2001年与2004年抗菌药物应用情况比较

目的　了解抗菌药物应用的基本情况。方法　将 2 0 0 1年 3月 14 3 0例住院患者病历与 2 0 0 4年 3月的 2 0 66例住院患者病历进行回顾性调查和对比分析。结果　 2 0 0 1年的 14 3 0例中有 948(66 3 % )例 ,和 2 0 0 4年的 2 0 66例有 10 60例 (5 1.3 % ) ,应用了抗菌药物。结论　定期检查考评 ,严格掌握用药指征 ,是加强抗菌药物应用管理的关键。     

甘露醇和低温对兔骨骼肌缺血再灌流损伤的保护作用

通过兔后肢缺血模型，观察了甘露醇和低温对骨骼肌缺血再灌流损伤的保护作用。结果：甘露醇和低温可以不同程度地降低再灌流后患肢静脉回流血中细胞内酶（ＣＰＫ、ＬＤＨ、ＡＳＴ）的活性和脂质过氧化反应终末代谢产物丙二醛（ＭＤＡ）的含量，减轻骨骼肌细胞超微结构的破坏。两者单独应用效果不明显（Ｐ＞０．０５），联合应用效果非常明显（Ｐ＜０．０１）。提示自由基介导的脂质过氧化反应参与骨骼肌缺血再灌流损伤，甘露醇和低温对其具有协同保护作用。     

根据桂枝汤的效应消除半衰期和表观消除半衰期制订给药方案的探讨

为探讨药效法估测的效应消除半衰期和效量法估测的表观半衰期对合理制订给药方案的意义和作用,以桂枝汤解热和抗炎的药物动力学实验中所得的相应参数值设计了给药方案,观察了它们在提高药效上的作用。结果表明在给药总剂量相等、首次给药同时开始的情况下,以半衰期设计的给药方案组的药效均明显高于习惯的一次给药组;而以效应消除半衰期设计给药方案组药效增强率又高于以表观半衰期设计的方案组。提示效应消除半衰期比表观半衰期似更有实践意义。     

中风后癫痫的临床研究

本文报告３６例中风后癫痫发作的临床和ＣＴ资料。通过回顾性病历复习和随访发现，中风后癫痫的发生率占同期住院中风患者的５．２６％，以蛛网膜下腔出血和脑栓塞发生癫痫比率最高，分别为１５％和１２．５％。癫痫发作与ＣＴ所见病灶分布密切相关，皮质病灶较皮质下病灶更易发生病病。癫痫发作可发生于中风后任何时期，但早期癫痫以出血性中风多见，而迟发性癫痫则更多见于脑梗塞患者。     

语言实验室教学的利与弊

通过期末考试成绩对实验班与参照班学生语言基础知识和应用能力2方面进行比较，分析产生差异的原因，以便更合理地利用现有教学资源，取得最佳教学效果。     

Advances in TCM Treatment of Senile Vascular Dementia

Senile vascular dementia refers to organic loss of intellectual function due to cerebral damages caused by insufficient blood supply. The following is a summaryon achievements in its etiology, pathogenic mechanism, type identification and treatment in TCM, and the compound formulas, special formulas and drugs, and thepatent drugs used successfully for its treatment.     

淋巴因子水平改变与妊高征的关系

近年来的研究结果发现由Th1/Th2细胞分泌的淋巴因子与妊娠高血压综合征联系密切 ,可能参与了其病因及病理生理过程 ,对它的深入研究有利于妊娠高血压综合征诊断、治疗水平的提高     

Prof. Shan Zhaowei＇s Experience in Treating Atrophic Gastritis

Prof. Shan Zhaowei （ 单兆伟 ）, the author＇s teacher, has been engaged in TCM for more than 30 years, with profound knowledge in the treatment of diseases of the spleen and stomach, which are introduced in the following.     

Role of mast cells and monoamines in the thrombocytopaenia and mortality elicited by tumour necrosis factor in mice.

We explored the thrombocytopaenia elicited by the i.v. injection of mouse recombinant tumour necrosis factor (TNF) in mice. Injection of 10 micrograms of TNF led to a thrombocytopaenia (evident after 0.5 hr) which was caused by decreased platelet survival, as seen by the injection of labelled platelets. TNF-induced thrombocytopaenia was not prevented by heparin, nor by depletion of either fibrinogen or C'. TNF-induced thrombocytopaenia was markedly attenuated in mice treated with reserpine, an agent that depletes monoamines from mast cells and other cells, and in the mast-cell-deficient WWv mice. In vitro, TNF elicited a modest release of monoamine from peritoneal mast cells and from a mast cell line. When mice are injected with 3H-serotonin (3H-5HT) before TNF, TNF injection increased the plasma 3H-5HT content 1 hr later, modifications absent in reserpine pretreated or mast-cell-deficient mice. 3H-5HT content of the small intestine was markedly depleted in TNF-injected mice, suggesting that this organ is the source of the plasma 3H-5HT. Drop in body temperature and mortality induced by TNF were also attenuated in mast-cell-deficient, and in reserpine pretreated mice. These results indicate that TNF can induce a release of monoamines from mast cells, mainly from those of the small intestine, a process that contributes to TNF-induced thrombocytopaenia and mortality.