导航在长骨干骨折髓内钉固定中的应用

目的阐述透视导航技术在长骨干(股骨和胫骨)骨折,特别是在术中远端交锁髓内钉固定中的应用。探索在导航条件下术中应用髓内钉图像库开展远端交锁固定的可行性。此外,医用机器人的开发旨在被进一步用来改善手术程序的精确性。方法导航手术下,55例行股骨远端交锁钉固定和36例行胫骨远端交锁钉固定。其中13例术中应用图像库开展远端交锁固定。结果远端交锁固定成功率为97%。结论透视导航在长骨干骨折术中,使远端髓内交锁钉固定成功率增高。图像库的应用可以进一步减少患者和手术人员的X线辐射剂量。     

微小切口胆囊切除术2260例效果观察

目的 总结微小切口胆囊切除术治疗胆道系统疾病的经验。方法 对2002-2004年连续收治的2260例胆囊、胆道系统疾病实施微小切口手术的临床观察资料进行回顾性分析。结果 本组2260例微小切口胆囊切除术的患者无一例因手术原因死亡；术后无残留小胆囊；无胆汁漏及腹腔脓肿，亦无伤口全层裂开及切口疝形成。结论 该术式损伤小、局部显露清楚、不易发生副损伤，可同时行胆总管探查术，特殊情况下可随时改变手术方式。     

通过三年资料实证医院检验科常规项目全成本

目的弄清医院常规检验项目的实际成本,为医院及卫生主管部门进行科学管理和政府物价部门制订科学合理的收费价格体系提供科学依据。方法对某二级甲等医院检验科3年中所开展的全部7大类16个项目组169个检验项目的成本按耗材、设备折旧、劳务费、房屋折旧、业务费与后勤管理费共5大类进行实证分析。结果该科的成本构成比是:耗材成本34.1%、设备折旧24.3%、劳务费30.0%、房屋折旧4.0%、业务费与后勤管理费7.6%;检验项目的每项次平均成本为7.17元;成本最低的两类检验项目是生化及定性免疫,其项次成本分别为3.18元和4.25元;最高的则为微生物和血库,项次成本分别为48.63元和35.21元;项次成本过百元的有7项,多为输血项目;5至10倍于平均成本的28项,2至5倍于全科平均成本的22项,其余112项介于全科平均成本上下。结论实证研究是准确掌握检验项目成本的有效方法。     

10例前置胎盘产后出血改良式宫腔纱布填塞临床分析

目的对改良式宫腔填塞治疗前置胎盘产后出血进行疗效分析。方法对我院手术室常规使用大尾纱行子宫下段胎盘附着面出血,填塞压迫止血进行回顾性分析。结果10例患者行子宫下段纱布填塞疗效明显,出血量400～600ml,均未输血,生命体征平稳,无产褥感染和晚期产后出血。结论子宫下段宫腔纱布填塞术治疗产后出血疗效显著。     

慢性多发性肌炎临床及病理分析

目的探讨慢性多发性肌炎的发病机制、临床和病理特征。方法回顾性分析95例慢性多发性肌炎患者临床表现、肌酶学和肌电图检查结果,总结肌肉病理学特征。结果慢性多发性肌炎以四肢近端肌无力、肌萎缩为主要表现,血清酶谱轻-中度增高,肌电图以肌源性损害为主,病理改变为灶性坏死、炎性细胞浸润与再生肌纤维共存。结论临床特点结合病理学检查有助于慢性多发性肌炎的诊断,多数患者激素治疗有效。     

The upregulation of glial glutamate transporter-1 participates in the induction of brain ischemic tolerance in rats.

Glial glutamate transporter-1 (GLT-1) plays an essential role in removing glutamate from the extracellular space and maintaining the glutamate below neurotoxic level in the brain. To explore whether GLT-1 plays a role in the acquisition of brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIP), the present study was undertaken to observe in vivo changes in the expression of GLT-1 and glial fibrillary acidic protein (GFAP) in the CA1 hippocampus during the induction of BIT, and the effect of dihydrokainate (DHK), an inhibitor of GLT-1, on the acquisition of BIT in rats. Immunohistochemistry for GFAP showed that the processes of astrocytes were prolonged after a CIP 2 days before the lethal ischemic insult, which could protect pyramidal neurons in the CA1 hippocampus against delayed neuronal death induced normally by lethal ischemic insult. The prolonged processes extended into the area between the pyramidal neurons and tightly surrounded them. These changes made the pyramidal layer look like a 'shape grid'. Simultaneously, the prolonged and extended processes showed a great deal of GLT-1. Western blotting analysis showed significant upregulation of GLT-1 expression after the CIP, especially when it was administered 2 days before the subsequent lethal ischemic insult. Neuropathological evaluation by thionin staining showed that DHK dose-dependently blocked the protective role of CIP against delayed neuronal death induced normally by lethal brain ischemia. It might be concluded that the surrounding of pyramidal neurons by astrocytes and upregulation of GLT-1 induced by CIP played an important role in the acquisition of the BIT induced by CIP.     

