Serum IgG, IgA, IgM, and IgE levels and allergy in Filipino children in the United States

The serum levels of IgE, IgG, IgA, and IgM of 27 American-born Filipino children 5 to 17 years of age were measured and found to be significantly higher than those of a control group of 24 Caucasian children of similar age distribution and attending the same general pediatric clinics. The geometric mean of serum IgE of the Filipinos was 227 U. per milliliter and of the Caucasians, 69 U. per milliliter (p < 0.01). The geometric means of other serum immunoglobulin levels of the Filipinos by comparison with the Caucasians were: IgG, 1,303 and 1,010 mg. per 100 ml. (p < 0.01); IgA, 195 and 120 mg. per 100 ml. (p < 0.001); and IgM, 141 and 92 mg. per 100 ml. (p < 0.02), respectively. The incidence of atopic disease was higher in the Filipino study group (48 per cent) than in the Caucasian control group (25 per cent); eczema was especially prevalent in the Filipino group. Elevated serum IgE levels were associated with atopic disease in both racial groups; however, there was no correlation between serum level of IgG, IgA, or IgM and atopy.     

Plackett–Burman randomization method for Bacterial Ghosts preparation form E. coli JM109

Plackett–Burman randomization method is a conventional tool for variables randomization aiming at optimization. Bacterial Ghosts (BGs) preparation has been recently established using methods other than the E lysis gene. The protocol has been based mainly on using critical concentrations from chemical compounds able to convert viable cells to BGs. The Minimum Inhibition Concentration (MIC) and the Minimum Growth Concentration (MGC) were the main guide for the BGs preparation. In this study, Escherichia coli JM109 DEC has been used to produce the BGs following the original protocol. The study contained a detail protocol for BGs preparation that could be used as a guide.     

DEC1基因过表达对人食管癌ECA109细胞增殖及侵袭能力的影响

目的:探讨DEC1基因过表达对人食管癌ECA109细胞增殖和侵袭能力的影响及可能机制。方法:将质粒pc DNA3.1(-)/DEC1(DEC1组)和pc DNA3.1(-)(vector组)利用脂质体分别转染至人食管癌ECA109细胞中,通过real-time PCR检测转染48 h后的细胞内DEC1 mRNA表达,Western blot分别检测转染72 h后细胞内DEC1、基质金属蛋白酶9(MMP9)及细胞周期蛋白cyclin D1的蛋白表达;采用CCK-8实验、平板集落实验及Transwell实验分别检测DEC1过表达对细胞的增殖和侵袭能力的影响。结果:与vector组相比,DEC1组中DEC1的表达明显增高(P0.01);cyclin D1和MMP9的表达明显降低(P0.05);细胞增殖与侵袭能力明显受到抑制(P0.01)。结论:过表达DEC1可明显抑制ECA109细胞的增殖和侵袭能力,DEC1可能通过影响MMP9和cyclin D1参与其中。     

An overview of new antitubercular drugs,drug candidates,and their targets

The causative agent of tuberculosis (TB), Mycobacterium tuberculosis and more recently totally drug-resistant strains of M. tuberculosis, display unique mechanisms to survive in the host. A four-drug treatment regimen was introduced 40 years ago but the emergence of multidrug-resistance and more recently TDR necessitates the identification of new targets and drugs for the cure of M. tuberculosis infection. The current efforts in the drug development process are insufficient to completely eradicate the TB epidemic. For almost five decades the TB drug development process remained stagnant. The last 10 years have made sudden progress giving some new and highly promising drugs including bedaquiline, delamanid, and pretomanid. Many of the candidates are repurposed compounds, which were developed to treat other infections but later, exhibited anti-TB properties also. Each class of drug has a specific target and a definite mode of action. These targets are either involved in cell wall biosynthesis, protein synthesis, DNA/RNA synthesis, or metabolism. This review discusses recent progress in the discovery of newly developed and Food and Drug Administration approved drugs as well as repurposed drugs, their targets, mode of action, drug-target interactions, and their structure-activity relationship.     

DTT与顺铂诱导对食管癌Eca109细胞磷酸化P38表达的影响

目的:探讨磷酸化P38在顺铂和DTT诱导的食管癌Eca109细胞凋亡中的作用.方法:分别用DTT与顺铂诱导处理食管癌Eca109细胞,未加药组作为对照.采用流式细胞仪技术检测细胞凋亡率;用免疫组化方法检测磷酸化P38的表达情况.结果:与对照组相比,DTT处理组及顺铂处理组细胞凋亡率明显升高.免疫组化结果显示:2处理组磷酸化P38的水平均明显高于对照组(P＜0.05);DTT处理组磷酸化P38大部分位于细胞核内,而顺铂组磷酸化P38则主要弥散于细胞浆内.结论:磷酸化P38在DTT和顺铂诱导的食管癌Eca109细胞凋亡时细胞内分布不同,激活的P38可能通过不同途径参与细胞凋亡.     

