TRAIL与kallistatin联合表达载体的构建及抗肿瘤活性分析

为研究肿瘤坏死因子相关凋亡诱导配体(TRAIL)与组织激肽释放酶结合蛋白(kallistatin)联合用药的抗肿瘤作用,构建TRAIL与kallistatin双表达的重组质粒pAM-CAG-Kal-IRES-TRAIL,将重组质粒转染A549,LO-2,NCI-H446和Hela细胞,考察其抗肿瘤活性.实验结果表明:构建的双表达载体能同时表达TRAIL与kallistatin,且均能分泌至培养基中;TRAIL与kallistatin联合表达对肿瘤细胞活力的抑制作用明显增强,诱导肿瘤凋亡的作用也明显增强,说明联合表达TRAIL与kallistatin能够增强抗肿瘤活性.     

凋亡抑制蛋白与肿瘤关系的研究

凋亡抑制蛋白(inhibitor of apoptosis proteins,IAPs)可以作为癌症诊断和治疗的靶点,在肿瘤研究方面备受关注,就凋亡抑制蛋白的结构、功能、在肿瘤中的表达与肿瘤的关系等研究进展作一综述,为凋亡抑制蛋白的研究提供信息和思路.     

农村工业化与城镇化

通过阐述农村工业化的发展脉络及存在的问题,揭示了农村工业化在农村城镇化发展过程中的作用,并提出了推动实现农村工业化与城镇化良性互动的相关建议。     

肿瘤患者的心理分析及护理

分析了肿瘤患者心理变化4个阶段的不同表现,并针对此提出相应心理护理的方式。指出加强肿瘤患者的心理分析及护理是保证顺利治愈的重要环节。     

鸭血烯酸对艾氏癌生长的抑制作用

鸭血烯酸是由鸭血清中提取的不饱和脂肪酸．在体外实验中具有使艾氏腹水癌细胞膨胀失活的作用．用于治疗艾氏癌患鼠,可抑制其腹水癌和实体瘤的生长．与环磷酰胺（CPA）或氟脲嘧啶（SFU）相比,鸭血烯酸的毒性较低,疗效较高,约20％～40％被治愈的患鼠,可长期存活．     

颈部肿块细针吸取细胞学诊断

2000—2002年进行颈部肿块细针吸取细胞学检查共600例，有病理组织学证实138例，其中恶性病变66例。淋巴结、甲状腺各占60．10％、23．50％。细胞学阳性158例，占26．33％，可疑恶性32例，占5．33％。和术后病理组织学诊断对照。恶性病变符合率80．30％，良性病变符合率为93．06％，总符合率为86．96％。敏感率(阳性 可疑)淋巴结、甲状腺分别为96．29％和90．00％。本文对假阳性、假阴性病例进行了分析。     

复方癌立消抗肿瘤活性的研究

癌立消为验方，取长白山新鲜中药配制而成，实验用NIH小鼠移植Ehrlieh癌造成实体瘤模型。随机分四组。对照组不给药，阳性对照组给环磷酰胺剂量100mg／kg、癌立消剂量为成人剂量5倍(2．6g／kg)和10倍(5．2g／kg)两组。结果表明：癌立消有明显的抑瘤作用。5倍成人剂量组抑瘤率为43．9％-50．4％，10倍成人剂量组为53．3％-56．3％，而且有统计学意义。     

InCl3/HMS中孔固体酸烷基化催化剂的制备和表征

研究以HMS中孔材料为裁体，用浸渍蒸发法制备了InCl3/HMS负载型固体酸催化剂，并考察了不同InCl3负载量催化剂对苯和氯苄的酸催化苄基化反应的催化活性．用XRD、FT—IR和N2等温吸附等技术表征催化剂．结果表明，所制备的InCl3/HMS具有中孔结构；活性组分InCl3负载量与催化烷基化活性相关．过多的负载量，造成InCl3积聚于HMS裁体孔道内，导致催化剂孔容和比表面积的降低，从而降低了催化活性；在InCl3负载量为1．41mmol／g裁体时，催化剂活性最高．FT—IR分析初步表明活性组分InCl3通过化学键合的方式结合于载体HMS表面上，而不是简单地物理吸附于载体表面．     

Inhibitory effect of the adenovirus type 5 E1A protein expressed in the yeast system

The human adenovirus type 5 E1A, a tumor- suppressor gene[1], codes for two major related proteins of 243 amino acids (12S) and 289 amino acids (13S) by al-ternative splicing in two exons[2]. Studies have been shown that E1A can regulate expression of many genes and cell cycle[3]. Both in vitro and in vivo experiments indicated that E1A could induce tumor cells differentia-tion, convert tumor cells into an epithelial phenotype, in-hibit tumor cell growth and metastasis and strongly en-ha…     

Inhibitory effect of the adenovirus type 5 E1A protein expressed in the yeast system of the human tumor cell growth

Adenovirus 5 type E1A as a tumor suppressor gene can inhibit tumor growth and enhance the censitivity of chemotherapy and radiotherapy.E1A have the ability to integrate into the host genome,resulting in long-time expres-sion that induces Rb gene inactivation and animal cells im-mortalization.This prompted us to select the E1A protein for treatment of cancer in order to overcome the limitations of E1A gene therapy.Thus,we firstly comstructed E1A eu-caryotic expression vector (pPIC9/E1A),transformated the pichia pastoris yeast cells(GS115) and screened the high-expressing recombinant strains.The positive yeast strains were cultured in the shake flask,and induced for 3d.The crude E1A protein was purified using two steps of col-umu chromatography on HiTrap Q and HiTrap SP.The pu-rified E1A protein was identified by SDS-PAGE and Western blot.E1A protein was mostly located at cellular unclear when Cheriot delivered E1A protein into cells.The analysis in vitro indicated that the E1A protein arrested LN686 cell cycle at G2/M phase,and significantly inhibited the growth of LN686 tumor cells.The current studies firstly provided an experimental basis to further develop E1A protein for tumor treatment.