目的 分析采用美托洛尔与厄贝沙坦氢氯噻嗪片治疗老年重症心衰的效果.方法 选取2018年1月～12月我院老年病科收治的老年重症心衰患者84例作为研究对象,将其随机分为对照组(强心剂配合利尿剂治疗)与实验组(联合美托洛尔与厄贝沙坦氢氯噻嗪片治疗),各42例,对比疗效.结果 实验组临床疗效优于对照组,差异有统计学意义(P<0.05),心功能指标优于对照组,差异有统计学意义(P<0.05).结论 对老年重症心衰患者在常规用药的基础上加用美托洛尔与厄贝沙坦氢氯噻嗪片能够明显提高疗效,效果理想.

目的：分析2008～2014年度永川区院前急救流行病学变化趋势，探讨院前急救策略，提高院前急救质量。方法按照制订的入组标准，从重庆市永川区急救中心系统数据库中调取2008～2014年度数据进行统计学分析。结果院前急救人次逐年递增，性别构成差异无统计学意义（χ2＝0．302，P＝1．000）。地域分布仍以环城路内的城区地域为主，但其构成比出现逐年下降（χ2＝38．437，P＝0．000）。疾病谱的构成中，车祸及非车祸创伤排前两位，但构成比在逐年下降（χ2＝90．178，P＝0．000）。转诊患者均以30～49岁为主，占比46．32％。转出医院等级以一级社区及乡镇卫生院为主，占比74．98％。结论院前急救流行病学变化趋势研究，有利于合理调配急救资源，有针对性地制订院前急救对策，同时增强基层卫生机构的专项培训，提高工作效率和医疗资源的合理利用，更好地为人民群众服务。

目的:研究星形胶质细胞在炎症状态下缺血损伤对内皮性脂酶(endothelial lipase,EL)表达及活性的影响.方法:实验分为正常对照组、单纯损伤组和炎症损伤组.取新生大鼠脑皮质,体外分离培养纯化星形胶质细胞;单纯损伤组为对星形胶质细胞进行缺血缺氧损伤,炎症损伤组为白细胞共培养下的星形胶质细胞进行缺血缺氧损伤;两组损伤后分别在0,1,3,6,12,24,48 h不同时间点用逆转录PCR、实时荧光定量PCR和WesternBlot检测EL的表达变化.结果:缺血损伤的星形胶质细胞中EL的表达比正常对照组偏高,并随着损伤时间的延长逐渐增高,在损伤后6h和12 h达到峰值、随后下降.当加入炎症细胞后,炎症反应进一步促进EL在缺血缺氧损伤星形胶质细胞中的表达增加.结论:缺血缺氧损伤所介导的星形胶质细胞内EL的表达变化以及对该过程的促进作用可能直接影响到星形胶质细胞脂质的再利用,对损伤神经元的修复有极其重要的参考价值和临床意义.

Objective: To investigate the effect of matrine on the expressions of SALL4 and downstream target genes of Wnt/β-catenin signaling pathway in erythroleukemia (EL) cell line TF-1. Methods: TF-1 cells were treated with matrine at various concentrations (0.5, 1.0 and 2.0 g/L) for 48 h, using those untreated as control. The expression levels of SALL4 mRNA and downstream target genes (β-catenin, C-myc and Cyclin DI) of Wnt/β-catenin signaling pathway in TF-1 cells of various groups were determined by real-time fluorescent quantitative PCR, between which the relationship was analyzed. The expression level of SALL4 protein in TF-1 cells was determined by Western blot. Results: The expression levels of SALL4, β-catenin, C-myc, Cyclin DI mRNAs as well as SALL4 protein in TF-1 cells 48 h after treatment with matrine at various concentrations decreased significantly in a dose-dependent pattern as compared with those in control group (P < 0.05). The expression of SALL4 gene was significantly related to those of β-catenin, C-myc and Cyclin DI genes, with rs values of 0.912, 0.818 and 0.832 respectively (each P < 0.01). Conclusion: The inhibitory effect of matrine on expressions of SALL4 gene and protein as well as downstream target genes β-catenin, C-myc and Cyclin DI of Wnt/β-catenin signaling pathway may play an important role in inhibiting cell proliferation and inducing cell apoptosis.

