or without acupuncture, and others with imitative operation but without bothcoronary artery ligation and acupuncture treatment were used as control. It was found in acupuncturegroup that the fibrillation-liability of ischemic myocardium was efficiently decreased, the affinity ofAch-M receptors on membranes of ischemic myocardium was markedly increased, and the tolerance ofischemic myocardium to atropine was elevated in the experiment of atropine inducing fibrillation.These results indicate that acupuncture may play a therapeutic role on ischemic arrhythmia throughactivating the activity of muscarine-like receptors of cholinergic nervous system.     

NGF对小脑皮质细胞凋亡影响的实验研究

目的　探讨神经生长因子 (NGF)对小脑皮质神经细胞凋亡的影响 ,为临床治疗小脑变性疾病提供新的措施。方法　以原代培养的新生SD乳鼠小脑皮质细胞建立谷氨酸诱导的神经细胞凋亡模型。为观察NGF对受损细胞的保护作用 ,应用MTT法测定细胞的存活率和细胞代谢情况 ;利用光学显微镜技术观察细胞凋亡的形态学改变。结果　Glu (5 0 0 μmol/L)作用 5min可诱导小脑神经细胞凋亡。MTT法计数结果显示 ,NGF高剂量治疗组细胞存活率显著高于模型组 (P <0 0 1) ,光学显微镜观察发现受损细胞的形态学变化也得到明显改善。结论　外源性NGF能够减轻大鼠小脑皮质神经细胞凋亡。     

Fatal encephalitis in a patient with refractory celiac disease presenting with myorhythmia and carpal spasm.

We report the case of a woman with refractory celiac disease who developed abnormal spontaneous movements of the extremities and face consistent with myorhythmia. Investigation led to a diagnosis of encephalitis, confirmed by postmortem examination. The movements were likely caused by nonparaneoplastic encephalitis associated with refractory celiac disease. Etiologic and diagnostic considerations and treatment options are discussed.     

成年男性舌下神经在舌根部的定位研究

目的:探讨成年男性舌根部舌下神经解剖走行特点,指导临床舌根部射频温控减容术治疗阻塞性睡眠呼吸暂停低通气综合征(OSAHS)时针形电极刺入舌根部的部位及深度,以避免损伤舌下神经。方法:选择10具成年男性的舌标本,定型后在冰冻状态下作冠状切面,通过计算机图像处理与测量系统行舌下神经定位测量,并进行相关的统计学分析。结果:(1)两侧舌下神经呈对称性分布。(2)成年男性舌下神经舌内部分的主干(本实验为舌盲孔前后15mm范围内)其垂直向解剖走行基本恒定,距舌表面(22.21±2.22)mm;水平向走行中,舌盲孔后一般位于舌中内(近中线侧)(28.61±2.66)％处,舌肓孔前为(21.89±1.93)％处。结论:本实验为舌根部射频温控减容术治疗OSAHS提供了一个相对安全的范围:在不超过(22.21±2.22)mm深度且舌盲孔后避开中内(近中线侧)(28.61±2.66)％区域、舌盲孔前避开中(内近中线侧)(21.89±1.93)％区域,基本不会损伤舌下神经。     

医源性桡神经损伤46例分析

目的阐述医源性桡神经损伤的伤因、治疗和预防措施。方法分析1991年～2003年间收治的46例医源性桡神经损伤的病例。结果伤因分为上肢手术误伤，肱骨干和桡骨上端闭合性骨折复位手法不当，头静脉穿刺致桡神经浅支损伤。本组21例保守治疗，22例手术治疗，3例行肌腱转位功能重建。结论手术误伤是医源性桡神经损伤的首要原因；临床医生丰富的解剖知识和细致、轻柔的操作是预防医源性桡神经损伤的关键。     

Responses of periodontal nerve terminals to experimentally induced occlusal trauma in rat molars: an immunohistochenmical study using PGP 9.5 antibody

The response of periodontal nerves to experimentally induced occlusal trauma in rat molars was assessed by immunohistochemistry for protein gene product 9.5 (PGP 9.5) at light and electron microscopic levels, and by computerized image analysis. The occlusal surface on the left upper first molar of 8-wk-old male Wistar rats was raised approximately 1 min under ether anaesthesia. The rats were perfusion-fixed on d 1, 2, 3, 4, and 7 after bite-raising and then decalcified for 2–3 wk. Frozen sagittal cryostat sections were stained by the avidin-biotin complex method. By the second day after bite-raising many Ruffini endings were swollen and their outline unclear at the light microscopic level. Transmission electron microscopy disclosed PGP 9.5 reaction products within Ruffini endings that had unusually long cytoplasmic projections extending through enlarged slits of the Schwann sheaths and also diffuse extracellular PGP 9.5-immunoreactivity near the Ruffini endings. From d 2 to 4, thin nerve fibres on the pressure side of the periodontal ligament were orientated irregularly and had a prominent beaded appearance. An increase in beaded nerve terminals occurred at d 2–4 post elevation, and decreased later. These results suggest that occlusal trauma induces specific changes in the distribution and shape of nerve terminals in the periodontal ligament.     

