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.     

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 …     

西地那非与真空抽吸装置联合应用治疗勃起功能障碍The Journal of urology．171（1）：292-295

真空抽吸装置和西地那非均是常见的治疗勃起功能障碍的治疗方式，而对于单独应用西地那非或真空抽吸装置（VED）治疗勃起功能障碍不完全满意的患者，通常给予侵袭性治疗。为了评估这类患者联合使用西地那非和真空抽吸装置的有效性。Chen J等人对此进行了一项前瞻性研究评估研究，     

桡动脉血采集方法讨论

动脉血气分析是临床上常用的一种血液检测方法 ,用于观察病人内环境的酸碱平衡。随着其在临床的广泛应用,护士接触到动脉血采集也相应增加,因股动脉管腔粗大,搏动感强,易于采取,临床中常选其作为采血部位。但临床中一些清醒患者，     

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。