阳离子脂质体VEGF反义寡核苷酸对白血病细胞凋亡的影响

目的观察阳离子脂质体VEGF反义寡核苷酸对白血病细胞凋亡的作用。方法应用阳离子脂质体VEGF ASODN转染H160细胞48h后，观察细胞形态，电泳法检测DNA梯状带和流式细胞仪Annexin V—FTC／PI检测细胞凋亡。结果VEGF ASODN组VEGF mRNA的表达完全抑制，VEGF MSODN组和空白对照组的VEGF、mRNA的表达没有明显变化，细胞生长受抑制可见细胞固缩，DNA电泳出现典型的梯状条形带，流式细胞仪分析细胞凋亡率可达23．28％，明显高于VEGF MSODN组的8．21％和空白对照组。结论VEGF ASODN可抑制白血病细胞VEGF mRNA的表达，导致白血病细胞的凋亡，VEGF基因与白血病细胞的凋亡有关。     

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血管内皮生长因子反义寡核苷酸对白血病细胞系HL-60细胞作用的研究

本研究探讨VEGF ASODN抑制白血病细胞内源性VEGF mRNA的表达作用及其与白血病细胞凋亡的关系。用阳离子聚合物介导硫代修饰VEGF ODN转染体外培养白血病细胞系HL-60细胞后,采用MTT法检测细胞增殖抑制率,RT-PCR检测VEGF mRNA表达,以细胞形态学,凝胶电泳,流式细胞术观察细胞凋亡。结果显示：反义组与错义组、空白对照组相比,在细胞增殖抑制率和VEGF mRNA的表达水平方面均具有显著性差异（p〈0.05）;错义组与空白对照组相比无统计学差异（p〉0.05）。反义组可见细胞皱缩,颗粒增多,核固缩并出现细胞碎片,而错义组、空白对照组细胞轮廓清楚,胞体透亮,生长旺盛;反义组有凋亡梯形带,错义组和空白对照组仅见1条DNA条带;反义组细胞凋亡率达19.46%,与错义组、空白对照组相比具有显著性差异（p〈0.05）;错义组与空白对照组相比,无统计学差异（p〉0.05）。VEGF ASODN联合VP16的细胞凋亡率与等同条件单用VP16组相比有统计学差异（p〈0.05）;且凋亡率具有时间和剂量依赖关系。结论：VEGF ASODN能抑制白血病细胞内源性VEGF mRNA的表达,诱导白血病细胞的凋亡,抑制增殖,且增强VP16对白血病细胞诱导凋亡作用,两者联合效应具有相加作用。     

脑栓通胶囊治疗急性脑梗死疗效的Meta分析

目的系统评价脑栓通胶囊治疗急性脑梗死的疗效。方法检索中文科技期刊全文数据库(VIP)、万方数据库、中国期刊全文数据库(CNKI)、中国生物医学文献系统(CMB)、MedLine、EMbase、PubMed数据库,收集脑栓通胶囊治疗脑梗死急性期或恢复期的随机对照试验(RCT),经过文献筛选和文献质量评价后,采用RevMan 5.3软件对纳入文献资料进行Meta分析。结果共纳入15项RCT研究,共1 619例病人,其中试验组809例,对照组810例。Meta分析结果显示,与对照组相比,脑栓通胶囊联合化学药物治疗组有效率升高[RR=1.23,95%CI(1.12,1.35),P<0.000 1];治疗前后中国卒中量表评分差值[MD=3.49,95%CI(2.18,4.81),P<0.000 01]、欧洲卒中量表评分[MD=12.12,95%CI(9.65,14.58),P<0.000 01]、Barthel指数[MD=7.77,95%CI(7.29,8.25),P<0.000 01]和改良Barthel指数[MD=11.41,95%CI(6.27,16.55),P<0.000 1]比较,差异均有统计学意义。结论脑栓通胶囊联合化学药物治疗急性脑梗死疗效明显优于单纯化学药物治疗。     

