氯沙坦心衰生存研究（ELITE Ⅱ）：氯沙坦和卡托普利对心衰相关预后和症状的作用比较氯沙坦心衰生存研究（ELITE Ⅱ）：氯沙坦和卡托普利对心衰相关预后和症状的作用比较

背景：利用血管紧张素转换酶抑制剂阻断肾素-血管紧张素系统可以改善心衰（HF）患者的预后和症状。在ELITEⅡ研究中，比较了氯沙坦和卡托普利对心衰患者死亡率、发病率以及功能状态方面的作用。方法和结果：总共3152例年龄≥60岁、NYHA心功能分级为Ⅱ-Ⅳ级、射血分数≤40％的HF患者入选研究，接受氯沙坦50mg1次／d或卡托普利50mg3次／d。判断预后的指标包括：全因或HF相关的死亡、住院和停止治疗；NYHA分级的变化；生活质量（QoL）。各治疗组问HF相关预后无显著性差异。两组的NYHA分级得到了相似的改善（P〈0．01）。观察1856例患者的QoL发现，1343例患者至少存活1年以上；两组中1年存活者的QoL均得到了改善（与基线相比，P〈0．001）。     

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。     

胸腰段椎间盘突出症诊断的临床研究

目的探讨胸腰段椎间盘突出症临床表现的特点与规律，提高胸腰段椎间盘突出症的诊断水平。方法回顾性分析1995年9月～2004年1月我院经X线、CT、MRI及手术证实的胸腰段椎间盘突出症65例的临床资料，并将其分为低位胸椎组（T10-T12L1）43例，高位腰椎组（L1-2-L2-3）16例，多节段突出组6例。结果躯体感觉障碍89．2％（58／65）和下肢无力83．1％（54／65）是最多见的症状。9．2％（6／65）表现为上运动神经元损害，47．7％（31／65）表现为下运动神经元损害，43．1％（28／65）表现为上、下运动神经元混合性损害。仅3例为单根神经根损害，其余表现为多根神经或马尾神经的损害。腰背痛44．6％（29／65）和下肢无力40．0％（26／65）是最常见的首发症状。低位胸椎间盘突出以混合性运动神经元损害为主，占58．1％（25／43），易导致行走障碍、足下垂、下肢肌张力升高和病理征阳性；而高位腰椎间盘突出则以下运动神经元损害为主，占93．8％（15／16），易造成腰背、下肢疼痛及马尾神经损害。结论胸腰段椎间盘突出症的症状广泛、体征多样，当临床上存在以下情况时应高度怀疑胸腰段椎间盘突出症：①大腿前方、外侧或腹股沟部位出现感觉障碍者；②下肢无力，股四头肌，胫前肌肌力减退者（如足下垂）；③下肢运动或感觉障碍范围广泛、不规则，缺乏根性分布特征者；④上、下运动神经元损害同时存在，或虽表现为下运动神经元损害，但难以用低位腰椎间盘突出症解释者。     

脾原发性淋巴瘤超微结构观察与流式细胞分析

目的 探讨诊断电镜（DEM）对脾原发性淋巴瘤的病理分型的超微结构特征。流式细胞术（FCM）测定瘤细胞DNA倍性与恶性程度的关系。方法 应用透射电镜和流式细胞术观察分析41例脾原发性淋巴瘤的超微结构和瘤细胞DNA倍性。结果41例脾原发性淋巴瘤中霍奇金淋巴瘤5例,电镜下R-S细胞呈双叶不规则核和对称致密大核仁,核内常染色质明显,胞质内见中等量线粒体,较长的粗面内质网。非霍奇金B细胞性淋巴瘤21例,裂细胞性5例,细胞核大,核伴有较深的裂沟,胞浆少,胞质见少数肿胀线粒体,无核裂细胞性7例,细胞核规则,呈圆或卵圆型,异染色质多呈条块状,核仁中等大,胞质少,见少量线粒体及长粗面内质网。混合细胞性,瘤细胞大小悬殊,大畸形核较多,核扭曲,不规则深沟及不对称分叶,形成多叶核。非霍奇金T免疫母细胞淋巴瘤11例,瘤细胞较大,核小胞质相对多,胞质透明,核多形性,有的呈圆或卵圆形,核膜薄,有深浅不一的凹陷,可见小核仁。淋巴母细胞性5例,淋巴母曲核性淋巴瘤,细胞为中小形,呈锯齿状核和扭曲状核,异染色质沿核膜聚集,核仁小。毛细胞性淋巴瘤1例,毛细胞的绒毛宽基底,核仁大,胞浆无核糖体板层复合物。组织细胞性淋巴瘤3例,细胞浆丰富,核圆或椭圆形,偶见核膜呈锯齿状或折叠,线粒体和溶酶体丰富,无细胞连接和Birbeck颗粒。FCM     

通心络胶囊对冠心病治疗效果的临床对照观察

目的观察通心络胶囊对冠心病（CHD）常见临床症状的改善效果。方法对照组维持原有药物治疗不变,治疗组在此基础上加服通心络胶囊4粒/次,3次/日,疗程4周。病人接受观察前进行常规化验检查,检测心率、血压、心功能等指标。疗程结束时对上述指标再进行检查,并观察病人的临床症状改善情况。结果两组病人的胸痛、胸闷、气憋、心悸、乏力等常见临床症状均有改善,且治疗组明显优于对照组（P〈0.05）;治疗组每搏量和心排血量的较对照组提高较为明显（P〈0.01）。结论加服通心络胶囊治疗CHD能增强西药的治疗效果,进一步改善CHD病人的常见临床症状。     

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.