甲状腺机能亢进危象：附14例临床分析

本文报道14例甲亢危象,其发病率为4.5％,其发病与感染、劳累、情绪激动及同位素治疗有关。指出同位素治疗甲亢初期应服用抗甲状腺药物,讨论了淡漠型危象的有关问题。     

马来酸罗格列酮胃漂浮型缓释片的研究

目的：根据流体动力学平衡控释原理（HBS）研制了马来酸罗列酮胃漂浮型缓释片。方法；以体外释放度和漂浮情况为筛选指标，采用单因素考察和正交试验设计相结合， 对胃漂浮缓释片的处方、制备工艺及体外释放条件进行优化筛选；采用γ闪烁照相技术对优化处方的内漂浮情况进行胃内动态观察。结果：马来酸罗格列酮胃漂浮缓释片在释放介质中迅速起漂，持漂时间超过12h,12h达最大累积释放；初步确定在胃内滞留时间达3h以上。结论：优化处方的释放过程符合Higuchi方程，释放机制为异常扩散；胃漂浮片在胃滞时间明显长于普通片。     

东莨菪碱诱发染色体畸变的剂量效应

东茛菪碱五个剂量(1、2、5、10、20μg/ml作用于12名健康成人外周血淋巴细胞培养液诱发染色体畸变,并设空白对照组(生理盐水)。染色体畸变率分别为3.±0.5,9.6±1.1,11.7±1.1,13.6±2.3,18.0±3.0和17.5±2.0％;细胞畸变率为3.1±0.6,9.2±0.6,10.0±0.8,10.8±1.5,11.6±1.8和12.2±14.％。各剂量组与对照组比较差异高度显著(P<0.01)。方差分析,各剂量组间变异的差异高度显著(P<0.01)。相关系数和回归系数也非常显著(P<0.01)。结果表明,东莨菪碱剂量与染色体畸变率和细胞畸变率有线性关系。     

功能性消化不良的药物治疗

功能性消化不良是一种高发性疾病,常影响着人们的生活质量,被视为重要的消化道疾病.虽然已有达成共识的罗马标准,功能性消化不良呈现出多种多样的症状.本文尝试为临床提供治疗的选择,包括幽门螺杆菌的清除、抑酸治疗、促胃肠动力药、抗抑郁药等.总的来说,根据主要症状来选择治疗方法是可行和有效的.     

环糊精在鼻腔给药系统中的应用

综述了环糊精作为鼻腔给药系统赋形剂的应用及安全性.     

酵母样真菌感染的菌群临床分布与药敏分析

目的了解临床酵母样真菌的感染类型、分布及其对常用抗真菌药物的敏感性,为临床诊断治疗提供正确的用药依据。方法采用常规方法分离培养真菌,用法国生物梅里埃公司生产的ATB Expression微生物自动鉴定/药敏分析仪进行真菌鉴定和药敏分析。结果396株酵母样真菌中,白色假丝酵母菌检出率最高(72.3%),其次为热带假丝酵母菌(15.91%),光滑假丝酵母菌(6.82%)。酵母样真菌对5-氟胞嘧啶、两性菌素B、氟康唑、依曲康唑的敏感性分别为98.02%,98.43%,77.38%,77.76%。结论临床酵母样真菌感染以白色假丝酵母菌为主,对5-氟胞嘧啶、两性菌素B敏感性较高,对氟康唑、依曲康唑有不同程度的耐药,因此,药敏监测是非常必要的,临床医生应根据药敏结果合理使用抗真菌药物。     

Molecular basis of severe myoclonic epilepsy in infancy

Severe myoclonic epilepsy (SMEI) or Dravet syndrome is caused by mutations of the SCN1A gene that encodes voltage-gated sodium channel alpha-1 subunit. Recently, we generated and characterized a knock-in (KI) mice with an SCN1A nonsense mutation that appeared in three independent SMEI patients. The SCN1A-KI mice well reproduced the SMEI disease phenotypes. Both homozygous and heterozygous knock-in mice developed epileptic seizures within the first postnatal month. In heterozygous knock-in mice, trains of evoked action potentials in inhibitory neurons exhibited pronounced spike amplitude decrement late in the burst but not in pyramidal neurons. We further showed that in wild-type mice the Nav1.1 protein is expressed dominantly in axons and moderately in somata of parbalbumin (PV) – positive inhibitory interneurons. Our immunohistochemical observations of the Nav1.1 are clearly distinct to the previous studies, and our findings has corrected the view of the Nav1.1 protein distribution. The data indicate that Nav1.1 plays critical roles in the spike output from PV interneurons and further, that the specifically altered function of these inhibitory circuits may contribute to epileptic seizures in the mice. These information should contribute to the understanding of molecular pathomechanism of SMEI and to develop its effective therapies.