安体维康诱导肝细胞凋亡实验研究及临床观察

目的 :评价中药制剂安体维康 ( Antivirus Compound,ATVC)诱导人肝癌细胞凋亡的作用及临床疗效。方法 :采用 MTT(细胞毒 )实验培养人肝癌细胞株 BEL - 740 2细胞 ,加入不同浓度安体维康药液进行培养与对照组进行比较。临床给原发性肝癌 1 0例服用安体维康胶囊 3个月。结果 :安体维康能抑制人肝癌细胞株 BEL- 740 2细胞生长 ,有诱导肝细胞凋亡的作用。其作用强弱在一定程度上存在剂量和时间效应。服用安体维康的肝癌患者临床症状明显改善。结论 :安体维康可诱导人肝癌细胞调亡 ,对原发性肝癌有一定临床疗效     

老年人视网膜中央血管在前部视神经的解剖特征

目的：观察老年人前部视神经视网膜中央血管的解剖特征。 方法：通过组织连续切片和计算机影像分析，观察60~82岁老年人的18只眼球标本中无解剖变异的视网膜中央动脉(CRA)15条，视网膜中央静脉（CRV）23条在筛板前、筛板区及筛板后的管径变化。 结果：老年人筛板前、筛板区、筛板后CRA平均面积的均值分别为（12.70,17.40,18.00）×10^-3mm^2_;平均周长的均值分别为0.56，0.56，0.57mm，平均周长之间相比无显著差异。CRV平均面积的均值分别为（7.00，5.40，7.90）×10^-3mm²；平均周长的均值分别为0.44，0.38，0.41mm；CRV平均周长筛板前与筛板区相比，筛板区与筛板后相比均有显著差异。 结论：老年人CRA眼球内外管径一致；CRV在筛板区管径最小。 （中华眼底病杂志，1997，13：213-214）
     

SOD-like Activity of Copper Salicylate Complex in Tween Micel-lar Systems

合成了水杨酸铜络合物并分析了其组成，提纯了Ｔｗｅｅｎ－２０，－４０，－６０，－８０，并测定了它们在ｐＨ７．４的磷酸缓冲液中的ＣＭＣ。用Ｃｙｔ．ｃ还原法分别测定了水杨酸铜络合物在不同介质中的ＳＯＤ样活性。详细研究了表面活性剂与水杨酸铜络合物协同清除Ｏ－２的作用。观察到在胶束体系中水杨酸铜络合物的ＳＯＤ样活性明显高于缓冲液体系无表面活性剂时的ＳＯＤ样活性，表面活性剂本身也具有清除Ｏ－２的功能。抗红细胞膜脂质过氧化实验也得到类似结果。这可用胶束催化解释。水杨酸铜－Ｔｗｅｅｎ体系可能是一种潜在的抗炎药物。     

膀胱移行细胞癌中P16及Rb基因表达的关系

应用免疫组织化学方法对５９例膀胱移行细胞癌中Ｐ１６及Ｒｂ基因的表达进行研究。结果显示：５９例中Ｐ１６及Ｒｂ基因阳性表达率分别为４７４６％、７１１９％，其中１１例肿瘤组织（１８６４％）Ｐ１６及Ｒｂ基因均阳性表达，未发现同一肿瘤组织中同时存在Ｐ１６及Ｒｂ基因的表达缺失。Ｐ１６及Ｒｂ基因在膀胱移行细胞癌中的阳性表达率在肿瘤病理分级及临床分期的差异中均有显著性（Ｐ＜００５）。结果提示：Ｐ１６及Ｒｂ基因的异常表达在膀胱肿瘤的发生、发展过程中起重要作用，膀胱肿瘤中Ｐ１６及Ｒｂ基因同时表达缺失是少见现象     

TGF—β1对膀胱移行细胞癌细胞粘附性的调节

为了解ＴＧＦβ１对肿瘤粘附性的调节，采用Ｎｏｒｔｈｅｒｎ杂交分析测定了两个膀胱癌细胞系ＴＧＦβ１及ＦＮｍＲＮＡ的表达，并用体外测定方法检测了ＴＧＦβ１对两细胞系粘附性质的调节。结果表明：ＴＧＦβ１仅可使低表达ＦＮ的２５３Ｊ细胞的粘附性增强，而这种增强与ＦＮ表达的增加成正比；同样浓度的ＴＧＦβ１对高表达ＦＮ的６４７Ｖ细胞的粘附性无明显影响。提示肿瘤细胞粘附能力的可变性是其具有转移能力的原因之一。     