血清低密度脂蛋白胆固醇直接测定与Friedewald公式计算结果比较

采用聚乙烯硫酸（ＰＶＳ）沉淀法测定血清低密度脂蛋白胆固醇（ＬＤＬ－Ｃ）值，同时应用Ｆｒｉｅｄｅｗａｌｄ公式计算ＬＤＬ－Ｃ含量，并对两法结果进行比较分析，提出当甘油三脂（ＴＧ）＜４．５２ｍｍｏｌ／Ｌ时，Ｆ公式计算法可代替ＰＶＳ法，当ＴＧ＞４．５２ｍｍｏｌ／Ｌ时，不宜用Ｆ公式计算ＬＤＬ－Ｃ的值。     

Kinetics and enzyme involvement in the metabolism of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in microsomes of rat lung and nasal mucosa.

The rat lung and nasal cavity are two target organs for carcinogenesis by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). In order to characterize further the enzymes involved in the bioactivation of NNK, detailed kinetic and inhibitory studies were conducted with rat lung and nasal mucosa microsomes, and the results were compared with previous studies. The enzymes in rat lung microsomes catalyzed the alpha-hydroxylation, pyridine N-oxidation and carbonyl reduction of NNK. The apparent Km for the formation of the NNK-derived keto aldehyde, NNK-N-oxide, the NNK-derived keto alcohol and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol were 28.8, 10.4, 7.0 and 178.1 microM respectively. In rat nasal microsomes, alpha-hydroxylation was the predominant pathway and the rate was approximately 200 times higher than that in lung microsomes. The apparent Kms for keto aldehyde and keto alcohol formation in rat nasal microsomes were 9.6 and 10.1 microM respectively. The cytochrome P450 inhibitors metyrapone and carbon monoxide markedly inhibited the metabolism of NNK in both rat lung and nasal microsomes. In rat lung microsomes, alpha-naphthoflavone and monospecific antibodies against P450s 1A2, 2A1 and 2B1 inhibited the formation of keto aldehyde by 39, 46, 64 and 23% respectively. In rat nasal microsomes, alpha-naphthoflavone and antibodies against P450s 1A2, 2A1 and 3A inhibited the metabolism of NNK by 80, 35, 20 and 14% respectively. The results indicate that cytochromes P450 play a major role in the metabolic activation of NNK in rat lung and nasal microsomes, and that there are tissue-related differences in NNK metabolism.     

预移植在胚胎移植中的意义

目的 :评价预移植在胚胎移植中的作用。　方法 :在超声波引导下胚胎移植 114个周期 ,其中 10 1个周期进行预移植。比较预移植与未预移植周期临床妊娠率和胚胎种植率 ;按预移植与实际胚胎放置深度差值分组 ,并比较两组妊娠率和胚胎种植率。　结果 :预移植周期与未预移植周期临床妊娠率和种植率统计学差异无显著性(5 9.4 1%和 6 1.5 4 % ,35 .81%和 31.4 3% ,P均 >0 .0 5 ) ;按预移植与实际胚胎放置深度差值分组后 ,两组妊娠率和种植率统计学差异也无显著性 (6 1.5 4 %和 5 8.6 7% ,4 0 .79%和 34.0 9% ,P均 >0 .0 5 )。　结论 :在胚胎移植技术中 ,预移植不能准确指引胚胎移植深度     

Effects of thiamine deficiency on hepatic cytochromes P450 and drug-metabolizing enzyme activities

To elucidate the mechanisms by which thiamine deficiency affects hepatic microsomal monooxygenase activities, the effect of thiamine deficiency on two constitutive cytochrome P450 isozymes, P450IIE1 and P450IIC11, was investigated, using weanling male Sprague-Dawley rats. The clinical signs of thiamine deficiency were apparent after feeding a thiamine-deficient diet for 3 weeks. Thiamine deficiency caused an increase in P450IIE1, which was determined by N-nitrosodimethylamine demethylase assay and immunoquantitation of P450IIE1. This increase in the P450IIE1 level was mainly attributed to thiamine deficiency per se but not to dietary restriction. Ketone bodies were not elevated in thiamine-deficient rats, whereas ketone bodies were elevated and may have served as inducing factors in calorically restricted pair-fed animals. Injections of pyruvate or pyrithiamine in addition to thiamine deficiency did not potentiate the induction effect. On the other hand, thiamine deficiency did not affect the level of P450IIC11 during the 3 weeks of feeding the thiamine-deficient diet. In addition, thiamine deficiency increased cytosolic glutathione S-transferase activity but not steroid isomerase activity. The present study demonstrates the specificity of thiamine deficiency per se in the induction of P450IIE1 which does not involve an increase in the ketone body level.