论文摘要
第一部分 Smad5基因敲除小鼠位听功能和内耳形态实验观察 目的:观察Smad5基因敲除嵌合体Smad5（+/-）小鼠听觉、前庭功能和前庭形态变化,探讨Smad5基因是否为一种听觉、前庭功能相关基因。方法:对照法对20只Smad5（+/-）小鼠和15只Smad5（+/+）小鼠进行颈髓膜表面短声诱发电位检测前庭功能和听功能（ABR）及耳蜗和前庭器官形态的改变实验观察。结果:ABR测听Smad5（+/-）小鼠平均听力为72.25±10.23dB（SPL）,Smad5（+/+）小鼠平均听力为35.75±16.65dB（SPL）二者有显著差异（P<0.01）;颈髓膜表面短声诱发电位检测Smad5（+/-）小鼠峰值潜伏期在85dB、95dB和105dB分别为6.85±0.23ms、6.78±0.20ms和6.70±0.43ms。Smad5（+/+）小鼠峰值潜伏期在85dB、95dB和105dB分别为6.35±0.28ms、6.22±0.49ms和6.17±0.73ms前者潜伏期长于后者,但差异无统计学意义（P>0.05）。耳蜗半薄切片显示Smad5（+/-）小鼠球囊斑、椭圆囊斑和壶腹嵴毛细胞,前庭神经节和螺旋神节细胞缺失明显,而Smad5（+/+）小鼠球囊斑、椭圆囊斑、壶腹嵴毛细胞,螺旋神经节及前庭神经节细胞为散在性缺失。在细胞缺失数量上比较有明显差异。结论:Smad5基因敲除导致小鼠中、重度ABR阈值下降,颈髓膜表面短声诱发电位的潜伏期明显延长;球囊斑,椭圆囊斑,壶腹嵴,螺旋神经和前庭神经节细胞形态发生改变。Smad5基因敲除小鼠颈髓膜表面短声诱发电位的潜伏期延长及内耳感觉细胞缺失的机理尚需进一步研究论证。 第二部分 胆脂瘤型中耳炎颅内外并发症的临床分析 目的 探讨胆脂瘤性中耳炎引起颅内外并发症的临床特点和处理方法。方法 1992年1月—2002年12月解放军总医院耳鼻咽喉-头颈外科
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标签：基因敲除论文; 小鼠论文; 前庭器论文; 毛细胞论文; 中耳炎论文; 胆脂瘤论文; 中耳论文; 并发症论文; 面瘫论文;