奈达铂与顺铂联合应用对人食管癌Eca-109细胞增殖与凋亡的影响

目的研究奈达铂(NDP)联合顺铂(DDP)对人食管癌细胞株Eca-109的增殖及凋亡的影响,并探讨其机制.方法采用MTT法对Eca-109细胞的增殖抑制率进行检测,中效原理法对联合用药的相互作用进行分析判断;采用流式细胞术分析早期凋亡细胞比例;采用RT-PCR和免疫细胞化学分析Ki-67及Bax、Bcl-2表达的变化.结果NDP、DDP均明显抑制Eca-109细胞的生长,且呈剂量依赖性;两者联合使用时,低浓度时呈拮抗效应,高浓度时呈协同效应; IC50浓度的NDP、DDP和1/2 IC50(NDP) 1/2 IC50(DDP)对Eca-109细胞的抑制率分别为(41.85±4.1)%,(47.38±2.9)%和(52.45±0.9)%;流式细胞术结果表明正常对照组、NDP组、DDP组、联合用药组细胞早期凋亡率依次增加,单独用药组与联合用药组相比有差异;与单独用药组比较,联合用药组Ki-67、Bcl-2表达率显著降低,而Bax表达显著增高.结论与两药高浓度单独应用相比,低浓度NDP和DDP联合应用对Eca-109细胞增殖的抑制作用和诱导凋亡能力均有明显增强.     

全反式维甲酸联合5-氟尿嘧啶对Eca109细胞增殖、迁移和VEGF表达的影响

目的:探讨全反式维甲酸(ATRA)、5-氟尿嘧啶(5-FU)单独或联合作用对Eca109细胞增殖、迁移和血管内皮生长因子(VEGF)表达的影响。方法:将常规传代的Eca109细胞分为4组:ATRA组、5-FU组、ATRA+5-FU组和对照组,采用MTT法检测各组细胞的增殖情况,通过划痕实验测定各组细胞的迁移能力,采用RT-PCR和免疫细胞化学法分别检测各组细胞VEGF mRNA和蛋白的表达情况。结果:作用24、48和72 h后,ATRA+5-FU组的细胞生长抑制率均高于其他2组(F=23.432、13.605、73.369,P均<0.05);作用24 h后,ATRA+5-FU组的迁移率均低于其他3组(P均<0.001);作用48 h后,ATRA+5-FU组细胞VEGF mRNA和蛋白的相对表达量均低于其他3组(P均<0.05)。结论:ATRA、5-FU均能抑制食管癌细胞的增殖,且联合用药效果更为显著,可能与其抑制肿瘤血管生成有关。     

DNA甲基转移酶抑制剂5-杂氮-2′-脱氧胞苷对人食管癌细胞株Eca109的影响

目的:探讨DNA甲基转移酶抑制剂5-杂氮-2′-脱氧胞苷(5-aza-CdR)对人食管癌细胞株Eca109增殖作用的影响。方法:应用不同浓度(10-7、10-6、10-5、10-4mol/L)的特异性DNA甲基转移酶抑制剂5-aza-CdR,于不同作用时间(24～168h)处理人食管鳞癌细胞株Eca109,采用四甲基偶氮唑蓝(MTT)法测定5-aza-CdR作用下Eca109细胞株的生存率,倒置显微镜观察细胞的形态学变化。结果:不同药物浓度组在同一作用时间下,细胞株生存率差异有统计学意义(P<0.05);同一药物浓度不同作用时间组之间(24～96h)的细胞生存率差异也有统计学意义(P<0.05),且96h时对人食管鳞癌细胞株Eca109生长抑制作用最明显。形态学观察显示:癌细胞体积缩小,核固缩,染色质凝聚成块。结论:5-aza-CdR有抑制人食管癌细胞株Eca109生长的作用,抑制作用呈时间依赖性及浓度依赖性;并且干预后癌细胞呈现典型的凋亡细胞形态改变。     

人CD154基因真核表达载体的构建及在Eca109细胞中的表达

目的：构建人CD154基因真核表达质粒pcDNA3．1-CD154,初步观察转染该质粒后Eca109细胞的细胞生物学特性。方法：人外周血单个核细胞体外经PHA激活后提取总RNA,用RT—PCR技术扩增人CD154cDNA全长并构建真核表达质粒pcDNA3.1—CD154,用Lipofectamine^TM 2000介导pcDNA3．1-cDl54质粒转染食管癌Eca109细胞株,RT—PCR检测转染细胞中CD154 mRNA的表达,观察细胞生长特征。结果：用T7／SP6通用引物测序证实重组质粒中插入片段为正向插入的人CD154基因。pcDNA3．1-CD154转染Eca109细胞后细胞异型性明显改善,生长速率减慢。结论：pcDNA3．1-CD154构建成功;转染该质粒的Eca109细胞生物学特性发生改变。