室内空气污染与女性肺癌

为探讨室内空气燃料污染,被动吸烟,烹饪与女性肺癌的关系。搜索经省级医院确诊的哈尔滨市女性原发性肺癌１１５例及对照１２４例进行调查及单因素Ｌｏｇｉｓｔｉｃ回归分析。结果表明冬天取暖和做饭室内有烟,被动吸烟年限均与女性肺癌有关系显著,女性患肺癌危险性与终动吸烟总量呈明显的剂量－效应关系。     

老年性白内障晶状体上皮细胞凋亡的DNA片段分析及TUNEL检测

目的 探讨老年性白内障晶状体上皮细胞凋亡的生化特征。方法 用ＤＮＡ片段分析及ＴＵＮＥＬ法共检测３１例老年性白内障患者晶状体上皮细胞凋亡。结果 ＤＮＡ片段分析显示,老年性白内障患者晶状体上皮细胞有ＤＮＡ“梯状”图谱,而健康成年人晶状体上皮细胞未见ＤＮＡ断裂现象;ＴＵＮＥＬ检测发现,老年性白内障患者晶本上皮细胞中有凋亡细胞,而健康成年人晶状体上皮中无明显的凋亡细胞。结论 老年性白内障发生与晶状体上皮细     

鼻内窥镜下经筛窦行眶内壁骨折整复术

探讨应用鼻内窥镜下经筛窦行眶内壁折整复术。方法前鼻孔入路,内窥镜观察下将嵌入筛房的眶脂肪及内直肌还纳回眶内,硅胶板修补充填孔洞。结果１６例患者,平均术后观察８个月,复视消失,眼球内陷矫正,无硅胶排异。结论内窥镜下经筛窦行眶内壁骨折整复术,具有无皮肤瘢痕,手术损伤小,并发症少,且手术安全可靠。     

Mitomycin C-induced apoptosis in cultured human Tenon's capsule fibroblasts

To investigate the mitomycin C-induced apoptotic cell death of fibroblasts, the primarily cultured human Tenon's capsule fibroblasts were exposed to a clinically used dosage of 0.4 mg/ml of mitomycin C for 5 minutes. TUNEL (TdT-mediated dUTP-biotin nick end labeling) assay and electron microscopic studies were performed to determine the extent of mitomycin C-induced apoptosis. A flow cytometric study was performed to quantify the apoptotic cell population over time. The TUNEL stains were positive and electron microscopy showed features of apoptotic cell death in some fibroblasts 3 and 5 days after treatment. Flow cytometric analysis using Annexin V-propidium iodide double staining detected apoptotic cells 3 days after treatment. These apoptotic cell populations increased at 4 days and were sustained for one week. This study revealed that the clinical effects of mitomycin C on fibroblasts may be mediated not only by antiproliferative but also apoptotic cell death to some degree. Therefore, the apoptotic cell death of fibroblasts induced by mitomycin C should be considered to properly understand the mechanism of wound healing after trabeculectomy with adjunctive mitomycin C.     

Early and delayed cardioprotection by heat stress is mediated by calcitonin gene-related peptide

Brief ischaemia or heat stress protects the myocardium against ischaemia-reperfusion injury. Heat stimulus evokes release of sensory nerve transmitters, including calcitonin gene-related peptide (CGRP). Since CGRP has been shown to play an important role in the mediation of ischaemic preconditioning, the present study examined whether early or delayed preconditioning induced by retrograde hyperthermic perfusion in vitro or by whole-body hyperthemia in vivo also involves endogenous CGRP. Isolated rat hearts were perfused in the Langendorff mode and subjected to 30 min global ischaemia and 30 min reperfusion. Heart rate, coronary flow, left ventricular pressure and its first derivatives (±dp/dt) were recorded and the CGRP-like immunoreactivity (CGRP-LI) content and the release of creatine kinase (CK) during reperfusion were measured. Retrograde hyperthermic perfusion (42 °C) for 5 min improved the recovery of cardiac function, decreased the release of CK and elevated the content of CGRP-LI in the coronary effluent. CGRP_8–37 (10^–7 mol/l), a selective CGRP receptor antagonist, abolished the cardioprotection by heat stress. Pretreatment with capsaicin (50 mg/kg s.c.), which specifically depletes sensory nerve transmitter content, abolished both the cardioprotection and the increased release of CGRP-LI. Whole-body hyperthermia (42 °C for 15 min) caused an increase in the plasma concentration of CGRP-LI. Early or delayed protection was shown in the hearts obtained from the animals subjected to whole-body hyperthermia 10 min or 48 h before the experiments. The early or delayed protection by heat stress was also abolished by pretreatment with capsaicin. The present study suggests that, in the rat, the early and delayed cardioprotection induced by heat stress involves endogenous CGRP. Received: 31 December 1998 / Accepted: 6 April 1999     

