胃管滴注对新生儿坏死性肠炎合并休克的治疗体会（附3例报告）

报告新生儿坏死性小肠结肠炎合并休克病儿３例，在抢救休克、抗炎和纠正水、电解质平衡的基础上，用胃管内滴注牛奶和药物的方法进行治疗。结果表明：３例病儿全部治愈。着重阐述了胃管滴注法在治疗新生儿坏死性肠炎中的作用。     

宫腔积脓并发穿孔误诊2例

例1，65岁，腹痛4d伴恶心、呕吐，发热2d。在当地医院给输液及抗生素治疗无好转，且腹痛较前明显加剧，于1995年2月4日以阑尾炎穿孔伴腹膜炎收入外科。绝经15年，G6P5．平时阴道有流液，体温37．5℃，脉搏84次／min，呼及21次／min．血压16／10kPa，急性病容、腹肌紧张，满腹压痛，下腹穿刺抽出脓性液体2ml．     

硒对大鼠血清蛋白,血脂的亚慢毒性作用研究

硒对大鼠血清蛋白、血脂的亚慢性作用研究结果表明，大鼠在长期高硒摄入的条件下，其血清蛋白、血脂等项生化指标，与对照组相比，均有不同程度的降低，且随摄入硒的剂量增大，降低得越多。说明高硒对肝脏具有一定的毒性作用。     

铝致神经细胞Ca^2＋浓度升高的可能机制

本文就Ａｌ＾３＋引起神经细胞内Ｃａ６２＋浓度升高的实验依据提出了几种可能性机制，着重介绍了Ａｌ＾３＋通过信号传导系统，谷氨酸，β－淀粉样蛋白聚保，钙调蛋白以及其它机制引起胞内Ｃａ＾２＋浓度升高的过程，指出了某些尚待深入研究之处，并揭示了目前和今后的研究动向。     

顺铂肾毒性动物模型的实验研究

顺铂(DDP)一次尾静脉注射8mg/kg可使大鼠血中尿素氮(BUN)明显增加,超微结构观察肾小管上皮细胞内线粒体肿胀,空泡增多,溶酶体及吞饮小泡体积变大,数量增加,至第49天仍未恢复,提示8mg/kg顺铂引起的大鼠不易恢复的肾毒性是研究预防减轻顺铂的肾毒性并提高临床疗效的一个良好的动物模型。     

地塞米松对布比卡因诱导小鼠神经元毒性的影响

Objective To investigate the effect of dexamethasone on the toxicity of bupivacaine in murine neurons.Methods Murine neuroblastoma cell line N2a was obtained from ATCC cell bank (USA). The cells were cultured in 10% fetal cow serum/MEM culture medium and divided into 4 groups voup I control (Con); group II bupivacaine ( Bup); group Ⅲ dexamethasone (Dex) and group IV Dex + Bup. The culture medium contained bupivacaine 900 μmol/L in group Bup and dexamethasone 1 μmol/L in group Dex respectively. In group Dex + Bup ( IV ) Bup was added to the culture medium with a final concentration of 900 μmol/L at 12 h after pretreatment with Dex 1 μmol/L. The cells were inoculated in 24 well plates (0.5 ml in each well, 24 wells in each group) and 10 cm culture dishes (7 ml in each dish, 4 dishes in each group). The release rate of LDH was calculated and the morphology of the cells and nucleus condensation (by Hoechst 3334224 fluorescent staining) was detected at 9 h of incubation in 24 well plates. The mitochondrial transmembrane potential (by JC-1 assay) and phosphorylation of Akt and ERKs (by Western blot) were measured at 5 h of incubation in 24 well plates and in culture dishes respectively. ResultsBupivacaine caused severe damage to the N2a cells as evidenced by increase in LDH release and nucleus condensation (apoptosis), dephosphorylation of Akt and ERKs, decrease in mitochondrial transmembrane potential and severe morphological changes. Dexamethasone pretreatment significantly attenuated bupivacaine-induced neurotoxicity. Conclusion Dexamethasone can protect N2a cells from bupivacaine-induced neurotoxicity through stabilization of mitochondrial transmembrane potential and inhibition of dephosphorylation of Akt and ERKs.