骨髓单个核细胞Coombs试验阳性血细胞减少患者骨髓巨噬细胞活化抗原表达及其临床意义

目的 探讨骨髓单个核细胞Coombs(BMMNC-Coombs)试验阳性血细胞减少(又称免疫相关性血细胞减少,IRP)患者骨髓巨噬细胞(MΦ)活化抗原表达及其临床意义.方法 采用流式细胞仪(FACS)检测61例IRP患者及10例重型再生障碍性贫血(SAA)(病例对照组)和13例正常人(正常对照组)骨髓造血细胞膜自身抗体类型、骨髓MΦ数量(CD_(68)~+/CD_(45)~+)%及MΦ活化抗原(CD_(69))表达水平(CD_(68)~+CD_(68)~+CD_(68)~+)%,并探讨其临床意义.结果 61例IRP患者其MΦ数量及活化抗原表达水平[(0.57±0.30)%和(40.30±18.49)%]均高于病例对照组[(0.46±0.08)%和(32.44±19.37)%]及正常对照组[(0.44±0.69)%和(29.71±11.67)%](P值均<0.05);且其MΦ数量与活化抗原表达水平呈明显正相关(r=0.89,P<0.01).根据MΦ数量分为A组(MΦ百分率≥0.5%)和B组(MΦ百分率<0.5%),A组34例患者中32例(94.1%)有自身抗体IgG,B组27例患者中仅2例(7.4%);A组患者骨髓MΦ活化抗原表达水平(49.19±16.63)%显著高于B组患者(29.11±14.30)%(P<0.05),而B组患者和病例对照组及正常组无统计学意义(P值均>0.05);A组患者的3、6个月的总有效率(分别为47.06%、79.41%)均明显优于B组患者同期的疗效(22.22%、51.85%)(P<0.05);并且A、B组患者6个月的总有效率(79.41%、51.85%)均明显高于3个月的疗效(47.06%、22.22%)(P值均<0.05).34例自身抗体IgG(+)IRP患者按MΦ数量分为高(≥0.75%)、低(<0.75%)水平2组,25例MΦ低水平组24例仅能检测到1系骨髓细胞(CD_(34)~+或CD_(15)~+或GlycoA~+)有自身抗体IgG(96%),1例检测到2系骨髓细胞有自身抗体1gG;9例MΦ高水平组有8例能检测到2系骨髓细胞有自身抗体Igc,1例为3系骨髓细胞均有自身抗体IgG;高水平组IRP患者MΦ活化抗原表达水平(56.12±15.11)%显著高于低水平组(44.58±18.16)%(P<0.05);外周血红细胞、血红蛋白、血小板计数均显著低于低水平组(P<0.05);而外周血网织红细胞比例、总胆红素、间接胆红素及胸骨红系比例均显著高于低水平组(P<0.05).结论 IRP患者(尤其有骨髓造血细胞膜自身抗体IgG的IRP患者)骨髓MΦ数量明显增多,活化抗原高表达,即多呈激活状态,激活的巨噬细胞可能参与IRP患者骨髓早期造血细胞的破坏.     

阳离子脂质体VEGF反义寡核苷酸对白血病细胞凋亡的影响

目的观察阳离子脂质体VEGF反义寡核苷酸对白血病细胞凋亡的作用。方法应用阳离子脂质体VEGFASODN转染HI60细胞48h后,观察细胞形态,电泳法检测DNA梯状带和流式细胞仪AnnexinVFITC/PI检测细胞凋亡。结果VEGFASODN组VEGFmRNA的表达完全抑制,VEGFMSODN组和空白对照组的VEGFmRNA的表达没有明显变化,细胞生长受抑制可见细胞固缩,DNA电泳出现典型的梯状条形带,流式细胞仪分析细胞凋亡率可达23.28%,明显高于VEGFMSODN组的8.21%和空白对照组。结论VEGFASODN可抑制白血病细胞VEGFmRNA的表达,导致白血病细胞的凋亡,VEGF基因与白血病细胞的凋亡有关。     

