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突发性感音神经性聋病人的血清TNFα和IL-6检测 总被引:4,自引:0,他引:4
为探讨突发性感音神经性聋发病与血清细胞因子的关系,采用夹心法ELISA检测了32例突聋病人、15例慢性进行性感音神经性聋病人和20例健康对照者血清肿瘤坏死因子和白细胞介素水平。 相似文献
74.
为探讨影响颞骨骨折性面瘫预后的主要因素和面神经减压术的意义,总结分析了64例面瘫预后的主要相关因素。制作面瘫实验西式,测定面神经骨管开放组和非开放线面神经膨胀率,并行电镜观察。结果表明,影响预后的主要因素是否行面神经减主及手术时机。骨管开放组面神经膨胀率显著大于非开放组,非开放组纤维损伤谋生时机提示早期行面神经减压术有 利于面神经功能恢复。 相似文献
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In order to study the interaction between mechanical-electrical and electrical-mechanical transductions of outer hair cells (OHCs) in vivo, we observed the acoustically induced changes in the electrically evoked otoacoustic emission (EEOAE). One pole of a bipolar electrode was placed in the round window niche and the other pole on the surface of the first cochlear turn in the gerbil. A microphone and a speaker were used to monitor the EEOAE and to deliver an acoustical tone, respectively. It was found that a high sound level acoustical tone enhanced the EEOAE fine structure at frequencies below the acoustical frequency, and suppressed the overall level of the EEOAE at frequencies above the acoustical frequency. In addition, the EEOAE at frequencies approximately one half octave lower than the acoustical frequencies were relatively more enhanced or showed relatively less suppression than at other frequencies. The amplitudes of these changes had a positive relationship with acoustical tone levels. Furosemide eliminated the acoustically caused EEOAE change indicating that the acoustically caused change in the EEOAE is a phenomenon of the normal cochlea. One possible mechanism for the results is that the electrically and acoustically evoked basilar membrane (BM) vibrations interact at the EEOAE generation site and change the local mechanical and electrical properties. The second possible mechanism is that the acoustical stimulus creates an impedance discontinuity at its characteristic frequency location leading to a change in the reflected electrically evoked traveling wave, which may enhance or suppress the EEOAE by the vector summation of two waves. 相似文献
76.
目的:研究基因CT120在胶质瘤组织中的表达及其与胶质瘤组织病理学的关系。方法:应用免疫组织化学方法检测50例胶质瘤手术切除标本、3例正常脑组织中CT120蛋白的表达:应用半定量RT—PCR检测20例胶质瘤、3例正常脑组织中CT120mRNA的表达。结果:免疫组织化学检测发现正常脑组织中CT120蛋白无表达.50例胶质瘤组织中CT120蛋白表达阳性率为50.9%,不同级别胶质瘤中的表达无显著差异(χ^2=2.99,P〉0.05);半定量RT—PCR检测正常脑组织中CT120 mRNA呈弱表达,不同病理级别胶质瘤CT120 mRNA表达无显著差异(χ^2=3.25.P〉0.05)。结论:基因120在胶质瘤有表达,但在胶质瘤发生发展中作用不明显。 相似文献
77.
Transporter reversal as a mechanism of glutamate release from the ischemic rat cerebral cortex: studies with DL-threo-beta-benzyloxyaspartate 总被引:8,自引:0,他引:8
Elevated levels of the excitotoxic amino acids, glutamate and aspartate, have been implicated in the pathogenesis of neuronal injury and death induced by cerebral ischemia. This study evaluated the contribution of reversed high-affinity, Na(+)-dependent, glutamate transport to the ischemia-evoked release of glutamate and aspartate using DL-threo-beta-benzyloxyaspartate (DL-TBOA), a newly developed competitive, non-transported blocker of the EAAT 1-3 transporters. Changes in the extracellular levels of these and other amino acids, and of glucose and lactate in cerebral cortical superfusates during four-vessel occlusion-elicited global cerebral ischemia were examined using a cortical window technique. Basal and ischemia-evoked amino acid, glucose and lactate efflux were compared in control versus DL-TBOA (100 microM; applied topically for 35 min prior to ischemia) animals. Twenty minutes of ischemia caused large increases in aspartate, glutamate, GABA and taurine effluxes into cortical superfusates, with non-significant effects on the efflux of glycine, glutamine, alanine and serine. Application of DL-TBOA caused a 2-fold increase in basal, preischemic, extracellular glutamate levels, but did not affect those of the other compounds. In the presence of DL-TBOA, ischemia-evoked release of aspartate, glutamate, taurine and glutamine was significantly reduced; that of the other amino acids was not affected. The ischemia-evoked declines in glucose were significantly attenuated, and lactate release was enhanced above that in control animals. The amino acid data are interpreted as indicating that aspartate and glutamate releases were reduced as a consequence of DL-TBOA inhibition of reversed transport by high-affinity, Na-dependent carriers, predominantly involving the glial EAAT 2 transporter. The reduction in ischemia-evoked taurine release is interpreted as being due to a decrease in cell swelling prior to and during the initial phase of ischemia due to reduced entry of the Na(+), and other ions, associated with a decreased glutamate uptake. Glucose-sparing and availability for lactate formation would also result from a reduced glutamate/Na(+) uptake. These results indicate that reversed transport, primarily from glial cells by the EAAT 2 carrier, is responsible for a substantial (42 and 56%) portion of the ischemia-evoked increase in extracellular glutamate and aspartate levels, respectively. As a potent, competitive, non-transported blocker of high-affinity, Na(+)-dependent, glutamate transporters, DL-TBOA promises to be a valuable new compound for the study of glutamatergic mechanisms. 相似文献
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目的:介绍世界卫生组织网站中的药物流行病学信息。方法:介绍世界卫生组织网站结构和药物流行病学信息所处栏目。结果:药物流行病学信息主要分布于健康主题和WHO子网站中。结论:世界卫生组织网站中有丰富的药物流行病学信息。 相似文献