Application of Electrospray Ionization Mass Spectrometry Combined with Sequential Tandem Mass Spectrometry Techniques for the Profiling of Steroidal Saponin Mixture Extracted from Tribulus terrestris

Using electrospray ionization mass spectrometry combined with sequential tandem mass spectrometry (ESI-MS (n)), the steroidal saponin mixture extracted from TRIBULUS TERRESTRIS was studied. The structures of five known steroidal saponins and two unknown steroidal saponins in the saponin mixture were investigated by sequential tandem mass spectrometry experiments. All of the steroidal saponins displayed similar fragmentation behavior in ESI-MS (n), and the characteristic cross ring cleavage pattern could be used as a fingerprint for the identification of steroidal saponins. The methodology has been established as a powerful tool for the profiling of mixtures, especially of crude plant extracts, and the structural elucidation of compounds.     

采用定点基因缺失突变技术在大肠杆菌中分泌鲑鱼生长激素

目的：为获得与天然鲑鱼生长激素一致的基因工程产物,对已构建的鲑鱼生长激素基因分泌型表达质粒ｐＯｓＧＨ１５３进行改造,删除所编码表达产物氨基端多余的９个碱基,方法：采用ＰＡＬＴＥＲ系统进行寡聚核苷酸指导下的基因定点缺失突变。突变质粒ｐＯｓＧＨ１５８经限制性酶切图谱及Ｓｏｕｔｈｅｒｎ印迹杂交分析加以证,结果：含有表达质粒ｐＯｓＧＨ１５８的大肠杆菌株经ＩＰＴＧ诱导后提取周质帽白,经ＳＤＳ－ＰＡＧＥ及免疫     

梗死前心绞痛发作对急性心肌梗死近期预后的影响

目的：评价急性心肌梗死发病前４８小时内的心绞痛发作对急性心肌梗死近期预后的影响。方法：将８７１例急性心肌梗死前４８小时内有心绞痛组３７８例,梗死前无心绞痛４９３例,对两组住院期间的并发症和病死率进行比较分析,结果：发生心绞痛组的心肌梗死范围较小,住院期间病率、心力衰竭、心源性休克、室速的发生率均低于梗死前无心绞痛组。末溶栓组和溶栓未再通组,梗死前有心绞痛发作者的近期预后较无心绞痛者好,而两组溶栓冠     

Delayed protection against ischaemia-induced ventricular arrhythmias and infarct size limitation by the prior administration of Escherichia coli endotoxin.

1. Bacterial endotoxin (lipopolysaccharide derived from Escherichia coli) was injected intraperitoneally in conscious rats in doses ranging from 0.5 to 2.5 mg kg-1. At various times afterwards the animals were anaesthetized and subjected to a 30 min period of left coronary artery occlusion. 2. Under these conditions the severity of ventricular arrhythmias was markedly suppressed, in comparison with saline-injected controls, but this was particularly marked with the higher doses (1.5 and 2.5 mg kg-1); the number of ventricular premature beats was reduced from 1687 +/- 227 over the 0.5 h coronary artery occlusion period to 190 +/- 46 in those rats administered 2.5 mg kg-1 endotoxin 8 h previously (P < 0.05). The duration of ventricular tachycardia was also significantly reduced (138 +/- 26 s to 8.9 +/- 4.2 s; P < 0.01) and there was a reduction in the incidence of ventricular fibrillation (from 56% to 10%). 3. The time course of this protection was studied following the administration of a single dose of 2.5 mg kg-1 of endotoxin by anaesthetizing rats 4, 8 or 24 h later. Protection was apparent at each time but was particularly marked at 8 h. 4. No rat given the highest dose of endotoxin (32 in all) died as a result of ventricular fibrillation, or from any other cause, during an occlusion, in contrast to a 26% mortality in the controls (P < 0.01). 5. Infarct size, measured following a 30 min period of coronary artery occlusion followed by a 3 h reperfusion period, was reduced both 8 and 24 h after the administration of 2.5 mg kg-1 endotoxin (reductions of 24.3 and 23.1% respectively; P < 0.05). Endotoxin had no significant effect on the area at risk. 6. The beneficial effects of endotoxin on infarct size and on ventricular arrhythmias were markedly attenuated by the prior administration of dexamethasone, 3 mg kg-1 given 1 h prior to endotoxin administration. Dexamethasone itself reduced infarct size (P < 0.05) but had no direct effect on arrhythmia severity following coronary artery occlusion. 7. The mechanisms of this "cross-tolerance' induced by bacterial endotoxin against ischaemia-reperfusion injury remain to be elucidated but the most likely mechanisms appear to be the induction of protective enzymes or proteins (e.g. nitric oxide synthase, cyclo-oxygenase (COX) 2) probably mediated by cytokine release.