骨髓单个核细胞Coombs试验阳性的血细胞减少患者补体水平变化及其意义

Objective To investigate the variation of bone marrow complement level in cytopenia pa-tients with positive BMMNC-Coombs test(CBCPC), and probe the role of complement in destroying hemato-poietic cells of CBCPC patients. Methods One hundred and twenty-four patients with CBCPC and twenty-three healthy donors as controls were enrolled in this study. The levels of CI-150, C3, C4, C5b-9 were tested with ELISA. The auto-antibodies on bone marrow hematupoietic cells (BMHC) were examined with flow cy-tometry. Results The level of C5b-9 in bone marrow(BM) of untreated CBCPC patients [(119.8 ± 54.0)μg,/L] was significantly higher than that of recovered patients [(100.7 ± 33.4) μg/L] or normal controls [(93.9 ± 28.8) μg/I.] (P < 0.05). The levels of CH50 in BM of untreated or recovered CBCPC patients [(33.3 ± 11.5) kU/L, (30.8 ± 10.3) kU/L] were significantly higher than that of normal controls [(24.1 ±6.4) kU/L] (P < 0.05). The level of C3 in BM of untreated or recovered CBCPC patients [(4.9 ± 2.2) mg/ L], (5.0 ± 3.5) mg/L] was significantly lower than that of normal controls [(7.0 ± 5.6) mg/L] (P < 0.05). The level of complement in peripheral blood was consistent with that in BM. CH50 in BM of CBCPC patients was negatively correlated with their C3 (r = - 0. 303, P = 0. 007) and positively correlated with their C5b-9(r = 0. 241, P = 0. 003) levels. The level of C5h-9 in BM of CBCPC patients was higher in the BMHC-IgM positive group [(117.6 ± 55.7) μg/L] than in the BMHC- IgM negative group [(99.2 ± 26.2)μg/L] (P < 0. 05). The positive rate of CD34+ -IgG or CD34 + -IgM of CBCPC patients was positively corre-lated with their C5 b-9 level (r = 0. 593, P = 0.000, r = 0. 326, P = 0. 049). The reticulocyte percentage (r =0. 421, P = 0.000) and serum indirect bilirubin level (r = 0. 230, P = 0. 032) of CBCPC patients were posi-tively correlated with their CHSO level. Conclusions The hematocytopenia of CBCPC patients might be re-lated to the hematopoietic cells destruction caused by auto-antibedy activated complements.     

骨髓单个核细胞Coombs试验阳性的血细胞减少患者补体水平变化及其意义

Objective To investigate the variation of bone marrow complement level in cytopenia pa-tients with positive BMMNC-Coombs test(CBCPC), and probe the role of complement in destroying hemato-poietic cells of CBCPC patients. Methods One hundred and twenty-four patients with CBCPC and twenty-three healthy donors as controls were enrolled in this study. The levels of CI-150, C3, C4, C5b-9 were tested with ELISA. The auto-antibodies on bone marrow hematupoietic cells (BMHC) were examined with flow cy-tometry. Results The level of C5b-9 in bone marrow(BM) of untreated CBCPC patients [(119.8 ± 54.0)μg,/L] was significantly higher than that of recovered patients [(100.7 ± 33.4) μg/L] or normal controls [(93.9 ± 28.8) μg/I.] (P < 0.05). The levels of CH50 in BM of untreated or recovered CBCPC patients [(33.3 ± 11.5) kU/L, (30.8 ± 10.3) kU/L] were significantly higher than that of normal controls [(24.1 ±6.4) kU/L] (P < 0.05). The level of C3 in BM of untreated or recovered CBCPC patients [(4.9 ± 2.2) mg/ L], (5.0 ± 3.5) mg/L] was significantly lower than that of normal controls [(7.0 ± 5.6) mg/L] (P < 0.05). The level of complement in peripheral blood was consistent with that in BM. CH50 in BM of CBCPC patients was negatively correlated with their C3 (r = - 0. 303, P = 0. 007) and positively correlated with their C5b-9(r = 0. 241, P = 0. 003) levels. The level of C5h-9 in BM of CBCPC patients was higher in the BMHC-IgM positive group [(117.6 ± 55.7) μg/L] than in the BMHC- IgM negative group [(99.2 ± 26.2)μg/L] (P < 0. 05). The positive rate of CD34+ -IgG or CD34 + -IgM of CBCPC patients was positively corre-lated with their C5 b-9 level (r = 0. 593, P = 0.000, r = 0. 326, P = 0. 049). The reticulocyte percentage (r =0. 421, P = 0.000) and serum indirect bilirubin level (r = 0. 230, P = 0. 032) of CBCPC patients were posi-tively correlated with their CHSO level. Conclusions The hematocytopenia of CBCPC patients might be re-lated to the hematopoietic cells destruction caused by auto-antibedy activated complements.     

炎症性贫血诊治新进展

炎症性贫血是一类促炎因子-铁调素-膜铁转运蛋白轴紊乱引发的“铁失利用”性贫血,是对传统“慢性病贫血”的完善和补充。炎症性贫血精准描述了此类贫血的发病机制,拓宽了疾病范畴,更新了诊断标准,使其治疗策略更加完善。