背景与目的:有研究表明放疗能够上调和强化肿瘤血管的生成过程,导致放疗耐受;重组人血管内皮抑制素(recombinant human endostatin,rh-endostatin)可抑制肿瘤血管生成,改善由放疗引起的耐受性。本研究旨在探讨rh-endostatin与顺铂(cispl...背景与目的:有研究表明放疗能够上调和强化肿瘤血管的生成过程,导致放疗耐受;重组人血管内皮抑制素(recombinant human endostatin,rh-endostatin)可抑制肿瘤血管生成,改善由放疗引起的耐受性。本研究旨在探讨rh-endostatin与顺铂(cisplatin,DDP)分别联合电子线照射对肺腺癌A549移植瘤的抑制作用。方法:建立A549肺腺癌移植瘤模型,待瘤径达1.0cm时,将实验鼠随机分成4组(每组6只):对照组、照射组、照射+DDP组和照射+rh-endostatin组。定期测量肿瘤最长径和最大垂直径,第16天时处死裸鼠,取出肿瘤组织,检测肿瘤细胞凋亡率,RT-PCR检测bFGF mRNA表达水平,免疫组织化学法检测VEGF表达水平。结果:对照组、照射组、照射+DDP组和照射+rh-endostatin组肿瘤的生长速率分别为(162±6)%、(131±8)%、(104±7)%和(108±11)%(P<0.05);照射+rh-endostatin组与照射组相比以及照射+DDP组与照射组相比,差异均具有统计学意义(P<0.01);照射+rh-endostatin组与照射+DDP组相比,差异无统计学意义(P>0.05)。肿瘤细胞凋亡率,对照组、照射组、照射+DDP组和照射+rh-endostatin组分别为(12.2±1.1)%、(16.5±0.8)%、(24.4±1.5)%和(20.5±1.9)%,各组间差异具有统计学意义(P<0.05)。照射组bFGFmRNA和VEGF表达水平高于对照组,照射+rh-endostatin组bFGF mRNA和VEGF表达水平明显低于对照组、照射组、照射+DDP组(P<0.05)。结论:rh-endostatin明显提高了照射对A549肺腺癌移植瘤的抑制情况;rh-endostatin联合照射肺腺癌A549移植瘤可取得与DDP联合放疗相似的结果。展开更多
目的探讨CT导引穿刺活检胰腺占位性病变的诊断价值。方法回顾性分析CT导引细针穿刺胰腺占位性病变68例,其中胰头区病变49例、胰体12例和胰尾7例。病灶直径2～7 cm,<3cm 10例,3～7 cm 58例。术前均作CT平扫和增强扫描,均采用前路进针...目的探讨CT导引穿刺活检胰腺占位性病变的诊断价值。方法回顾性分析CT导引细针穿刺胰腺占位性病变68例,其中胰头区病变49例、胰体12例和胰尾7例。病灶直径2～7 cm,<3cm 10例,3～7 cm 58例。术前均作CT平扫和增强扫描,均采用前路进针,使用20 G细针穿刺。活检标本送病理科作组织病理检查。结果68例患者均安全地穿刺到病变内,活检成功率为100%。穿刺活检诊断率为恶性病变46例,良性17例,5例未见病变。5例中2例经临床和CT随访均无异常,另3例最终证实胰腺囊腺癌2例和胃癌转移1例。穿刺活检总正确率、灵敏度和特异度分别为96%、95%和100%。CT导引活检对恶性、良性病变的正确率为94%和100%(P>0.05)。较大肿块病灶(≥3.0 cm 97%,<3 cm90%)和病变位于胰尾(胰尾100%,胰头96%,胰体92%)的正确率稍高,但经统计学检验正确率差异并无统计学意义(P>0.05),未发现严重的并发症。结论CT导引经皮细针穿刺活检胰腺占位性病变是一种安全的有效的诊断和鉴别诊断的方法。展开更多
In order to investigate the inhibitory effects of Endostar(rh-endostatin,YH-16)in combination with radiotherapy on lung adenocarcinoma A549 in mice and the interaction mechanisms of combined therapy,the transplantatio...In order to investigate the inhibitory effects of Endostar(rh-endostatin,YH-16)in combination with radiotherapy on lung adenocarcinoma A549 in mice and the interaction mechanisms of combined therapy,the transplantation tumor models of A549 lung adenocarcinoma were established.When the largest diameter of tumor reached 1.0cm,all nude mice were randomly divided into 4 groups:Endostar group,radiotherapy group,radiotherapy plus Endostar(combined treatment)group,and control group(n=6 in each group).The largest diameter and the vertical diameter of tumor were measured at different time points.At the 16th day,mice were executed,and the tumors were applied to analysis of rate of tumor cell