Background. Cerebral state index (CSI) has recently been introduced as an intra-operative monitor of anaesthetic depth. We compared the performance of the CSI to the bispectral index (BIS) in measuring depth of anaesthesia during target-controlled infusion (TCI) of propofol. Methods. Twenty Chinese patients undergoing general anaesthesia were recruited. CSI and BIS, and predicted effect-site concentration of propofol were recorded. The level of sedation was tested by Modified Observer's Assessment of Alertness/Sedation Scale (MOAAS) every 20s during stepwise increase (TCI, 0.5ugml-1) of propofol. The loss of verbal contact (LVC) and loss of response (LOR) were defined by MOAAS values of 2-3 and less than 2, respectively. Baseline variability and the prediction probability (PK) were calculated for the BIS and CSI. The values of BIS05 and CSI05, BIS50 and CSI50, BIS95 and CSI95 were calculated at each end-point (LVC and LOR). Results. Baseline variability of CSI was more than that of BIS. Both CSI and BIS showed a high prediction probability for the steps awake vs LVC, awake vs LOR, and LVC vs LOR, and good correlations with MOAAS values. Conclusion. Despite larger baseline variation, CSI performed as well as BIS in terms of PK values and correlations with step changes in sedation.

The present study investigated the expression patterns of glial cells and interleukin-1b (IL-1b) in the rat spinal cord after a surgical incision, which is closely related with clinical postoperative pain. Microglia and astrocytes became activated in the spinal cord following incision. Real-time polymerase chain reaction (PCR) and immunohistochemisty showed that IL-1b mRNA and protein level in the spinal cord was transiently upregulated after surgical incision. The increased IL-1b-immunoreactivity (IR) was mainly localized in neurons but not the activated microglia or astrocytes. Although obvious increase in IL-1b-IR could be observed in the lumbar segments of the spinal cord ipsilateral to a hind paw incision, significant upregulation of IL-1b was not detected in the lumbar segments following thoracic incision. The present study indicated that surgical incision could induce glial activation and segmental upregulation of IL-1b in the spinal cord. The activated glial cells and upregulated IL-1b, in turn, may be involved in the incision-induced pain hypersensitivity.

目的 对单纯疱疹病毒I型扩增子质粒装载脑啡肽基因，并进行包装和扩增后，评价其在疼痛的转基因治疗上的作用。方法 将pCMVHPPE质粒中的人前脑啡肽原基因插入单纯疱疹病毒I型扩增子质粒pHSVIRESlacZ，再用单纯疱疹病毒温敏株辅助在BHK-2l细胞中包装、扩增，通过检测lacz的表达反映扩增子病毒滴度。结果 酶切鉴定证实重组子构建成功，重组扩增予质粒的包装、扩增由BHK-21细胞的形态变化和x.gal原位检测载体lacZ的表达证实. 扩增子假型病毒滴度达1×106TU/ml。结论 本研究构建、包装、扩增的携带外源脑啡肽基因的假型病毒有较高感染性，这种扩增子病毒可作为疼痛基因治疗的实验研究的有力工具。

目的 探讨缺血预处理对神经细胞凋亡的影响。方法 采用四动脉阻断法大鼠全脑缺血模型，21只Wistar大鼠，腹腔注射戊巴比妥钠麻醉。大鼠分四组：A组，假手术对照组（n=5），未予脑缺血处理；B组，预处理对照组（n=5），予3min全脑缺血后未再次缺血；C组，预处理缺血组（n=5），予3min全脑缺血，再灌24h后，再次全脑缺血10rain；D组，脑缺血组，予全脑缺血10rain。各组动物均在再灌72h后断头取脑。采用流式细胞计数仪检测大鼠前脑皮质凋亡细胞的百分数。结果 A组的凋亡细胞百分数是（O.2680±0.2035）%，B组（O.2780±0.1780）%，C组（O.3500±0.0744）%，D组（0.6280±0.2181）%。A、B及C组间无显著性差异（P<O.05）。D组凋亡细胞百分数显著高于A、B及C组（P<0.05）。结论 脑缺血预处理可抑制缺血诱导的神经细胞凋亡。

目的 研究采用单纯疱疹病毒I型扩增子载体将脑啡肽基因导入神经细胞，观察载体lacZ基因和外源脑啡肽基因的表达。方法 实验共分4组：A组为对照组，未加病毒悬液的神经细胞；B组，加病毒悬液的神经细胞培养2d；C组，加病毒悬液的神经细胞培养3d；D组，加病毒悬液的神经细胞培养至第lOd，留培基用放射免疫法检测外源脑啡肽基因的表达。用X-gal原位检测lacZ基因表达反映扩增子病毒的存在和滴度。结果 L-脑啡肽放射免疫检测证实转基因神经细胞L一脑啡肽含量较对照组明显升高（P<0.05），x.gal染色证实加入假病毒悬液的神经细胞有30%以上的细胞蓝染。结论 HSV-I扩增子假病毒能将外源脑啡肽基因导入神经细胞，并使之有效表达。