21纪我国医药行业的创新与发展

在分析我国医药行业发展现状及存在问题的基础上,研究了加入WTO后医药行业所面临的机遇与挑战,以及当前医药企业技术创新存在的不足,提出了21世纪我国医药行业创新与发展的对策和建议。     

12例腰椎间盘突出合并腰骶神经背根节嵌压

目的：了解腰椎间盘同合并腰骶神经背根节（ＤＲＧ）嵌压的机制。方法：１２例腰椎间盘突出患者术中发现：髓核切除后神经根张力仍较大并固定,沿神经根探查发现腰骶神经ＤＲＧ充血并肿大,直径０．８－１．２ｃｍ,平均１．１ｃｍ。嵌压物为增生的上关节突和增生肥厚的关节囊韧带。１２例病人共探查１５个ＤＲＧ,其中位于椎间孔６例,椎管和椎间孔交界７例,椎间孔外２例同时合并腰神经在椎间孔外嵌压。     

舰艇用防火漆热解气急性吸入毒性试验

目的 :观察舰艇用防火漆热解气小鼠急性吸入毒性。方法 :急性试验用鼠 6 0只 ,随机分为 6组 ,每组 10只 ,各组试验浓度呈等比级数 ,染毒柜为六面体的玻璃柜。启动热解气循环系统后 ,用煤气火焰烧烤干漆膜试样 ,直到全部炭化 ,小鼠在染毒柜内静式吸入 2h ,观察小鼠在染毒期间的活动情况 ,存活小鼠饲养观察 2周 ,解剖作病理检查。结果 :染毒后急性死亡小鼠以肺的急性损害为主要特征。存活小鼠镜下所见各脏器与正常对照组无明显差异。结论 :通过防火漆热解气小鼠急性吸入毒性试验 ,求得LC50 为 5 7.72mg/L ,舰艇用防火漆属低毒类。     

飞行员不成熟防御机制与心理健康、 个性、生活事件、社会支持的相关性研究

目的　探讨飞行员心理防御机制与心理社会因素的相关性。方法　对312 例飞行员进行防御方式问卷,卡特尔16 种个性因素问卷,症状自评量表,紧张性生活事件量表,社会支持评定量表测评。结果　揭示飞行员不成熟防御机制与心理健康水平,生活事件,社会支持显著相关,个性因素明显的影响不成熟防御机制;患病飞行员采用不成熟防御机制明显的多。结论　在飞行员心理卫生保健工作中,揭示并修正飞行员不成熟防御机制是十分必要的。     

Kentanserin对大鼠心肌缺血 再灌注损伤的影响

为探讨５ ＨＴ２受体与心肌缺血 再灌注损伤的关系,观察５ ＨＴ２受体阻断剂ｋｅｎｔａｎｓｅｒｉｎ对心肌缺血 再灌注大鼠室颤及左室内压＋ｄｐ／ｄｔｍａｘ及－ｄｐ／ｄｔｍａｘ的影响。结果表明,ｋｅｎｔａｎｓｅｒｉｎ可拮抗缺血性心功能障碍和再灌室颤。提示５ ＨＴ２受体参与了缺血性心功能障碍和再灌室性心律失常的发生。     

重组人神经营养因子-4/5蛋白抗三氧化二砷神经毒作用

目的初步观察重组人神经营养因子-4／5（hNT－4／5）蛋白对三氧化二砷毒性的抑制作用。方法利用hNT－4／5蛋白具有抗神经毒性的特点,采用本实验室克隆表达及部分纯化的具有天然hNT－4／5蛋白生物学活性的重组hNT-4／5蛋白,以不同水平的重组hNT4／5蛋白（0－100μl）与不同浓度的As2O3（0－160μmol／L）同时加入各组鸡胚前脑神经细胞和PC12细胞培养液中共同孵育24－48小时,观察其对染毒鸡胚前脑神经细胞存活和PC12细胞突起生长的影响作用。结果在鸡胚前脑神经细胞和PC12细胞中与As2O3共同培养48小时后,对照组与实验组的细胞存活率差异有显著性,而且细胞存活率和突起数目随hNT－4／5浓度增高而提高和增加。结论初步观察到重组hNT4／5蛋白具有抑制As2O3的毒性作用,为从基因工程途径寻找抗环境毒物因子提供了依据。     

