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目的通过改进直接体绘制技术(DVR)算法中的关键步骤,绘制能表达数据场中不同层次组织的内部结构。方法根据界面对光线的反射和物质本身对光线的衰减,将数据场划分为边界不丰富的简单数据场和边界丰富的复杂数据场,从而采用分段线性函数来构造阻光度传递函数(TF);将数据场中低灰度体素点看为一种不发光但会导致采样光线衰减的物质;根据采样结束时采样光线的阻光度分布来调整TF,完成三维绘制。结果绘制出了不同层次组织的内部结构。结论本算法有效地解决了体素点相互遮挡的问题,实现了医学三维整体可视化。  相似文献   
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While adult mice receiving picrotoxin (PTX) alone responded with clonic and tonic-clonic seizures, this response was greatly suppressed for mice simultaneously injected with 2,3-butanedione monoxime (BDM). For example, 60% and 10% of the mice convulsed when injected (i.p.) with 3.0 mg/kg PTX alone or PTX plus 205 mg/kg of BDM, respectively. In contrast, a non-oxime analogue of BDM, 2,3-butanedione (BTD), did not have this anticonvulsant effect. In order to explore the basis for the anticonvulsant effect of BDM, we recorded GABA-activated currents (IGABA) of frontal cortical as well as ventromedial hypothalamic neurons before, during and after exposure to this oxime. BDM had a biphasic effect on concentrations (100 μM-40 mM) decreased and lower concentrations (0.01 μM–0.001 μM) potentiatedIGABA; these effects of BDM reversed upon washout of the oxime. In contrast, BTD had no effect onIGABA. Finally, when 0.001 μM BDM, 10–30 μM PTX and GABA were co-applied the inhibitory effect of the toxin onIGABA was markedly suppressed. These data suggest that the anticonvulsant effect of oximes involves facilitation of the inhibitory action of GABA.  相似文献   
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The thiadiazinone derivative [+]-EMD 60263 ((+)-5-(1-(α-ethylimino-3,4-dimethoxybenzyl)-1,2,3,4- tetrahydroquinoline-6-yl)-6-methyl-3,6-dihydro-2H-1,3,4 -thiadiazine-2-on) is a Ca2+-sensitizing agent with only minor phosphodiesterase inhibitory activity. Our aim was to characterize the inotropic and electrophysiological effects of [+]-EMD 60263 and its enantiomer [-]-EMD 60264 in several cardiac muscle preparations. The Ca2+-sensitizing activity resided in the [+]-enantiomer only. [+]-EMD 60263 (3 μM) shifted the EC50 of Ca2+ for contractile activation of skinned fibers of pig heart from 2.41 μM to 0.73 μM, whereas [-]-EMD 60264 (30 μM) was ineffective. In Langendorff-perfused guinea pig hearts, [+]-EMD 60263 and [-]-EMD 60264 induced concentration-dependent positive and negative inotropic effects, respectively; both enantiomers reduced spontaneous heart rate but did not influence perfusion pressure. The maximum increase in force of human atrial trabeculae was 35 % of pre-drug control with [+]-EMD 60263 in comparison to 113 % with forskolin. In guinea-pig papillary muscles, [+]-EMD 60263 and [-]-EMD 60264 had opposite inotropic responses, however, both agents similarly prolonged action potential duration. Both enantiomers concentration-dependently blocked the rapidly activating component IKr of the delayed rectifier in guinea-pig myocytes. The block saturated at potentials positive to +30 mV, closely resembling the effects of the antiarrhythmic agent E-4031 which had been originally used to define IKr. It is concluded, that the positive inotropic action of [+]-EMD 60263 can be explained by prevalence of the Ca2+-sensitizing effect. The accompanying prolongation in action potential duration is caused by block of the IKr component of the delayed rectifier. While the inotropic effects are stereoselective, most of the electrophysiological actions are clearly independent of sterical configuration. The combination of Ca2+-sensitizing with class-III antiarrhythmic action may provide an interesting pharmacological profile of potential therapeutic use. Received: 7 January 1997 / Accepted: 25 February 1997  相似文献   
