E1 Tor Vibio Cholerae Strain SM_6 and Jiangsu 1d Strain

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中西医结合治疗眼内出血50例

自2000年以来,采用中西医结合方法治疗眼内出血50例,疗效满意,现总结报道如下.     

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 …     

抗癌药物安全应用与护理

抗癌药物不但能对患者产生许多不良反应，而且对长期接触抗癌药物的工作人员尤其是护士也具有极大的危害性。因此，抗癌药物安全应用与护理也就成了临床积极研究的一个重要课题。     

危重病患者血浆胰岛素水平与细胞因子含量的关系

目的探讨危重病患者是否存在高胰岛素血症、胰岛素抵抗(IR)及与肿瘤坏死因子(TNF-α)、白细胞介素-6(IL-6)的关系.方法测定危重病患者123例和对照组30例的空腹血糖(FBG)、空腹胰岛素(FINS)、TNF-α、IL-6的水平,并计算胰岛素敏感性指数(IAI),以评估危重病患者IR的严重程度,并分析各参数之间的相关性.结果危重病组与对照组的IAi分别为-1.95±0.38和-1.5±0.29,两者差异显著(P＜0.01).危重病按病因分组后各组IAI相比无显著差异(P＞0.05).IAI与危重病严重程度、TNF-α及IL-6的直线回归分析,直线关系r分别为0.86,-0.89,-0.87,差异有显著性(P＜0.01).结论危重病患者存在高胰岛素血症及IR.IR的程度与危重病程度、TNF-α、IL-6的水平有显著相关性.危重病患者的IR与TNF-α的升高有关,提示IAI可作为危重病患者病情严重程度的预测指标.     

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。