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1.
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. 相似文献
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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. 相似文献
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中药材在贮藏过程中,受自身性质及外界贮藏因素的影响,容易发生虫蛀现象。虫蛀后的中药材,轻则影响外观,降低消费者的购买力;重则影响品质,降低其药用价值,并产生虫体、排泄物及分泌物等杂质,严重污染中药材。该研究对影响中药材虫蛀发生的相关因素和虫蛀后的成分变化进行文献整理,对预防虫蛀发生的养护措施进行系统总结,首次对可应用于中药材贮藏过程中的虫蛀发生检测技术进行综述。在贮藏过程中,虫蛀的发生是生物因素(害虫的来源、种类和虫口密度等)、内在因素(水分、化学成分和自身的新陈代谢等)和环境因素(温度、相对湿度和环境含氧量等)共同作用的结果。虫蛀发生后,中药材所含的成分含量存在明显的变化。通过对中药材入库前的严格检查、入库后的定期养护及采用恰当的贮藏养护方法,可降低虫蛀发生率,提高中药材的保存完好率。中药材的贮藏养护是保证质量的关键环节,通过科学规范的贮藏,严格执行操作管理规范,就能降低被虫蛀的风险,保证中药材的品质。 相似文献
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目的 探讨直肠痛肿瘤组织内术前放疗后浸润淋巴细胞(TIL)数量改变对预后的影响.方法 搜集近8年余接受30 Gy分10次12 d完成的术前放疗的直肠癌患者107例,分析TIL分级与术前放疗后病理消退程度及预后关系.结果 直肠癌放疗前TIL 1级75例,2级16例,3级16例,4级0例,术前放疗后TIL 1级19例,2级43例,3级35例,4级10例.放疗后病理消退分级1级36例,2级57例,3级14例.单因素分析发现放疗前及放疗后TIL对局部病理消退影响有统计学意义(X2=36.80,P<0.01;X2=14.00,P<0.01);术前放疗后癌巢内TIL及病理消退对预后影响显著(X2=24.00,P<0.01;X2=12.17,P<0.01).Logistic多元分析提示放疗后TIL与病理消退关系密切(X2=8.05,P<0.01).结论 放疗前及放疗后TIL与直肠癌术前放疗局部病理消退相关.直肠癌术前放疗后癌巢TIL是影响生存预后的因素之一. 相似文献
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自1996年~2004年1月,笔者采用闭合复位经皮交叉穿针内固定的方法治疗距骨颈骨折,效果满意,现报告如下: 相似文献
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目的探讨左西孟旦、重组人脑利钠肽联合米力农治疗顽固性心力衰竭(RHF)患者对其血清内皮素-1(ET-1)、醛固酮(ALD)水平的影响。方法选取2018年8月至2020年8月于本院进行治疗的80例RHF患者作为研究对象,采用简单随机分组法分为A组和B组,各40例。A组采用左西孟旦(LEV)联合米力农治疗,B组采用重组人脑利钠肽(rh-BNP)联合米力农治疗,比较两组临床疗效、不良反应发生情况、ET-1、ALD、左心室射血分数(LVEF)、N末端B型利尿钠肽原(NT-proBNP)水平以及6 min步行试验距离(6MWT)。结果 A组治疗总有效率为97.50%,高于B组的85.00%(P<0.05)。治疗7 d后,两组LVEF和6MWT距离均大于治疗前(P<0.05),NT-proBNP水平均低于治疗前,且A组LVEF和6MWT距离大于B组,NT-proBNP水平低于B组(P<0.05)。治疗7 d后,两组ET-1、ALD水平均低于治疗前,且A组低于B组(P<0.05)。A组不良反应发生率为12.50%,低于B组的32.50%(P<0.05)。结论 LEV、r... 相似文献
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