前列腺带性结构及其雄激素、雌激素、表皮生长因子受体分布特征的研究

为了探讨雄激素受体（ＡＲ）、雌激素受体（ＥＲ）、孕激素受体（ＰＲ）和表皮生长因子受体（ＥＧＦＲ）在前列腺带性结构中的分布，应用单饱和剂量测定法，分别测定了前列腺移行带、外周带组织中ＡＲ、ＥＲ、ＰＲ和ＥＧＦＲ的含量。结果表明，在１１例前列腺增生症（ＢＰＨ）患者２２份标本中，移行带和周围带ＡＲ全部阳性；尽管ＡＲ浓度个体差异很大，但是两带之间仍有密切相关性（Ｐ＜０００１）；周围带ＡＲ浓度高于移行带，两带ＡＲ浓度均高于ＰＲ、ＥＲ；ＰＲ和ＥＲ在前列腺带性结构上没有明显差异。ＥＧＦＲ在移行带明显高于周围带。研究证实了ＡＲ、ＥＲ、ＰＲ，ＥＧＦＲ在前列腺移行带和周围带上的分布特征。     

人卵巢癌中肿瘤转移抑制基因nm23-H1编码蛋白的表达

目的：探讨人卵巢癌标本中，肿瘤转移抑制基因ｎｍ２３－Ｈ１编码蛋白ＮＤＰＫ－Ａ表达的临床意义及其与预后的关系。方法：应用免疫组织化学抗生蛋白链菌素－过氧化酶结合（Ｓ－Ｐ）法，检测５８例人卵巢癌标本中ｎｍ２３－Ｈ１蛋白水平。结果：ｎｍ２３－Ｈ１蛋白的表达与患者手术时是否有淋巴结及大网膜转移相关（Ｐ〈０．０５），但原发灶与转移灶间的阳性表达率相差不显著；与患者术后生存时间密切相关（Ｐ〈０．０１），术后生     

A novel cognition enhancer NS-105 modulates adenylate cyclase activity through metabotropic glutamate receptors in primary neuronal culture

The effect of (+)-5-oxo-D-prolinepiperidinamide monohydrate (NS-105), a novel cognition enhancer, on adenylate cyclase activity was investigated in cultured neurons of the mouse cerebral cortex. NS-105 (10^–7 and 10^–6 M) inhibited forskolin-stimulated cyclic AMP formation, an action that was dependent on pertussis toxin-sensitive G proteins. Conversely, in pertussis toxin-pretreated neurons, NS-105 (10^–7 –10^–5 M) significantly enhanced the forskolin-stimulated cyclic AMP formation, and this action was completely reversed by cholera toxin. A metabotropic glutamate receptor agonist (1S, 3R)-1-aminocyclopentane-1, 3-dicarboxylic acid (1S, 3R-ACPD) produced similar bi-directional actions on the cyclic AMP formation. Both of these inhibitory and facilitatory actions of NS-105 and 1S, 3R-ACPD were blocked by L(+)-2-amino-3-phosphopropinoic acid (L-AP3). NS-105 (10^–6 M) and 1S, 3R-ACPD (10^–4 M) significantly enhanced isoproterenol- and adenosine-stimulated cyclic AMP formation. The enhancement of such Gs-coupled receptor agonists-stimulated cyclic AMP formation was also produced by quisqualate but not by L(+)-2-amino-4-phosphonobutanoate (L-AP4). The phosphoinositides hydrolysis was enhanced by 1S, 3R-ACPD (10^–4 M) but not by NS-105 (10^–6 M), however, 1S, 3R-ACPD-induced increase in phosphoinositides turnover was attenuated by NS-105. These findings suggest that NS-105 stimulates metabotropic glutamate receptor subclasses that are coupled both negatively and positively to adenylate cyclase, but it acts as an antagonist at the receptor subclasses that are linked to phosphoinositides hydrolysis. Received: 3 February 1997 / Accepted: 25 April 1997     

Hereditary characteristics of enzyme deficiency and dermatoglyphics in congenital color blindness

The hereditary characteristics of enzyme deficiency and dermatoglyphics in congenital color blindness (CCB) were studied. We propose that there is a linkage between the two loci on the X-chromosome determining CCB and glucose-6-phosphate dehydrogenase (G6PD), based on our study of a high incidence of G6PD deficiency in 156 male cases with CCB. The CCB gene is closely linked with that of G6PD deficiency from our pedigree investigations. The rise in the frequency of eight or more whorls, the low value of atd angle and the presenting rate of real palmar patterns of the thenar, hypothenar and I, areas presented the hereditary traits of congenital color blindness.