窥镜下激光治疗前列腺增生症

目的 评价经尿道激光前列腺切除术（ＴＵＬＰ）的疗效及其与前列腺大小的关系。方法 回顾分析了１９８８年至１９９８年１０年,采用ＴＵＬＰ治疗的４６９例前列腺增生症患者对手术技术、手术前后的症关改善情况进行比较,并对２３３例符合条件的患者ＴＵＬＰ手术效果与前列腺大小的相关性进行了研究。结果 ４６９例患者前列腺症状评分（ＩＰＳＳ）平均值由术前的２６．７降到术后的１４．２;最大尿流率平均值由６．２ｍｌ／ｓ上     

B型超声检查对渗出型老年性黄斑变性的诊断价值

目的:探讨渗出型老年性黄斑变性(Age-related macular degeneration,AMD)的B型超声影象特征。方法:采用NIDEKUS-3300型超声诊断仪,对31例(54只眼)渗出型AMD进行了观察。结果:视网膜色素上皮脱离时,眼内后极部出现膜状弧形回声,光带与眼球壁之间,可见一个梭形透声区;渗出或出血未完全吸收阶段,呈混合性回声;渗出或出血逐渐吸收并为瘢痕组织所替代时,可见实体性小隆起物,强回声,形状似凸透镜或三角形,凸起端指向球后,玻璃体腔面平坦。结论:B型超声在渗出型AMD的诊断、治疗随访观察中具有实用价值。眼科学报1999;15:233-235。     

Establishment and characterization of a cytotrophoblast cell line from normal placenta of human origin

A cell line has been established from human placentae at thefirst trimester of normal pregnancy. The cell line was obtainedby culture of purified cytotrophoblast cells in serum-free mediumsupplemented with epidermal growth factor, insulin, dexamethasoneand 0.1% bovine serum albumin. The cells can be subculturedfor >30 passages in one to three splits. All the cells weremononuclear epithelial-like cells positive to cytokeratin 18,gonadotrophin-releasing . hormone (GnRH), neuropeptide Y, neurotensin,leucine-enkephalin, dopamine and 5-hydroxytryptamine inununo-cytochemicalstaining. The cells secreted GnRH, progesterone and oestradiol(in the presence of testosterone) but little human chorionicgonadotrophin and no -endorphin. The cell line showed humankaryotypes and had a population doubling time of 48 h in serum-freemedium. However, the cells would stop growing in the mediumcontaining fetal bovine serum. A normal cytotrophoblast cellline established in serum-free medium will be particularly usefulin the study of cytotrophoblast cell proliferation and differentiation.     

活血益气药不同剂量配伍对心梗后心衰大鼠心脏系数及功能的影响

目的 :观察相同种类活血益气药的不同剂量配伍对心梗后心衰大鼠心脏系数、功能的影响。方法 :采用左冠脉结扎术致心梗后心衰大鼠模型 ,分别用活血益气方 (全方活血药量占全方 75% )、益气活血方 (活血药量占全方25% )、气血方 (活血药量占全方 50%)于术后 4周给药至 8周 ,每日灌胃 ,以卡托普利作为阳性药。用阻抗法观察给药前后大鼠心脏功能、心脏系数的变化。结果 :心梗后心衰大鼠经 4周给药治疗后 ,心功能每搏输出量 (SV)、心输出量 (CO)、心脏指数 (CI)值都明显升高 (P<0.01) ;同时 ,活血益气方 (活血药量占全方 75 % )、气血方 (活血药量占全方50% )对模型动物治疗后心脏系数改善与假手术组相似 (P>0.05) ,而益气活血方 (活血药量占全方 25% )、卡托普利与假手术组比较 ,对其无改善 (P<0.01)。结论 :活血益气药通过改善心梗后心衰模型大鼠心脏系数及功能 ,达到治疗心衰作用 ;同时 ,方剂配伍中多量活血药的应用 (活血药 /益气药为 75%和 50%)可以较明显改善心衰大鼠的组织学指标心脏系数。     

三七总皂苷抗缺氧缺糖再给氧诱导大鼠海马神经细胞凋亡的研究

目的 :以原代培养的大鼠海马神经细胞缺氧 /缺糖再给氧为模型 ,观察三七总皂苷对神经细胞凋亡的抑制作用。方法 :流式细胞仪检测凋亡细胞百分率 ,激光共聚焦扫描显微镜检测细胞内Ca²⁺浓度 ,荧光显微镜观察细胞形态学变化和坏死细胞百分率 ,同时 ,测定细胞乳酸脱氢酶 (LDH)的释放。结果 :神经细胞缺氧 /缺糖 5h后再给氧可诱导神经细胞凋亡和细胞坏死 ,并显著增加细胞内Ca²⁺浓度和LDH的释放 ,并随再给氧时间的延长而增加。三七总皂苷能降低神经细胞凋亡及坏死的百分率 ,降低细胞内Ca²⁺浓度 ,减少LDH的释放 ,三七总皂苷的作用随剂量增加而作用增强。结论 :三七总皂苷对缺血再灌注损伤后海马神经元的凋亡过程具有抑制作用 ,这种作用可能与其能降低细胞内Ca²⁺浓度有关。     

