放射线联合p53基因及内皮抑素治疗小鼠前列腺癌皮下移植瘤

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.     

辐射调控自杀基因的腺病毒载体在胰腺癌细胞中的表达

早期生长反应基因-1(Egr-1)启动子可由电离辐射诱导,使得转导基因的表达可从时间与空间上进行调控,由此驱动单纯疱疹病毒胸苷激酶基因(TK)在胰腺癌细胞中高效表达,提高杀伤胰腺癌细胞的效率,本研究旨在观察辐射调控下的自杀基因的腺病毒载体在胰腺癌细胞中的表达。     

适应和开拓市场 加快医院发展

适应和开拓市场加快医院发展段沛奇，刘运生，胡铁辉，吕琳近年来，我院转变观念，向市场要效益，以质量求发展，不断加强经营成本核算，使医院在经济效益与社会效益上取得了新的成效。１．转变思想观念，适应市场经济体制：建国以来，我国医疗体制尽管发展缓慢，但基本保...     

壮医药罐疗法对痹病患者免疫功能影响的测定

壮医药罐疗法对痹病患者免疫功能影响的测定陈秀珍，吕琳，韦金育，叶琦丽，陈超树壮医药罐疗法是广西壮族自治区具有独特风格的一项传统疗法。主治风湿痹病及其他多种疾病。经临床１５２例验证观察，对风关痛，风关炎，类关炎治疗有效率分别达９４．９％，８９．８％，８...     

1988～1992年兰空机关大院计划免疫工作情况

1988～1992年我们坚持开展儿童计划免疫及新兵预防接种工作,增强了集体免疫力,提高了健康水平,现将主要情况分析如下: 1 基本情况 兰空机关大院每年有500多名儿童及100多名新兵为接种重点。对学龄前儿童进行“四     

人体活动的静电起电及防静电危害措施

静电现象是日常生活中司空见惯的 ,但是 ,在计算机房工作的操作者和从事电子仪器调试的技术人员带电时 ,在操作中产生的放电将成为机器故障或者错误动作的原因。许多情况下的静电危害主要起源于人体的静电起电。1　人体活动的静电起电过程1 1　不同固态介质之间的接触起电人在绝缘地面 (如橡胶板地面 )上走路时 ,鞋底和地面不断紧密接触、分开 ,发生接触起电。人坐在表面为绝缘材料的椅子上活动后起立时 ,人身穿的衣服与椅面接触后分离 ,使人体起电。穿尼龙羊毛混纺衣服 ,从人造革面椅子上起立时 ,人体可产生近万伏高压静电。在干燥的冬天…     

低血钾致单纯性ST段下垂型下移1例

患者 ,女 ,5 1岁。因间歇性肢体麻木 3周 ,伴胸闷憋气加重 1天来院就诊。既往有高血压病史 1年 ,近半年口服吲达帕胺片 (商品名 :寿比山 ) 2 .5ｍｇｑｄ。体检 :血压 110 /70ｍｍＨｇ (1ｍｍＨｇ =0 .133ｋＰａ) ,心率 70次 /ｍｉｎ ,律齐 ,无病理性杂音。实验室检查 :血Ｋ+2 .77ｍｍｏｌ/Ｌ ,Ｎａ+134.1ｍｍｏｌ/Ｌ ,Ｃｌ-94 .8ｍｍｏｌ/Ｌ。临床诊断 :低钾血症。心电图 (图1Ａ)示 :窦性心律 ,心率 73次 /ｍｉｎ ,Ｐ Ｒ间期 0 .16ｓＳＴⅡ ,Ⅲ ,ａＶＦ ,Ｖ3,Ｖ5,Ｖ6 下垂型下移 >0 .10ｍＶ ,ＳＴＶ4 下移 0 .15ｍＶ ,ＴⅡ ,ａＶＦ ,Ｖ2～ 6…     

维丁胶性钙治疗婴幼儿非感染性腹泻106例观察

我院儿科自1989年以来应用维丁胶性钙治疗婴幼儿非感染性腹泻,效果较好。现将资料完整的1992年4月～1993年9月诊治的106例临床观察报告如下。 1 临床资料 1.1 男24例,女32例。年龄42d～3岁,1岁以内78例(73.6％)。母乳喂养66例(62％),混合喂养21例(20％),人工喂养19例(18％)。对照组98例。两组年龄,喂养及临床表现基本相同。病例选择除外有脓血便及中度以上脱水患儿。腹泻天数1～4d72例(68％),≥     

放射线联合p53基因及内皮抑素治疗小鼠前列腺癌皮下移植瘤

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.