Objective: To investigate the influence of Bortezomib (Bor) on proliferation and apoptosis of acute promyelocyte leukemia NB4 cell strain and acute erythroleukemia TF1 cell strain as well as on expressions of SALL4 gene and C-mye and CCND1 genes downstream in Wnt/β-catenin signaling pathway. Methods: NB4 and TF1 cells were treated with 10, 30 and 50 nmol/L Bor for 12, 24 and 48 h separately, using those untreated as control, then determined for proliferation activity by MTT method, for apoptosis rate by flow cytometry, and for expressions of SALL4, C-mye and CCND1 genes by RT-PCR and fluorescent quantitative PCR. Results: Bor showed time- and dose-dependent inhibitory effect on proliferation of NB4 and TF1 cells, with IC50 values of 23.97 and 25.36 nmol/L respectively 48 h after treatment. Bor induced the apoptosis of two kinds of cells in dose-dependent mode. The apoptosis rates of NB4 cells 24 after treatment with 30 and 50 nmol/L Bor and TF1 cells 24 h after treatment with 50 nmol/L Bor showed significant difference with those in control group (both P < 0.05). Bor inhibited the expressions of SALL4, C-mye and CCND1 genes in the two kinds of cells significantly. Twenty-four hours after treatment with 50 nmol/L Bor, the expression levels of the three genes in both NB4 and TF1 cells were significantly higher than those in control group (each P < 0.05). The expression of SALL4 gene was closed related to those of C-mye and CCND1 genes (r. = 0.857, 0.929, both P < 0.01). Conclusion: The inhibition of SALL4 gene as well as target genes C-mye and CCND1 downstream in Wnt/β-catenin signaling pathway may play an important role in induction of apoptosis of NB4 and TF1 cells.

目的探讨蛋白酶体抑制剂硼替佐米（bortezomib、Bor）诱导急性红白血病细胞株（TF1）和急性早幼粒白血病细胞株（NB4）凋亡及其对SALL4基因表达的影响。方法 MTT法检测细胞的增殖情况;流式细胞术检测细胞凋亡;免疫细胞化学检测SALL4蛋白表达;实时荧光定量PCR检测SALL4 RNA的表达变化;Western Blotting检测SALL4蛋白的表达情况。结果 MTT结果显示,硼替佐米能够抑制两种细胞的增殖,呈时间和计量依赖性,TF1细胞和NB4细胞48 h IC50分别为（29.15±0.55）和（30.55±0.74）nmol.L-1;流式细胞术结果显示,细胞凋亡率随着硼替佐米浓度的增加而增加,呈剂量依赖性。免疫细胞化学显示两种细胞均表达SALL4蛋白,定位于细胞核;实时荧光定量PCR结果表明,经不同浓度Bor（10,30,50 nmol.L-1）处理24 h后,两种细胞的SALL4 RNA均出现了不同程度的下调,50 nmol.L-1 Bor作用后,SALL4基因表达下降为对照组的45.11%（TF1）和69.77%（NB4）,差异均具有统计学意义（P＜0.05）;Western Blotting结果表明,Bor能够抑制两种细胞中SALL4B蛋白的表达,具有时间剂量依赖性。结论硼替佐米能够抑制TF1、NB4细胞的增殖并促进细胞凋亡,同时抑制SALL4基因表达。

