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目的　探讨血浆脂蛋白相关磷脂酶A2（Lp-PLA2) 联合预后营养指数（PNI)对急性脑出血（AICH)患者预 后的评估价值。方法 98例AICH患者为AICH组，根据预后情况分为预后不良和预后良好，另选取同期50例体检 健康志愿者作为对照组。检测血浆Lp-PLA2水平并计算PNI。采用多因素Logistic回归分析AICH患者预后不良的 影响因素，受试者工作特征（ROC) 曲线分析血浆 Lp-PLA2、PNI对 AICH 患者预后的评估价值。结果　与对照组比 较，AICH 组血浆 Lp-PLA2 水平升高，PNI 降低（P 均<0. 05)。随访 90 d，98 例 AICH 患者预后不良发生率为 34. 69% （34/98)。AICH患者预后不良的独立危险因素为血肿体积、美国国立卫生研究院卒中量表评分增加和Lp-PLA2升 高，独立保护因素为 PNI升高（P均<0. 05)。血浆 Lp-PLA2、PNI 单独与联合评估 AICH 患者预后不良的曲线下面积 （AUC)分别为0. 778、0. 785、0. 891，血浆Lp-PLA2联合PNI评估AICH患者预后不良的AUC最大。结论 AICH患者血 浆Lp-PLA2和PNI与预后有关，血浆Lp-PLA2联合PNI评估AICH患者预后不良的价值较高，可能成为AICH患者预 后不良的辅助预测指标。 [ABSTRACT FROM AUTHOR]

Objective To observe the effects of dichloroacetate (DCA)on the proliferation and apoptosis of bladder cancer cells T24 in vitro and to study the underlying mechanism. Methods The bladder cancer cells T24 were randomly divided into four groups: experimental group 1, experimental group 2, experimental group 3, and the control group. Cells in the experimental groups 1, 2, and 3 were added with 5, 10, and 20 mmol/ L DCA, respectively; cells in the control group were added with 0. 1% dimethyl sulfoxide (DMSO). The cell proliferation of T24 cells were detected by MTT assay at 24, 48, and 72 h after DCA treatment. At 48 h, the apoptosis was examined by Hoechst33258 staining,the mitochon-drial membrane potential was detected by using JC-1 staining,and the expression levels of Bax protein, Bcl-2 protein and Caspase-3 protein were determined by Western blotting. Results The cell proliferation in the experimental groups 1, 2, and 3 was lower than that of the the control group at 24, 48 and 72 h, and with the time and increasing concentrations of DCA, the inhibition of cell proliferation was more significant (all P < 0. 05). The number of apoptosis cells in the experimental groups 1,2 and 3 was higher than that of the control group, and the mitochondrial membrane potential was lower than that of the control group (all P < 0. 05). Compared with the control group, the expression of Bax protein and Caspase-3 protein significantly increased, while the expression of Bcl-2 protein significantly decreased in the experimental groups 1, 2, and 3 (all P < 0. 05). Conclusions DCA can inhibit the proliferation and induce the apoptosis of bladder cancer cell line T24, which suggests that the mechanism may be related to the decrease of mitochondrial membrane potential level,up-regulation of Bax protein and Caspase-3 protein, and down-regulation of Bcl-2 protein. [ABSTRACT FROM AUTHOR]

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