Effects of heroin,alone or in combination with other drugs,on the locomotor activity in two inbred strains of mice

The locomotor activity of C57B1/6J and DBA/2J mice was studied, under the influences of heroin, amphetamine, strychnine, or ethanol, and of combinations of the opiate with each one of the other drugs. Heroin treatment was followed by the typical running fit in the C57 mice, while the DBA strain was unaffected. Amphetamine enhanced the activity in the C57 strain only. The combination of heroin with amphetamine or ethanol increased the locomotor activity only in the DBA strain, while heroin + strychnine exerted a clear stimulating effect on the activity of the C57 mice. The strychnine + heroin mixture was more toxic than heroin alone when the lethal doses (LD50) were determined in the 2 strains.     

乙醇诱导肝癌细胞凋亡的实验研究

目的研究低浓度乙醇对肝癌细胞的影响及作用机制。方法采用噻唑蓝比色法观察乙醇对细胞增殖的影响；采用流式细胞仪法观察乙醇对肝癌细胞内活性氧的影响；采用琼脂凝胶电泳法观察DNA片断化条带。结果低浓度乙醇可明显抑制细胞增殖；乙醇作用于细胞后2h内引起活性氧产生，24h后细胞出现典型的凋亡表现。结论乙醇能够通过诱导细胞内活性氧的产生引起细胞凋亡，呈明显的剂量依赖性。     

中晚期肝癌双介入治疗10例分析

（目的）评价肝动脉灌注化疗栓塞（HACE）和B超引导下经皮穿刺注射无水乙醇（PEI）联合治疗中晚期肝癌的疗效。（方法）10例中晚期肝癌患者采用HACE加PEI或HACE加手术切除。（结果）全组观察有效率为60％（CR＋PR），症状缓解率为90％。半年、一年生存率分别为70％和50％，未发生明显副作用。（结论）HACE加PEI是治疗中晚期肝癌较好方法，可取得良好的疗效，且直在基层医院推广。     

Opposite effects of sulpiride and SCH 23390 on ethanol-induced striatal ascorbic acid release in intact and 6-hydroxydopamine lesioned rats

The effects of L-sulpiride and SCH 23390 on ethanol-induced striatal ascorbic acid (AA) release in normal and 6-hydroxydopamine-lesioned rats were studied by using microdialysis coupled to high performance liquid chromatography with electrochemical detection. Ethanol (3.0 g/kg i.p.) significantly stimulated striatal AA release by 200% above the baseline in normal, 6-hydroxydopamine-lesioned, and reserpine-treated rats. L-Sulpiride, a dopamine D(2) antagonist, at the dose of 100 mg/kg i.p., decreased basal ascorbic acid release and showed an inhibitory tendency on ethanol-induced ascorbic acid release. However, at the higher dose of 200 mg/kg i.p., L-sulpiride significantly inhibited ethanol-induced ascorbic acid release in both normal and 6-hydroxydopamine-treated rats. SCH 23390, a dopamine D(1) antagonist, at the doses of 0.5 and 1.0 mg/kg i.p., potentiated ethanol-induced ascorbic acid release in normal rats. However, the potentiation of SCH 23390 on ethanol effect was not significant in 6-hydroxydopamine-treated rats at the dose of 1.0 mg/kg i.p. The present study demonstrates that opposite actions exist in the regulation of ethanol-induced ascorbic acid release in the striatum by dopamine D(1) and D(2) receptor blockade. It also suggests that the postsynaptic dopamine receptors are involved in mediation of ethanol-induced ascorbic acid release in rat striatum.     

Effects of ethanol on hippocampal place-cell and interneuron activity

Mounting evidence suggests that ethanol exerts effects on learning and memory by altering cellular activity in the hippocampus and related structures. However, little is actually known regarding ethanol's effects on hippocampal function in awake, freely-behaving animals. The present study examines the effects of ethanol on hippocampal place-cell and interneuron activity in freely-behaving rats. Signals from individual hippocampal neurons were isolated while subjects traversed a symmetric Y-maze for food reward. Following 15 min of baseline recording, subjects were injected with one of four doses of ethanol (0.0, 0.5, 1.0 and 1.5 g/kg), and cellular activity was monitored for a 1-h time period. Following sufficient time for recovery (minimum of 3 h post injection), cellular activity was monitored for an additional 15-min period. Both 1.0 and 1.5 g/kg ethanol potently suppressed the firing of hippocampal place-cells without altering place-field locations. Ethanol did not significantly suppress out-of-field firing rates, leading to a decrease in spatial specificity (i.e. the ratio of in-field/out-of-field firing rates). Interneuron activity was not altered by 1.0 g/kg ethanol, but was occasionally suppressed by 1.5 g/kg ethanol. Results are interpreted in light of recent behavioral and electrophysiological studies examining the effects of ethanol on hippocampal function.     

