Axon terminals of the intrinsic neurons in the nucleus lateralis of the cerebellum an electron microscope study

Summary The large projection neurons of the lateral nucleus have long axons, which leave the cell mass in the superior cerebellar peduncle. These axons emit myelinated recurrent collaterals which have synaptic varicosities en passant. The varicosities are 2–5 m in diameter and contain round, agranular synaptic vesicles ranging between 280 and 480 Å with diameters of approximately 400 Å. The vesicles lie in a moderately dark axoplasmic matrix with a mean packing density of 281/m². The varicosities synapse through Gray's type 1 junctions with dendrites and thorns of large and small neurons. They constitute 22% of the total axonal population on dendrites of large neurons and 10% on dendrites of small neurons. The recurrent collateral system may provide a means for positive feedback to the same neuron and other neurons of the neuropil.The small neuron or interneuron has a short axonal plexus. The axon is myelinated, and is distinctive with a light axoplasmic matrix and varicosities containing elliptical synaptic vesicles. The vesicles are loosely dispersed with a mean population density of 44/m². These varicosities synapse through an intermediate type of junction upon the somata of certain large and small neurons and they consitute 14% and 22% of the axosomatic synapses respectively. They also make synapses on dendrites, constituting 12% and 25% of the total population of axons synapsing with dendrites of large neurons and those of small neurons respectively. It is suggested that these are the inhibitory interneurons of the lateral nucleus.The corticonuclear input through Purkinje axons is the dominant influence on the lateral nucleus neurons. This inhibitory input is considerably larger on the large neurons than on the small ones. It is speculated that the axosomatic synapses are inhibitory. Excitatory influences, through the collaterals of mossy and climbing fibers and the recurrent collaterals of the large intrinsic neurons, impinge upon the dendrites, where the axons of both Purkinje cells and interneurons also terminate.Supported in part by U.S. Public Health Service grants NS10536, NS03659, Training grant NS05591 from the National Institute of Neurological Diseases and Stroke, and a William F. Milton Fund Award from Harvard University.     

多激励次数自由呼吸T1 VIBE序列在肝脏MR中的应用

目的探讨多激励次数自由呼吸VIBE序列在肝脏MR中的应用价值。方法选取40例屏气效果不佳肝脏MR检查患者(无法配合屏气15s)分别行多激励次数自由呼吸T1 VIBE扫描和常规屏气T1 VIBE扫描,扫描结果按自由呼吸组及常规屏气组分组;采用"5分法"对每组图像总体质量进行主观评分,并分别测量肝右叶、肝左叶及脾脏的SNR,比较两组图像差异。结果多激励次数自由呼吸T1 VIBE序列图像主观评分明显高于常规屏气T1 VIBE序列,差异有统计学意义(P<0.01)。多激励次数自由呼吸T1 VIBE序列的平均SNR为:肝右叶71.6,肝左叶64.11,脾脏59.53,常规屏气T1 VIBE序列的平均SNR为:肝右叶23.18,肝左叶18.58,脾脏18;多激励次数自由呼吸T1 VIBE序列的SNR均高于常规屏气T1 VIBE序列(P<0.01)。结论多激励次数自由呼吸T1 VIBE序列可明显减少腹部呼吸运动伪影,提高图像整体质量增加SNR;在肝脏MR检查中具有重要的应用价值。     

陈旧性和近发性脊髓损伤幻觉痛的痛觉及心理的对比研究

采用莫克吉尔疼痛答卷、斯戴答卷和毕迪埃答卷等方式，对２２例“近发性”（Ｘ１）及２８例“陈旧性”（Ｘ２）脊髓损伤幻觉痛患者的疼痛、焦虑和抑郁等特点进行了观察和对比。结果发现：疼痛测定指数总分及疼痛强度的评分趋势，３０～３９岁组（Ａ组）及４０一４９岁组（Ｂ组）Ｘ１＞Ｘ２，５０一５９岁组（Ｃ组）为Ｘ１＜Ｘ２．而且疼痛对睡眠的影响与此趋势相一致；Ｘ１各年龄组幻觉痛的痛感觉成分均大于Ｘ２，Ｘ１各年龄组幻觉痛的痛情绪成分均小于Ｘ２；焦虑和抑郁对疼痛无直接影响。这一结果初步揭示了“近发性”与“陈旧性”脊髓损伤幻觉痛的规律，并可为采取有针对性的措施提供依据。     

Cardiac vulnerability to electric shocks during phase 1A of acute global ischemia

OBJECTIVES: The purpose of this study is to characterize the changes in vulnerability to electric shocks during phase 1A of global ischemia in the rabbit ventricles and to determine the mechanisms responsible for these changes. BACKGROUND: Mechanisms responsible for the changes in cardiac vulnerability over the course of ischemia phase 1A remain poorly understood. The lack of understanding results from the rapid ischemic change in cardiac electrophysiologic properties, which renders experimental evaluation of vulnerability difficult. METHODS: To examine dynamic changes in vulnerability to electric shocks over the course of acute global ischemia phase 1A, this study used a three-dimensional anatomically accurate bidomain model of ischemic rabbit ventricles. Monophasic shocks are applied at various coupling intervals to construct vulnerability grids in normoxia and at various stages of ischemia phase 1A. RESULTS: Our simulations demonstrate that 2 to 3 minutes after the onset of ischemia, the upper limit of vulnerability remains at its normoxic value (12.75 V/cm); however, arrhythmias are induced at shorter coupling intervals. As ischemia progresses, the upper limit of vulnerability decreases, reaching 6.4 V/cm in the advanced stage of ischemia phase 1A, and the vulnerable window shifts towards longer coupling intervals. CONCLUSIONS: Changes in the upper limit of vulnerability result from an increase in the spatial extent of the shock-end excitation wavefronts and the slower recovery from shock-induced positive polarization. Shifts in the vulnerable window stem from decreases in local repolarization times and the occurrence of postshock conduction failure caused by prolonged postrepolarization refractoriness.