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Objectives Recent studies have described regional differences in the electrophysiology and pharmacology of ventricular myocardium in canine, feline, rat, guinea pig, and human hearts. This has been shown to be due to a smaller IKs and a lager sodium-calcium exchange current (INa-Ca) and late INa in M region (deep subepicardial to midmyocardial). Studies from our laboratory have found a new repolarization current-nonselective cation current (NSCCs) existing in rabbit right ventricular myocytes. Methods We examined the characteristics of NSCCs in epicardial, M region, and endocardial cells isolated from the rabbit left ventricle with standard microelectrode and whole-cell patch-clamp techniques. The permeability to Na , K , Li , Cs but not to Cl- indicating that it was a nonselective cation current. Gd3 (0.1 mmol/l) and La3 (0.1 mmol/l) can block the current markedly. Results Further characterization of NSCCs was significantly smaller in M cells than in epicardial and endocardial cells. NSCCs current density was significantly smaller in M cells than in epicardial and endocardial cells. With repolarization to -80 mV, INs current density was (-0.44±0.05) PA/PF in endocardial cells, (-0.12±0.05) PA/PF in M cells and (-0.28±0.07) PA/PF in epicardial cells; and with repolarization to 30 mV, INs current density was (1.09±0.29) PA/PF in endocardial cells, (0.38±0.09) PA/PF in M cells and (0.91±0.32) PA/PF in epicardial cells. Conclusions Transmural dispersion of repolarization was due to the heterogeneity of NSCCs in rabbit left ventricle epicardial, endocardial myocytes and M cells. These findings may advance our understanding of the ionic basis for our understanding of factors contributing to the development of cardiac arrhythmias.  相似文献   
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目的 探讨实验性内听动脉阻断与术后听力改变的关系及术中听觉监控的方法。方法 实验兔乙状窦后进路暴露小脑桥脑角,下压小脑暴露内听道及第Ⅷ神经复合体,分辨出内听动脉,予阻断不同时间,分别行蜗神经直接复合动作电位(DCAP)和畸变产物耳声发射记录(DPOAE)。结果对照组DCAPN1波潜伏期值无明显改变。内耳血供阻断10s和30s组在压迫开始后3min,DCAPN1波潜伏期值均恢复为初始值。内耳血供阻断1min组在压迫开始后3h,DCAPN1波潜伏期值未恢复为初始值假手术组DPOAE幅值无明显改变,内耳血供阻断10s、30s对DPOAE幅值无影响,内耳血供阻断1min使得DPOAE幅值下降结论兔内耳血供阻断1min可能造成兔听觉不可逆损伤。DCAP、DPOAE能有效、持续地监控内耳血供阻断,是耳神经外科手术中实用的听觉监测手段。  相似文献   
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目的了解SysmexXE-2100全自动血细胞分析仪嗜酸性粒细胞绝对值计数的准确性。方法分别用仪器法和目测法计数60份抗凝静脉血的嗜酸性粒细胞数,再将两者的结果进行比较;并对5份嗜酸性粒细胞数值不同的抗凝静脉血分别用仪器法和目测法计数,每份标本重复计数10次,然后计算出CV值进行比较。结果60份抗凝静脉血仪器法和目测法计数结果之间无显著性差异,P>0.05;相关系数(r)为0.9996,P<0.01。仪器法和目测法对5份嗜酸性粒细胞数值不同的标本重复计数的平均CV值分别是1.98%和6.63%,显示仪器法的精密度明显高于目测法。结论用SysmexSE-2100全自动血细胞分析仪计数嗜酸性粒细胞绝对值(0~9.02×109/L)是一种快速和较准确的方法,可满足临床诊断、治疗和疗效观察的需要。  相似文献   
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Stefan I McDonough 《Toxicon》2007,49(2):202-212
Some of the most potent and specific inhibitors of voltage-gated calcium channels are peptide toxins that inhibit channel function not by occlusion of the channel pore, but rather by interfering with the voltage dependence and kinetics of channel opening and closing. Many such gating modifier toxins conform to the inhibitor cystine knot structural family and have primary sequence or functional mechanism similar to toxins that target voltage-gated sodium or potassium channels. This review introduces known gating modifiers of calcium channels, discusses the selectivity, binding sites, and mechanism of the toxin-channel interaction, and reviews the usefulness of these toxins as research tools and as the basis for novel calcium channel pharmacology and therapeutics.  相似文献   
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