心脏传导的变异性裂隙现象

在连续３６１例患者心内电生理检查中，发现４例有心脏传导的裂隙现象。其特点表现为激动传导方向上远端平面相对不应期（ＲＲＰ）长，程序刺激中先出现传导延缓，随后近端平面也进入ＲＲＰ使传导变为延缓，激动经过近端平面延缓传导后，到达远端平面时其已脱离了ＲＲＰ，使已经在远端传导延缓的情况变为传导正常，与经典的裂隙现象相比，这种裂隙现象的发生机制，与心内电图的表现均有不同，暂定名为变异性裂隙现象。     

指末端毛细血管血检测CMV抗体的研究

本文用ELISA方法对110名住院病儿指末端毛细血管血和静脉血配对血标本中巨细胞病毒(CMV)抗体进行了对照研究。配对血标本检测CMV IgM、IgG抗体的一致性分别为99.09％和96.36％;敏感性分别为87.5％和95.58％;特异性分别为100％和98.48％。反复多次重复检测配对血标本中CMV抗体,结果均呈正相关。本结果表明:指末端毛细血管血可代替静脉血检测儿科病血中CMV抗体.这对儿科CMV感染病儿进行动态血清学监测具有重要意义。     

地膜覆盖条件下红花生长发育规律及其与产量关系的研究

对地膜覆盖条件下红花生长发育规律及其与产量的关系进行了研究。结果表明,地膜红花与露地红花生长发育规律基本一致,但地膜红花生育进程明显提前,各个阶段的生长量明显增多,花的产量及籽粒产量极显著提高。     

不同繁殖材料对半夏产量的影响

实验表明:半夏有性繁殖种子田间出苗率为0～25%,且实生苗当年不能形成商品;无性繁殖则以珠芽和小块茎作种明显优于大块茎。     

显微内窥镜下治疗腰椎间盘突出症和腰椎管狭窄症

目的探讨显微内窥镜(MED)治疗腰椎间盘突出症和腰椎管狭窄症的临床效果。方法MED下切除增生内聚的关节突、肥厚的黄韧带及突出的椎间盘，彻底解除对硬膜、神经根的压迫。结果随访324例，按中华骨科学脊柱学组腰背痛手术评定标准，优297例，良14例，差13例，疗效优良率达96．0％，结论MED损伤小、恢复快、疗效好。     

~3H-α-第二丁基对羟基苄醇在家兔体内的药物动力学研究

本文报道给家兔注入不同剂量的~3H-α-第二丁基对羟基苄醇,观察该药在其体内的药物动力学。结果表明,血中分布相快,消除相慢,消除半衰期T_1/1β为12h。经F值检验和理论计算值与实测值的契合程度比较,表明该药在兔体内的运转符合二室开放模型的动力学方程。     

54例严重缓慢心律失常病人的起搏器治疗

1978年～1987年用永久起搏器治疗54例严重缓慢心律失常的病人,共进行103次手术。随访8年多,发现7例死亡,其中6例死亡原因与起搏器治疗无关,1例死于与起搏器并发感染密切相关。本文就严重缓慢心律失常的类型、病因、安装永久起搏器的指征、手术并发症等加以讨论。     

Effects of cerulenin on the endogenous fatty acid synthetic activity in squamous cell carcinoma of the oral cavity.

PURPOSES: Inhibition of cerulenin on the endogenous fatty acid synthetic activities of oral squamous cell carcinoma (OSCC) and normal oral mucosa was assayed. METHODS: Squamous cell carcinoma and normal oral mucosa were collected fresh from surgical specimens. The collected tissues were minced in RPMI 1640 and divided into 3 groups: cerulenin treated, dimethylsulfoxide treated, and control. The tissues were incubated in [1(2)-(14)C]acetic acid, sodium salt for the last 2.5 hours of the treatment at 37 degrees C in 5% CO(2). After labeling, total lipids were extracted and counted for (14)C by scintillation counting. RESULTS: Endogenous fatty acid synthetic activities of oral squamous cell caranoma in the cerulenin-treated group decreased by 19% at 1 hour, 64% at 2 hours, and 87% at 4 hours; remained nearly unchanged in the dimethylsulfoxide-treated group; and increased slightly in the control group. The oral mucosa tissues were only mildly affected by cerulenin in fatty acid synthesis. CONCLUSIONS: Cerulenin significantly inhibits fatty acid synthetic activity in squamous cell carcinoma and only mildly affected the oral mucosa, indicating that the fatty acid synthetic pathway may be exploited as a target for developing anticancer drugs.     

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.