Release of cholecystokinin from rat cerebral cortex in vivo: role of GABA and glutamate receptor systems

Using cortical cups in chloralose-urethanized rats, the in vivo release of cholecystokinin-like immunoreactivity (CCK-LI) from cerebral cortex was examined. Resting levels of cholecystokinin-like immunoreactivity ranged from 20 to 30 pg/20 min sample. The addition of potassium (40 mM) in excess, resulted in a highly significant elevation in the levels of CCK-LI in the cortical superfusate. Deletion of calcium and the substitution of cobalt (10 mM), resulted in a significant reduction in both resting release and the release otherwise evoked by the addition of potassium. Focal electrical stimulation of the cortex (20 Hz), resulted in a significant (1.9 +/- 0.2-fold, n = 8) increase in the levels of CCK-LI. The addition of glutamate (10(-6)-10(-4) M) of kainic acid (10(-8)-10(-6) M), also resulted in significant elevations in the levels of CCK-LI. The co-administration of a putative glutamate receptor antagonist, kynurenic acid (10(-4) M) resulted in a significant reduction in the levels of release otherwise evoked by the addition of glutamate, but not by electrical stimulation. The addition of GABA (10(-5)-10(-3) M) resulted in a dose-dependent decrease in the resting release of CCK-LI, and the release evoked by glutamate. Picrotoxin (10(-6)-10(-4) M), resulted in a highly significant increase in the levels of CCK-LI in the cortical effluent. These results are consistent with a tonic GABAergic inhibition of CCK-releasing neurons. The treatment of the animal with diazepam (30 mg/kg, i.p.) also resulted in a significant reduction in resting release and the release otherwise evoked by focal cortical stimulation.     

HBsAg母婴传播的研究

对HBsAg(+)母亲所生婴幼儿,连续两年的动态观察,发现这些婴幼儿的感染绝大多数皆在出生3个月后,其感染频率与母亲HBsAg的滴度成正相关,表明母婴传播阻断应以HBsAg(+)母亲所生之子女为重点对象。     

人血清胰岛素抗体、猪胰岛素原抗体和胰多肽抗体的放射免疫检测法

作者用自制的[~(125)I]标记激素,参考国外经验,建立了人血清胰岛素抗体、猪胰岛素原抗体和胰多肽抗体等三种放射免疫检测法,并对方法的主要实验条件进行了优选,对方法的质量控制参数作了验证。结果发现:在使用国产胰岛素的糖尿病人血清中,三种抗体的检出率分别为90.8％、48.3％和36.5％;抗体特异性结合值分别为21.2±17.4％、41.8±27.4％和25.6±28.4;而正常人和糖尿病人未用胰岛素者全部为阴性,显示国产胰岛素具有明显的免疫原性。     

同种原位肝移植围手术期的处理

目的 总结我院自1999年8月以来,开展的3例同种异体原位肝移植（Orthotopic livertransplantation,OLT）围手术期的处理过程及经验体会。方法　2例原位肝移植、1例肝-肾联合移植术。均在术前12h口服环孢霉素A（CsA）和骁悉（MAP）,术中用甲基强的松龙（MP）1000 mg静脉冲击防止排斥,术后MP+CsA+MAP三联用药。结果 ①文中3例病人手术均获成功,其中2例原位肝移植病人存活至今,生活质量良好。肝肾联合移植病人于术后第76d死于严重混合感染。②移植肝的功能维护是肝移植术后处理的重点,其中包括急性排斥反应的诊断和处理,以及其它可能引起肝移植肝功能损害、衰竭等问题的处理。③全身非移植器官的功能恢复:包括呼吸系统、感染、出血、胸水、腹水等并发症的处理过程。结论 肝移植围手术期的处理是肝移植成功与否的关键,其中包括肝移植的排斥反应及各系统的功能支持与维护。     

大肠肿瘤组织中EB病毒的原位杂交检测

目的：探讨EB病毒感染与人大肠癌发生的关系。方法：用原位分子杂交法对130例人大肠癌标本中EB病毒小分子RNA片段进行检测。结果：130例标本中有6例（4.48％）癌组织呈阳性反应，其中4例为男性，4例有明显淋巴细胞浸润。结论：EB病毒感染可能与我国部分大肠腺癌的发生有关，肿瘤细胞间质中大量淋巴细胞浸润可能是EB病毒感染的重要病理学特征。     

蛇床子水提取液抑瘤作用的实验研究

目的 :研究蛇床子水提取液的体内抗肿瘤作用。方法 :通过 S180 肉瘤移植建立荷瘤小鼠模型 ,给予不同剂量蛇床子水提取液后观察 S180 荷瘤小鼠肿瘤生长曲线、血清唾液酸 (SA)、瘤重及小鼠生存天数的变化。结果 :蛇床子水提取液能明显抑制肿瘤生长 ,降低荷瘤小鼠血清 SA水平 ,0 .0 6mg/(g· d) ,0 .1 1 mg/(g· d)、0 .2 1 mg/(g· d)剂量组平均瘤重低于肿瘤对照组 (P<0 .0 5 ) ,抑瘤率依次为 2 3 .2 %、2 9.1 %和 2 4 .8%,且能延长荷瘤小鼠生存天数 (P<0 .0 1 ) ,动物生命延长率依次为 :2 6 .9%、3 4 .8%和 2 6 .6 %。结论 :蛇床子水提取液具有较强的抗肿瘤效应 ,有很好的利用前景 ,值得对其进行深入研究。     

Comparative study of long-term effects of surgical excision and excision combined with radiotherapy or chemotherapy in breast cancer: an analysis of 192 cases

Clinical data of 192 patients with breast cancer with a primary lesion of 2-5 cm (stage II according to the criteria recommended by the UICC) and with histopathologically confirmed positive axillary lymph nodes were analyzed. The patients were divided into three groups: 1) surgical excision alone; 2) surgery plus irradiation; and 3) surgery plus chemotherapy. It was shown that the 5-year survival rates for these groups were 40.5%, 61.0%, and 62.0%, respectively (P less than .05).     

创伤后肝细胞凋亡与坏死的检测及其意义

目的 探讨严重创伤后肝细胞凋亡及坏死在急性肝功能障碍发病机制中的作用。方法复制多发性骨折合并休克的大鼠创伤模型,采用 Annexin－V－Flous、碘化丙锭(propidium iodid,PI)双标法经流式细胞仪检测创伤后各时间点肝细胞凋亡与坏死的数量变化,结合光镜、电镜和电泳观察细胞凋亡与坏死,并与肝功能变化相比较。结果创伤后早期肝细胞即发生凋亡和坏死,坏死肝细胞的数量进行性升高,与肝功能变化显著呈正相关;凋亡肝细胞在创伤后3h达高峰,部分凋亡肝细胞发生继发性坏死,其数量与肝功能变化显著正相关。结论肝细胞坏死与凋亡是严重创伤后肝功能损害的重要原因,坏死肝细胞是肝功能损害的直接因素,凋亡肝细胞通过发生继发性坏死加重肝功能损害。