超声引导经皮瘤内注射醋酸和无水酒精治疗肝癌的比较

目的比较经皮瘤内注射无水酒精和醋酸对肝癌的治疗效果.方法肝癌患者12例,病灶46个,1.0～3.5cm大小.分别于超声引导下经皮瘤内注射无水酒精(21个)和75%醋酸(25个).2个月后复查,观察肿瘤的变化情况.结果治疗前两组肿块大小无差别(P>0.05),治疗后复查,PEI组肿块明显大于PAI组(P＜0.05),局部复发率PEI组(10/21)明显高于PAI组(3 / 25)(P＜0.01).结论 PAI术对肝癌的治疗效果优于PEI术.     

吴茱萸乙醚提取物抗角膜真菌作用研究

目的：体外检测中药吴茱萸乙醚提取物对串珠镰孢菌、茄病镰孢菌、黄曲霉菌3种真菌的抗菌作用。方法：采用体外药基法进行检测．测定中药吴茱萸乙醚部分提取物的最小抑菌浓度（MIC）值。结果：吴茱萸乙醚部分提取物抗串珠镰孢菌的MIC为2．5mg／ml；茄痔镰孢菌MIC为5mg／ml；黄曲霉菌MIC为10mg／ml。结论：吴茱萸乙醚部分提取物对串珠镰孢菌、茄病镰孢菌、黄曲霉菌3种真菌的抗菌作用中，抗串珠镰孢菌的效果最好。     

Dissociation between the locomotor and anxiolytic effects of acetaldehyde in the elevated plus-maze: Evidence that acetaldehyde is not involved in the anxiolytic effects of ethanol in mice

Acetaldehyde, the first product of ethanol metabolism, has been suggested to play a major role in many behavioral effects of ethanol. However, very few studies have directly tested the behavioral effects of the acute administration of acetaldehyde. In particular, the role of this metabolite in ethanol-induced anxiolytic effects has never been extensively tested. The aim of the present study was to characterize the anxiolytic effects of acetaldehyde in two strains of mice, C57BL/6J and CD1 mice with the elevated plus-maze procedure. The results show that acute injections of ethanol (1–2 g/kg) induced significant dose-dependent anxiolytic effects in both strains of mice. In contrast, acetaldehyde failed to produce any anxiolytic effect, although it induced a significant hypolocomotor effect at the highest doses. In an independent experiment, cyanamide, an aldehyde dehydrogenase inhibitor, prevented the locomotor stimulant effects of ethanol, although it failed to alter its anxiolytic effects. Together, the results of the present study indicate that acetaldehyde is not involved in ethanol-induced anxiolytic effects, although it may be involved in its sedative/hypolocomotor effects.     

Antioxidant properties of black tea in alcohol intoxication

Food ingredients such as alcohol may modify cellular redox state. Ethanol metabolism is accompanied by generation of free radicals that can damage cell components especially when antioxidant mechanisms are no able to neutralize them. However black tea is a source of polyphenol antioxidants that may enhance cellular antioxidant abilities. The aim of this study was to investigate the effect of black tea on antioxidant abilities of the liver, blood serum and brain of 12-months old rats sub-chronically (for 28 days) intoxicated with ethanol. Administration of black tea alone caused increase in the activity and concentration of antioxidant parameters more extensively in the liver and serum than in the brain. Alcohol caused decrease in the liver glutathione peroxidase and reductase and catalase activity but increase in activity of superoxide dismutase. Moreover, decrease in the level of non-enzymatic antioxidants, such as reduced glutathione, vitamin C, A and E and β-carotene was observed. The activity of serum glutathione peroxidase and reductase decreased while superoxide dismutase activity was not changed. The level of non-enzymatic antioxidants in serum was also decreased. However brain activity/level of all examined antioxidants enzymatic as well as non-enzymatic was decreased after ethanol intoxication. Black tea considerably prevented antioxidant parameters against changes caused by ethanol. These results indicate beneficial antioxidant effect of black tea regarding all examined tissues, but especially the liver.