Effects of chronic treatment with a nitric oxide donor on nerve conduction abnormalities and endoneurial blood flow in streptozotocin-diabetic rats

Abstract. This study examined the ability of nitrova-sodilator treatment with isosorbide dinitrate to prevent the development of reduced nerve conduction velocity and nutritive blood flow in streptozotocin-induced diabetes mellitus in rats. Two month untreated diabetes caused approximately 23% and 13% reductions in sciatic motor and saphenous nerve sensory conduction velocity ( P < 0.001). Isosorbide dinitrate treatment provided 64.6 and 67.6% protection for motor and sensory nerves, respectively ( P < 0.01). Sciatic endoneurial nutritive blood flow was measured by microelectrode polarography and a hydrogen clearance technique. After 1 month untreated diabetes, flow was reduced by 41.9% ( P < 0.001). Isosorbide dinitrate treatment for 1 month in non-diabetic and diabetic rats significantly increased blood flow ( P < 0.01). When between-group variations in blood pressure were taken into account, vascular conductance increased by 29% and 31% in non-diabetic and diabetic rats, respectively ( P < 0.01). Thus, nitrovasodilator treatment improves nerve perfusion and function in experimental diabetes, probably by compensating for reduced endothelium-derived nitric oxide release or action.     

Deficient activation of microglia during optic nerve degeneration

Transection of an optic nerve (ON) is followed by slow removal of myelin. We studied microglia for the expression of molecules that characterize activated myelin phagocytosing macrophages: MAC-1, FcγII/III receptor (FcR), MAC-2, and F4/80. In-vitro, microglia expressed all molecules and phagocytosed myelin. In-vivo, intact ON displayed high levels of MAC-1, little FcR and F4/80, and no MAC-2. The expression of these molecules was upregulated differentially in in-vivo degenerating ON: MAC-1 uniformly, FcR and F4/80 variably, and MAC-2 sporadically. The distribution of MAC-2 expression correlated best with a pattern of sporadic structural degeneration. Thus in-vivo, ON injury is followed by deficient microglia activation, which we suggest contributes significantly to the slow clearance of myelin.     

Localization of Putative Receptors for Tetanus Toxin and Botulinum Neurotoxin Type A in Rat Central Nervous System

Clostridial neurotoxins (tetanus and botulinum toxins) are potent blockers of neurotransmitter release. These toxins act specifically on the nervous system by interacting with still non-identified protein receptors together with gangliosides. Whereas many biochemical data are available on their binding properties to neuronal membranes in vitro , there is poor morphological evidence of their binding to mammalian central nervous system. In the present study, the binding of tetanus and botulinum neurotoxin type A to rat brain sections is reported. Both toxins bound to nerve terminals with a broad distribution in brain. Tetanus toxin additionally bound to nerve fibres. The staining patterns were clearly shown to be due to the interaction of the heavy chains, which contain the binding moiety, with the tissue. In an attempt to investigate the nature of the acceptors present in the tissue, some sections were pre-incubated with periodic acid. This treatment resulted in the additional binding of botulinum neurotoxin type A to nerve fibres. Since the extended staining of nerve terminals was not modified by this pretreatment, it is suggested that protein receptors of clostridial neurotoxins are located at the nerve terminals, which may be common constituents of the synapses.     

Facial nerve reconstruction in neurofibromatosis 2

Summary Between 1979 and 1989, 13 patients with neurofibromatosis 2 underwent reconstructions of the facial nerve after removal of bilateral acoustic or facial neurinomas. Seven patients received hypoglossal-facial nerve anastomosis, and five reveived sural nerve grafting in the cerebellopontine angle. End-to-end anastomosis and intracranial-intratemporal sural grafting were performed for one patient each, respectively. Re-innervation was seen in all cases. The results were good in 11 cases. Two patients presented with poor results due to development of neurinomas close to the site of the nerve reconstruction. The importance of reconstructive surgery in patients with neurofibromatosis is stressed. The problems regarding failure of re-innervation in some cases and difficulties in their management are discussed.