多普勒超声心动图评估左心室舒张末压的研究

目的探讨多普勒超声心动图评估左室舒张末压的有效方法与指标。方法对６８例病人采用左心导管测压及经胸多普勒超声心动图检测。结果对比研究显示,联合肺静脉与二尖瓣血流频谱分析优于二尖瓣血流频谱分析,肺静脉Ａ峰和二尖瓣Ａ峰时限差值（ＰＡｄ－Ａｄ）与左室舒张末压实测值呈最佳相关性（ｒ＝０．７２,Ｐ＜０．０１）。结论认为应用多普勒超声心动图测定ＰＡｄ与Ａｄ,并以其差值估测左室舒张末压,是一项简便、可靠的无创性评估左室舒张末压的方法。ＰＡｄ－Ａｄ≥０可作为临床判断左室舒张末压增高［≥２．０ｋＰａ（１５ｍｍＨｇ）］的一项半定量指标。     

Does glutathione-S-transferase dethiolate lens protein-thiol mixed disulfides?-A comparative study with thioltransferase.

Protein S-thiolation is a process in which under oxidative stress, vulnerable sulfhydryl groups of proteins are conjugated to non-protein thiols such as glutathione (GSH) or cysteine resulting in the formation of protein-thiol mixed disulfides, protein-S-S-glutathione (PSSG) and protein-S-S-cysteine (PSSC). This process spontaneously disrupts the redox homeostasis of the cells, which in turn leads to functional disturbances in the respective tissue. In the ocular lens, such modification of proteins may trigger a cascade of events starting with the alteration of protein conformation, protein/enzyme deactivation, protein-S-S-protein aggregation and eventually lens opacification or cataract. Generally, the first line of defense system in the cells protects the lens proteins against such damage. Recent studies in our laboratory have shown that in addition to this defense system, lens cells also possess a well developed system to repair the oxidative damage to the lens proteins. We have identified this repair system as thioltransferase (TTase) and have proved that TTase by its dethiolase activity reverses the protein S-thiolation process which returns the oxidatively damaged lens proteins/enzymes to their original reduced state and restores their physiological functions. We investigated if this repair mechanism was mediated by enzymes other than TTase. We studied glutathione S-transferase (GST) and report here for the first time the cloning, high level expression, and purification of human lens mu and pi isoforms of GST. A comparative study of recombinant human lens TTase and GST (mu and pi) on their dethiolating abilities using lens crystallin-thiol mixed disulfides showed that the lens TTase is 60-70% more efficient in the dethiolation/repair process than GST. When TTase and GST were tested in conjunction for the dethiolation of thiol mixed disulfides, there was no significant enhancement of dethiolase activity. These findings suggest that TTase by itself is an efficient enzyme in the dethiolation/repair process and hence can be considered a crucial system to counteract oxidative stress in the lens.     

Modulation of Ca2+/calmodulin-dependent protein kinase II activity by acute and chronic morphine administration in rat hippocampus: differential regulation of alpha and beta isoforms

Calcium/calmodulin-dependent protein kinase II (CaMK II) has been shown to be involved in the regulation of opioid receptor signaling. The present study showed that acute morphine treatment significantly increased both Ca2+/calmodulin-independent and Ca2+/calmodulin-dependent activities of CaMK II in the rat hippocampus, with little alteration in the protein level of either alpha or beta isoform of CaMK II. However, chronic morphine treatment, by which rats were observed to develop apparent tolerance to morphine, significantly down-regulated both Ca2+/calmodulin-independent and Ca2+/calmodulin-dependent activities of CaMK II and differentially regulated the expression of alpha and beta isoforms of CaMK II at protein and mRNA levels. Application of naloxone or discontinuation of morphine treatment after chronic morphine administration, which induced the withdrawal syndrome of morphine, resulted in the overshoot of CaMK II (at both protein and mRNA levels) and its kinase activity. The phenomena of overshoot were mainly observed in the beta isoform of CaMK II but not in the alpha isoform. The effects of both acute and chronic morphine treatments on CaMK II could be completely abolished by the concomitant application of naloxone, indicating that the effects of morphine were achieved through activation of opioid receptors. Our data demonstrated that both acute and chronic morphine treatments could effectively modulate the activity and the expression of CaMK II in the hippocampus.