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.     

Parkinson''''s Disease and Smoking: An Integral Part of PD''''s Etiological Study

INTRODUCTION Parkinson抯 disease (PD), a debilitating neurodegenerative disorder, is featured with bradykinesia, resting, muscular rigidity, gait disturbances, and postural reflex impairment[1]. PD is rare before age of 50 years, but it increases dramatically with older ages, with peak onset occurring during the age of 70-85 years. In the United States, prevalence of PD in all age groups is approximately 150 per 100 000 and is roughly 30 per 100 000 at age of less than 50 years and 800 …     

鼻中隔前脱位及软骨部歪鼻手术矫正30例分析

对３０例鼻中隔前脱位伴软骨部歪血进行手术矫正，结果２８例治愈２例好转，均无处梁下塌及鼻尖疤痕性回缩，作者认为（１）松解四方软骨周边，特别是上下两个固定点是矫正歪鼻的关键；（２）鼻中隔软骨尽量保留，以防除过多而影响鼻中隔支撑力，（３）保留一侧粘软骨膜下或前部部少分；（４）注意矫正后新的位置固定。     

青少年初始血压高者在高血压发生中的预测意义

为探讨初始血压偏高者在高血压发生中的预测意义，对汉中农村４６２３名年龄６～１５岁青少年血压，经过８年随访（末次随访率为８２．０７％）证明，基线调查收缩压百分位与８年后的收缩压相关系数，男为０．３３，女为０．２８，舒张压均为０．２０；基线调查收缩压在第７５百分位（Ｐ７５）以上者，８年后血压≥１８．７／１２．０ｋＰａ（１４０／９０ｍｍＨｇ）的机率是＜Ｐ５０以下的３．９１倍，初始血压百分位愈高相对危险性愈大；如同时初始收缩压≥Ｐ７５、体重指数≥Ｐ９０，并有高血压病家族史者，发生高血压的机率为２７．６％，是收缩压＜Ｐ７５、体重指数＜Ｐ９０和无高血压家族史者的６．５７倍。我们认为，青少年初始血压高者是成年高血压的易感人群，特别当伴有肥胖或超重及高血压家族史者，预测意义更大。     

原发性干燥综合征合并大量胸腹水1例

患者女性，５５岁。近半年来间断发热，体温３７℃～３９℃，伴四肢乏力，口眼干燥，进干食困难，食欲减退，夜尿增多，无肌肉及关节疼痛，抗生素治疗无效。一周前出现明显腹胀，不思饮食，于１９９５年１２月５日入院，体检：体温３７．６℃，体质消瘦，皮肤干燥，右下肺...     

儿童近视化长期观察及在临床治疗中的指导意义

为指导临床治疗，我们对1984～2004年间我院就诊的屈光不正的儿童87例148只眼进行了长期观察。现报道如下：[第一段]     

治疗牛皮癣的药物致骨髓重度受抑与急性再生障碍性贫血的鉴别

目的：进一步探讨临床应用牛皮癣药物导致的骨髓重度受抑与急性再生障碍性贫血（以下简称急性再障）之间的实验室鉴别诊断的主要依据。方法：药物导致的骨髓重度受抑和急性再障患者行骨髓涂片、骨髓活检和末梢血涂片瑞姬氏染色后进行骨髓象和血象的检测；另外采静脉血应用血细胞自动化分析仪进行血常规检测。结果：治疗牛皮癣药物导致的骨髓重度受抑与急性再障患者外周血象极为相似，但骨髓重度受抑患者的骨髓涂片、活检不同于急性再障患者的显示，各系、各阶段有核细胞比例大致正常，巨核细胞、血小板数量虽少但还可见；此类药物导致的骨髓重度受抑患者骨髓涂片的骨髓小粒并不少，且虽有部分空虚，但其中网络的是三系造血细胞。结论：通过了解病史和使用牛皮癣药物的治疗史，骨髓象和血象的实验室分析，可以进一步找出此类药物导致的骨髓重度受抑与急性再障之间的实验室鉴别依据。     

Axin1调节骨骼肌GLUT4蛋白表达的作用研究

目的：探讨体轴发育抑制因子（Axin1）调节骨骼肌葡萄糖转运蛋白4(GLUT4)蛋白表达的作用及其机制。方法：利用RNAi干扰的Axin1腺病毒（Ad-siAxin1）感染C2C12小鼠骨骼肌细胞敲低Axin1,荧光显微镜和MTS实验明确Ad-siAxin1最佳感染浓度和时间。分别用携带绿色荧光蛋白的腺病毒（Ad-GFP）、Ad-siAxin1、载体质粒（vector）和Axin1质粒转染C2C12小鼠骨骼肌细胞敲低或过表达Axin1蛋白,Western印迹检测Axin1、端锚聚合酶蛋白（TNKS）和GLUT4蛋白水平。结果：荧光显微镜和MTS实验结果显示,在C2C12小鼠骨骼肌细胞中Ad-siAxin1作用的最佳浓度和时间分别为160μL和48 h。Western印迹结果显示,与Ad-GFP组相比,Ad-siAxin1组中Axin1蛋白降低（t=6.746,P<0.01）。Ad-siAxin1组TNKS蛋白水平降低（t=4.019,P<0.05）,GLUT4蛋白水平下调（t=3.248,P<0.05）。与vector组相比,转染Axin1质粒后,Axin1蛋白水平上...     

胎盘生长因子串联scFv质粒构建表达及亲和力测定

目的:构建并表达胎盘生长因子串联scFv,提升对胎盘生长因子的亲和力。方法:设计不同长度的柔性连接子连接的串联scFv,构建串联scFv质粒,并分别将串联scFv与亲本scFv于原核表达系统进行表达。通过间接ELISA分别测定串联scFv及对应亲本scFv亲和力,分别对数据进行单因素ANOVA方差分析,并使用Dunnett-t检验进行组间比较。结果:柔性连接子长度的不同,会对串联scFv亲和力造成差别。单因素ANOVA方差分析结果表明,各组亲和常数间存在明显的统计学差异,Dunnett-t检验组间比较结果可知,当串联scFv间柔性连接子（GGGGS）n长度n=4和n=5时,亲和力较亲本提升不明显（P＞0.05）;但亲和力在n=6（t335=33.90,t7A10=32.00,均P<0.000 1）及n=7（t335=91.68,t7A10=90.71,均P<0.000 1）时较两亲本均有明显提升。结论:串联scFv可以明显提高单体scFv亲和力。