椎管肿瘤的显微外科治疗

椎管肿瘤的早期手术治疗是该病的最佳方案,随着显微神经外科技术的日趋成熟,其疗效及预后较常规手术有明显改善,我科2000年6月至2005年3月对18例椎管肿瘤采用显微手术,取得良好效果,现报道如下。临床资料1.一般资料:本组男11例,女7例,年龄18~53岁,平均37岁,病程3个月~5年,平均1.1年。临床表现:以进行性一侧或双下肢肌力下降为首发症状5例,以感觉障碍为首发症状10例,以神经根痛为首发症状3例。影像学检查:本组18例患者均行MR平扫及增强扫描,均可清楚显示肿瘤的部位、大小及同脊髓的解剖关系,其中硬脊膜外2例,跨椎管内外哑铃形肿瘤3例,髓外硬…     

Effect of water restrictions on the physiological parameters,psychological behavior and brain c-Fos expression in rat

1 Introduction Exposure to hostile stressors causes a series of coor- dinated responses in the body, such as alterations of neu- roendocrine secretion, immune reaction and behavioral manifestation to maintain homeostasis stability and sur-vival of the organisms. Stressors are divided into two main categories: physical, or systemic, and psychological, or emotional / processive. Each stressor might activate a spe- cific central pathway to induce a special neuroendocrine response, even cause stre…     

一氧化氮诱导肝癌细胞凋亡过程bcl-2和bax mRNA表达水平的变化

目的 探讨在一氧化氮(NO)诱导肝癌细胞凋亡过程bcl-2和bax mRNA表达水平的动态变化。方法 用NO供体硝普钠(SNP)诱导SMMC-7721和HepG2肝癌细胞株凋亡，RT-PCR的方法检测bcl-2、ba xmRNA表达水平，并采用凝胶分析系统进行半定量分析。结果 1．0mmol/L可降低SMMC-7721和HepG2细胞bcL2、bax mRNA的表达水平，提高bax/bc1-2 mRNA的比值并呈时间依赖性。HepG2细胞bcl-2和bax mRNA降低的幅度较SMMC-7721细胞小(P＜0．05)，开始变化的时间也较SMMC-7721细胞迟。结论 NO诱导肝癌细胞株的凋亡，可能与其bcl-2、bax mRNA表达水平变化导致bax/bc1-2 mRNA比值上升有关。     

国外山羊肉的生产和销售

地球上广泛分布的山羊是人类最早利用的动物之一。它对人类生存和发展的贡献是不可低估的。现代畜牧业中,山羊,特别是肉用山羊不受人们的欢迎,更谈不上对山羊肉生产的投资、建设和研究,致使世界山羊肉资源得不到充分挖掘和利用。而在另一方面,人们却越来越重视膳食结构,追求瘦肉蛋白,还有世界人口迅速增长所带来的蛋白质短缺问题都迫使人们重新认识和利用山羊,山羊肉也有可能受到越来越多人的青睐。     

E1 Tor Vibio Cholerae Strain SM_6 and Jiangsu 1d Strain

Ｅ１ＴｏｒＶｉｂｉｏＣｈｏｌｅｒａｅＳｔｒａｉｎＳＭ_６ａｎｄＪｉａｎｇｓｕ１ｄＳｔｒａｉｎ￥ＪｉａｎｇＸｉａｏｗａｎ，ｅｔａｌ．ＡＣＴＡＡＣＡＤＥＭＩＡＥＭＥＤＩＣＩＮＡＥＮＡＮＪＩＮＧ，１９９４，１４（２）：１６３－１６４ＡｂｓｔｒａｃｔＥ１Ｔｏ?..     

Morphine Preconditions Purkinje Cells against Cell Death under In Vitro Simulated Ischemia-Reperfusion Conditions

Background: Morphine pretreatment via activation of [delta]1-opioid receptors induces cardioprotection. In this study, the authors determined whether morphine preconditioning induces ischemic tolerance in neurons.

Methods: Cerebellar brain slices from adult Sprague-Dawley rats were incubated with morphine at 0.1-10 [mu]m in the presence or absence of various antagonists for 30 min. They were then kept in morphine- and antagonist-free buffer for 30 min before they were subjected to simulated ischemia (oxygen-glucose deprivation) for 20 min. After being recovered in oxygenated artificial cerebrospinal fluid for 5 h, they were fixed for morphologic examination to determine the percentage of undamaged Purkinje cells.

Results: The survival rate of Purkinje cells was significantly higher in slices preconditioned with morphine (>= 0.3 [mu]m) before the oxygen-glucose deprivation (57 +/- 4% at 0.3 [mu]m morphine) than that of the oxygen-glucose deprivation alone (39 +/- 3%, P < 0.05). This morphine preconditioning-induced neuroprotection was abolished by naloxone, a non-type-selective opioid receptor antagonist, by naltrindole, a selective [delta]-opioid receptor antagonist, or by 7-benzylidenenaltrexone, a selective [delta]1-opioid receptor antagonist. However, the effects were not blocked by the [mu]-, [kappa]-, or [delta]2-opioid receptor antagonists, [beta]-funaltrexamine, nor-binaltorphimine, or naltriben, respectively. Morphine preconditioning-induced neuroprotection was partially blocked by the selective mitochondrial adenosine triphosphate-sensitive potassium channel antagonist, 5-hydroxydecanoate, or the mitochondrial electron transport inhibitor, myxothiazol. None of the inhibitors used in this study alone affected the simulated ischemia-induced neuronal death.     

Isoflurane Preconditions Hippocampal Neurons against Oxygen-Glucose Deprivation: Role of Intracellular Ca2+ and Mitogen-activated Protein Kinase Signaling

Background: Isoflurane preconditions neurons to improve tolerance of subsequent ischemia in both intact animal models and in in vitro preparations. The mechanisms for this protection remain largely undefined. Because isoflurane increases intracellular Ca2+ concentrations and Ca2+ is involved in many processes related to preconditioning, the authors hypothesized that isoflurane preconditions neurons via Ca2+-dependent processes involving the Ca2+- binding protein calmodulin and the mitogen-activated protein kinase-ERK pathway.

Methods: The authors used a preconditioning model in which organotypic cultures of rat hippocampus were exposed to 0.5-1.5% isoflurane for a 2-h period 24 h before an ischemia-like injury of oxygen-glucose deprivation. Survival of CA1, CA3, and dentate neurons was assessed 48 later, along with interval measurements of intracellular Ca2+ concentration (fura-2 fluorescence microscopy in CA1 neurons), mitogen-activated protein kinase p42/44, and the survival associated proteins Akt and GSK-3[beta] (in situ immunostaining and Western blots).

Results: Preconditioning with 0.5-1.5% isoflurane decreased neuron death in CA1 and CA3 regions of hippocampal slice cultures after oxygen-glucose deprivation. The preconditioning period was associated with an increase in basal intracellular Ca2+ concentration of 7-15%, which involved Ca2+ release from inositol triphosphate-sensitive stores in the endoplasmic reticulum, and transient phosphorylation of mitogen-activated protein kinase p42/44 and the survival-associated proteins Akt and GSK-3[beta]. Preconditioning protection was eliminated by the mitogen-activated extracellular kinase inhibitor U0126, which prevented phosphorylation of p44 during preconditioning, and by calmidazolium, which antagonizes the effects of Ca2+-bound calmodulin.