灶

Results The model showed serious edema, proteinuria, hypoproteinemia, and hyperlipidemia. Podocytes were swollen and mesangial cells developed mild hyperplasia at the end of the fourth week. The nephric tubule atrophied at the end of the eighth week accompanied with adhesion between glomeruli and Bowman's capsule. Glomeruli sclerosis of mild or medium degree was observed at the end of the twelfth week with obvious lymphocyte infiltration in the renal interstitium as well as the formation of collagen fibers.

结果 该模型表现为严重水肿、大量蛋白尿、低蛋白血症和高脂血症；病理学检查显示，4周末肾小球足细胞肿胀，系膜细胞轻度增生；8周末有球囊粘连，肾小管上皮细胞萎缩；12周末部分肾小球节段性轻、中度硬化，间质内有明显灶性淋巴细胞浸润，并有轻度纤维化。

Objective To study the effects of IL-1 receptor antagonist（IL-1ra）on neurocyte apoptosis in cerebral ischemia in rats.

目的 探讨白细胞介素1受体拮抗剂（IL-1ra）对大鼠局灶性脑缺血再灌注神经细胞凋亡的影响。

Objective To study the mechanism of neurocyte on inhibitor of nitric oxi-de synthase in the focal cerebral ischemic reperf us ion and the relationship between inhibitor of NOS and apoptosis especially.

目的 研究一氧化氮合酶抑制剂在局灶性脑缺血再灌流过程中对神经细胞的作用机理，特别是NOS抑制剂与细胞凋亡的关系。

Moutains of evidences from laboratary and clinical data show that gene abnormality is the major etiological factor of over 40% patients affected with epilepsy.There were also 6 epilepsy genes been cloned successfully, and mutations of over 1000 genes maybe related to epilepsy. These abnormal genes influence many aspects from molecular level to the neuronal plasticity, such as the development of brain,neuronic degeneration, remodeling of neural circuits, energy metabolism, ion channel and so on.These factors would at last affect the formation of epilepsy focus, propagations of epileptic potentials, vulnerability of epilepsy cells.

大量的实验和临床资料提示基因异常是40%以上癫痫患者的病因，有6种常见全身癫痫的基因已被成功克隆，1000种以上的基因突变可能与癫痫的发作有关，这些表达异常的基因分布在脑发育、神经元变性及神经环路重组、能量代谢、离子通道等多个环节，从分子、细胞、神经元可塑性等多个方面影响着癫痫灶的形成、痫性放电的扩布及癫痫细胞的损伤，构成了癫痫的基因机制。

Overall these studies demonstrate that the assessment of regional atrophy can be a useful addition to routine neuropathological examination.

所有这些研究均表明，对局灶性萎缩的评估可作为痴呆的常规神经病理学检查以外的一个辅助方法。

Based on the knowledge above, we carry out the study on the neurotrophy mechanism of qingkailing effective composition antagonizing focal cerebral ischemic injury in rats.

基于以上认识，本课题进行了清开灵有效组分抗大鼠局灶性脑缺血损伤的神经营养机制研究。

In the second part, we investigate the neurotrophy mechanism of qingkailing effective composition antagonizing ischemic injury, and comprehensively analyze the experimental results and come to the conclusions as follows: 1. Qingkailing effective composition can promote the activation of astrocyts during the early period after ischemia.

第二部分采用线栓法大鼠MCAO模型，围绕神经营养因子，从不同家族、同一家族的不同成员、同一成员的因子及其受体三个层次，探讨了清开灵有效组分抗局灶性脑缺血损伤的神经营养机制及效应特征。

In the whole group, of the 18 cancer sites, 8 nidi were less than 3cm.

两个癌灶应在811同时或间隔半年以内诊断；6。

Results Cerebral blood flow values were significantly lower in depressed patients than in nondepressed patients in the frontal cortex of the affected hemisphere.

结果 抑郁组与非抑郁组相比，梗死灶同侧的额叶皮层的脑血流明显减少，这种血流的降低与抑郁的严重程度相关。

Results:The rate of tumor shrinkage and necrosis was 46.8% and 20.7%,while the contrast group was 78.9%,49.2% respectively(P＜0.05).There were significant difference(P＜0.05)for 2year survival rate in singlelesion group,nondistant metastasis group and combinedtherapy group.

结果：单纯TACE组的肿瘤总缩小率和肿瘤完全坏死率分别为46.8%和20.7%，联合治疗组分别为78.9%、49.2%（P均＜0.05），单病灶组、无转移灶组及联合治疗组的2年生存率高于多病灶组、有转移组和单纯TACE组（P均＜0.05）。

The split between the two groups can hardly be papered over.

这两个团体间的分歧难以掩饰。

This approach not only encourages a greater number of responses, but minimizes the likelihood of stale groupthink.

这种做法不仅鼓励了更多的反应，而且减少跟风的可能性。