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61.
普通人的八条保健规刚1.找到一位受过良好教育的,可以信赖的保健专家.2.具备健康知识,有能力处置健康风险,确定你自己的生命质量标准.3.广泛利用预测医学和预防医学.4.虽期望通过医疗得到康复或缓解,但也意识到医疗本身的局限和风险.5.要从医生和其他保健专家那里得到信息和咨询,在治疗中做他们的负责的和可靠的同伴.  相似文献   
62.
程美 《中国交通医学杂志》1995,9(1):101-101,146
<正>我院自1993年6月至9月选择持硬麻醉的手术病人54例,用曲马多作硬膜外注射,观察术后止痛效果、持续时间及副作用等,现报告如下。 临床资料 男性18例,女性36例,年龄最小18岁,最大76岁,体重45~77kg,择期手术48例,急诊手术6例,病情按ASA分级:Ⅰ~Ⅱ级45例,Ⅲ级8例,Ⅳ级1例。  相似文献   
63.
E1TorVibioCholeraeStrainSM_6andJiangsu1dStrain¥JiangXiaowan,etal.ACTAACADEMIAEMEDICINAENANJING,1994,14(2):163-164AbstractE1To?..  相似文献   
64.
65.
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.  相似文献   

66.
Background: Carbon dioxide is an important vasodilator of cerebral blood vessels. Cerebral vasodilation mediated by adenosine triphosphate (ATP)-sensitive K+ channels has not been demonstrated in precapillary microvessel levels. Therefore, the current study was designed to examine whether ATP-sensitive K+ channels play a role in vasodilation induced by mild hypercapnia in precapillary arterioles of the rat cerebral cortex.

Methods: Brain slices from rat cerebral cortex were prepared and superfused with artificial cerebrospinal fluid, including normal (Pco2 = 40 mmHg; pH = 7.4), hypercapnic (Pco2 = 50 mmHg; pH = 7.3), and hypercapnic normal pH (Pco2 = 50 mmHg; pH = 7.4) solutions. The ID of a cerebral parenchymal arteriole (5-9.5 [mu]m) was monitored using computerized videomicroscopy.

Results: During contraction to prostaglandin F2[alpha] (5 x 10-7 m), hypercapnia, but not hypercapnia under normal pH, induced marked vasodilation, which was completely abolished by the selective ATP-sensitive K+ channel antagonist glibenclamide (5 x 10-6 m). However, the selective Ca2+-dependent K+ channel antagonist iberiotoxin (10-7 m) as well as the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester (10-4 m) did not alter vasodilation. A selective ATP-sensitive K+ channel opener, levcromakalim (3 x 10-8 to 3 x 10-7 m), induced vasodilation, whereas this vasodilation was abolished by glibenclamide.  相似文献   

67.
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.  相似文献   

68.
放大胃镜在胃病中的应用   总被引:1,自引:0,他引:1  
放大内镜由于具有变焦放大的功能,可以在消化道检查中清晰显示胃肠黏膜的腺管开口、微细血管等微细结构的变化,结合黏膜色素染色,可以比较准确地反映病变组织的病理学背景,更容易地在镜下区分不同性质的病变,提高了早期癌的镜下检出率。使得镜下诊断出现了新的标准,使内镜诊断提高到了一个新的水平,是医学发展的又一次革命性进步。  相似文献   
69.
70.
南四湖区渔民发汞含量的调查   总被引:3,自引:0,他引:3  
长时间食用被水体污染的生物,会造成机体生理、生化功能的改变。我们从1985年开始,对南四湖湖区渔民进行了发汞含量的调查,以评价人体对汞的蓄积水平。  相似文献   
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