重组人生长激素治疗15例原发性扩张型心肌病的初步观察

目的　观察重组人生长激素 (rh GH)对扩张型心肌病 (DCM)患者左心室形态及功能的影响、疗效及安全性。方法　 2 8例 DCM心力衰竭患者随机分为 rh GH治疗组 (1 5例 )和对照组 (1 3例 )。两组病例均接受常规抗心衰治疗 (ACEI、利尿剂、地高辛 ) ,rh GH治疗组在常规抗心衰治疗的基础上肌肉注射 rh GH8.0 IU,每周 2～3次 ,共 3个月 ,治疗前后记录观测指标。以二维超声心动图、 X线胸片及心功能变化评价左心室形态及功能的改变。结果　 rh GH治疗组 3个月后左心室舒张末期内径 (L VED)由治疗前 (70 .0 4± 2 .2 1 ) mm缩小至治疗后 (6 0 .2 0±2 .32 ) mm ,P<0 .0 1 ;心胸比率由治疗前 0 .6 6± 0 .0 6缩小至治疗后 0 .5 5± 0 .0 5 ,P<0 .0 1 ;左心室射血分数(L VEF)由治疗前 (31 .30± 2 .89) %提高到治疗后 (4 3.32± 4 .78) % ,P<0 .0 1。结论　初步临床观察表明 ,基因重组分泌型人生长激素对 DCM心力衰竭患者左心室形态及心功能改善具有一定的作用 ,近期治疗中未发现明显不良作用     

南昌链霉菌生物合成梅岭霉素种子制备优化

以参数相关理论为指导,优化南昌链霉菌生物合成梅岭霉素种子制备工艺。结果表明,培养20～35h后,pH7.30～7.50,总糖<0.35%,pmv>10%,溶磷<100μg/ml,菌丝分化启动有利于提高梅岭霉素的发酵效价。     

氨茶碱血药浓度与平喘疗效的关系评估

目的　观察氨茶碱治疗支气管哮喘的临床疗效与有效血药浓度之间的关系 ,指导临床合理用药。方法　给予患儿氨茶碱负荷量 3～ 4 m g/ kg静脉滴注 ,于 2 0～ 30 min内完成 ,维持量 0 .8～ 1.0 m g· kg- 1 · h- 1 。治疗后第 2天测定氨茶碱血药浓度并进行疗效判断。结果　治疗后氨茶碱平均血药浓度为 (8.80± 3.84 ) mg/ L,临床总显效率为 82 .8%。根据血药浓度将其分为 A组 (≤ 5 mg/ L )、B组 (5～ 10 mg/ L )和 C组 (10～ 2 0 m g/ L )三组。 A组和 B组、A组和 C组的临床疗效差异有非常显著性 (P<0 .0 1) ,B组和 C组的临床疗效差异无显著性 (P>0 .0 5 )。结论　氨茶碱血药浓度在 5～ 2 0 m g/ L ,能确保临床疗效并防止药物副反应的发生。     

Cloning and characterization of a blood coagulation factor IX-binding protein from the venom of Trimeresurus stejnegeri.

A blood coagulation factor IX-binding protein (TSV-FIX-BP) was isolated from the snake venom of Trimeresurus stejnegeri. On SDS-polyacrylamide gel electrophoresis, TSV-FIX-BP showed a single band with an apparent molecular weight of 23,000 under non-reducing conditions, and two distinct bands with apparent molecular weights of 14,800 and 14,000 under reducing conditions. cDNA clones containing the coding sequences of TSV-FIX-BP were isolated and sequenced to determine the structure of the precursors of TSV-FIX-BP subunits. The deduced amino acid sequences of two subunits of TSV-FIX-BP were confirmed by N-terminal protein sequencing and trypsin-digested peptide mass fingerprinting. TSV-FIX-BP was a non-enzymatic C-type lectin-like anti-coagulant. The anti-coagulant activity of TSV-FIX-BP was mainly caused by its dose dependent interaction with blood coagulation factor IX but not with blood coagulation factor X.     

Inhibition of Amiodarone‐Induced Lung Fibrosis but not Alveolitis by Angiotensin System Antagonists

Abstract: Earlier work in this laboratory showed that amiodarone induces apoptosis in alveolar epithelial cells by a mechanism inhibitable by angiotensin system antagonists. A variety of recent studies suggests a critical role for alveolar epithelial cell apoptosis in the pathogenesis of lung fibrosis. On this basis we hypothesized that amiodarone‐induced alveolar epithelial cell apoptosis and lung fibrosis in vivo might be inhibitable by the angiotensin converting enzyme inhibitor captopril or the angiotensin receptor antagonist losartan. Amiodarone‐induced lung fibrosis was induced in male Wistar rats by oral adminstration over six months. Replicate groups of rats received captopril or losartan in addition to amiodarone. Apoptosis was detected by increased total lung activity of caspase 3 and in situ end labeling (ISEL) of fragmented DNA. Collagen was localized and quantitated by the picrosirius red technique. Alveolar epithelial cell apoptosis was detected in amiodarone‐treated animals as early as three weeks after the start of amiodarone administration; by six months exposure, the incidence of alveolar epithelial cell apoptosis was significantly reduced by coadministration of captopril or losartan. Alveolar wall collagen accumulation also was significantly attenuated by captopril (100%) or losartan (74%), but neither agent blunted the accumulation of alveolar macrophages evoked by amiodarone (5.3‐fold at 6 months). Lung neutrophil content was unchanged by amiodarone treatment for three weeks or six months. These results indicate that amiodarone induces alveolar epithelial cell apoptosis in vivo that is inhibitable by angiotensin antagonists. They also support the hypothesis that blockade of angiotensin formation or function attenuates amiodarone‐induced lung fibrosis irrespective of the severity of alveolitis.