OBJECTIVE To explore the mechanism of matrine (Mat) induced human erythroleukemia TF-1 cell apoptosis and its effect on SALL4 expression. METHOD Different concentrations of the Mat (0.5, 1.0, 1.5, 2.0 g x L(-1) ) were cultured in vitro in TF-1 cells at different time (24, 48, 72 h). Cell proliferation was assayed by MTT. Cell cycle was determined by flow cytometry (FCM). Cell apoptosis was detected by Annexin V and PI double staining method. SALL4 mRNA expression was detected by reverse transcription RT-PCR (RTT-PCR). RESULT Administrated with Mat (0.5-2.0 g x L(-1)) after 24, 48, 72 h, the proliferation of TF-1 cells were inhibited (P < 0.01) , and in dose- and time-dependent manner. Half inhibitory concentration (IC50 ) was 1.0 g L(-1) at 48 h. After 48 h that the Mat acted on TF-1 cells, the proportion of G0/G1 phase cells increased while compared with the control group, and S phase cells decreased (P < 0.01). Apoptosis were 8.6% , 11.21%, 15.26% , 17.63%, which showed statistically significant difference (P < 0.01) compared with the control group (5.05%). RT-PCR results showed the ratio between SALL4 mRNA expression and beta-actin (internal reference) expression significantly decreased (P < 0.01) with Mat dose increased. CONCLUSION In a certain range of concentration and time, Mat can inhibit TFT-1 cells proliferation. The mechanism is to make the cells G0/G1 phase blocked, to inhibit SALL4 gene expression and induce cell apoptosis.

SALL4 gene is closely related to body malformations related diseases, embryonic stem cell development, and hematopoietic malignancies. SALL4 can activate hematopoietic stem cell through Wnt signaling pathways, and promote continued proliferation of leukemia stem cells, leading to leukemia. In-depth study of SALL4 gene and its protein function will help clarify the pathogenesis of leukemia, providing a new target for the treatment of leukemia.

Objective:To investigate the effect of bortezomib on proliferation and apoptosis of human erythroleukemia cells TF-1,and its influence on the expression of Sall4 mRNA.Methods:(1)The level of cell proliferation was analyzed by MTT assay.(2)Morphological changes were observed by microscope.(3)Morphological changes were observed by electron microscope.(4)Flow cytometry with Annexin-V staining was used to analyze cell apoptosis rate.(5)Flow cytometry was used to analyze and cell cycle distribution.(6)The level of the expression of Sall4 mRNA was detected by RT-PCR.Results:(1)Bortezomib inhibited TF-1 cells in a time-and-does dependent manner.The IC50 at 24 and 48 h were 52 nmol/L and 27 nmol/L respectively.(2)Under microscope,it could be observed that the density of cells declined while cell fragments increased.(3)Moreover,under electron microscope,there appeared some apoptotic bodies.(4)Bortezomib could induce apoptosis of TF-1 cells in a dose-dependent manner.(5)At the same time,it caused an increase in G2/M phase and a marked decrease in G0/G1 and S phases in a time-dependent manner.(6)It was found by RT-PCR that the level of Sall4 mRNA was down-regulated with the treatment of bortemomib.Conclusion:Bortezomig can cause apoptosis of TF-1 cells and down-regulate the expression of Sall4 mRNA in a time-and-does dependent manner.

Objective To investigate the expression of oncogene SALL4 in martine-induced apoptosis of human acute leukemia THP-1 cells as well as its significance.Methods THP-1 cells were treated with 1.0,1.5 and 2.0 g / L matrine respectively and observed for morphological change by electron microscopy 24,48 and 72 h later,while determined for proliferative activity by MTT method,for apoptosis rate by flow cytometry,and for expression of SALL4 mRNA by RT-PCR.Results The THP-1 cells 24 h after treatment with matrine showed apoptotic morphology at various degrees.The matrine at various concentrations inhibited the proliferation and promoted the apoptosis of THP-1 cells significantly,both in dose-and time-dependent modes(P 0.05).However,the expression levels of SALL4 mRNAs in THP-1 cells treated with martine at various concentrations decreased significantly as compared with those in control group,in dose-and time-dependent mode(P 0.05).Conclusion The down-regulation of SALL4 gene expression might play an important role in martine-induced apoptosis of THP-1 cells.