apoptosis,and the expression levels of basic fibroblast growth factor(bFGF)mRNA were detected by reverse transcription-polymerase chain reaction(RT-PCR)and those of vascular endothelial growth factor(VEGF)by immunohistochemistry.The results demonstrated that the rate of tumor inhibition in combined treatment group was higher than that in other groups.And the rate of tumor cell apoptosis in combined treatment group was also higher than that in other groups.Meanwhile,the levels of bFGF mRNA and VEGF expression in combined treatment group were lower than those in other groups.It was concluded that Endostar obviously enhanced the curative effectiveness of radiotherapy on lung adenocarcinoma A549 in mice.The underlying mechanisms may involve the down-regulation of bFGF mRNA and VEGF expression to inhibit angiogenesis by Endostar and the cooperative effect of Endostar and radiotherapy to synergistically promote tumor cell apoptosis.And Endostar inhibits angiogenesis by down-regulating the expression of bFGF mRNA and VEGF.展开更多
文摘背景与目的:有研究表明放疗能够上调和强化肿瘤血管的生成过程,导致放疗耐受;重组人血管内皮抑制素(recombinant human endostatin,rh-endostatin)可抑制肿瘤血管生成,改善由放疗引起的耐受性。本研究旨在探讨rh-endostatin与顺铂(cisplatin,DDP)分别联合电子线照射对肺腺癌A549移植瘤的抑制作用。方法:建立A549肺腺癌移植瘤模型,待瘤径达1.0cm时,将实验鼠随机分成4组(每组6只):对照组、照射组、照射+DDP组和照射+rh-endostatin组。定期测量肿瘤最长径和最大垂直径,第16天时处死裸鼠,取出肿瘤组织,检测肿瘤细胞凋亡率,RT-PCR检测bFGF mRNA表达水平,免疫组织化学法检测VEGF表达水平。结果:对照组、照射组、照射+DDP组和照射+rh-endostatin组肿瘤的生长速率分别为(162±6)%、(131±8)%、(104±7)%和(108±11)%(P<0.05);照射+rh-endostatin组与照射组相比以及照射+DDP组与照射组相比,差异均具有统计学意义(P<0.01);照射+rh-endostatin组与照射+DDP组相比,差异无统计学意义(P>0.05)。肿瘤细胞凋亡率,对照组、照射组、照射+DDP组和照射+rh-endostatin组分别为(12.2±1.1)%、(16.5±0.8)%、(24.4±1.5)%和(20.5±1.9)%,各组间差异具有统计学意义(P<0.05)。照射组bFGFmRNA和VEGF表达水平高于对照组,照射+rh-endostatin组bFGF mRNA和VEGF表达水平明显低于对照组、照射组、照射+DDP组(P<0.05)。结论:rh-endostatin明显提高了照射对A549肺腺癌移植瘤的抑制情况;rh-endostatin联合照射肺腺癌A549移植瘤可取得与DDP联合放疗相似的结果。
文摘目的探讨CT导引穿刺活检胰腺占位性病变的诊断价值。方法回顾性分析CT导引细针穿刺胰腺占位性病变68例,其中胰头区病变49例、胰体12例和胰尾7例。病灶直径2～7 cm,<3cm 10例,3～7 cm 58例。术前均作CT平扫和增强扫描,均采用前路进针,使用20 G细针穿刺。活检标本送病理科作组织病理检查。结果68例患者均安全地穿刺到病变内,活检成功率为100%。穿刺活检诊断率为恶性病变46例,良性17例,5例未见病变。5例中2例经临床和CT随访均无异常,另3例最终证实胰腺囊腺癌2例和胃癌转移1例。穿刺活检总正确率、灵敏度和特异度分别为96%、95%和100%。CT导引活检对恶性、良性病变的正确率为94%和100%(P>0.05)。较大肿块病灶(≥3.0 cm 97%,<3 cm90%)和病变位于胰尾(胰尾100%,胰头96%,胰体92%)的正确率稍高,但经统计学检验正确率差异并无统计学意义(P>0.05),未发现严重的并发症。结论CT导引经皮细针穿刺活检胰腺占位性病变是一种安全的有效的诊断和鉴别诊断的方法。
文摘In order to investigate the inhibitory effects of Endostar(rh-endostatin,YH-16)in combination with radiotherapy on lung adenocarcinoma A549 in mice and the interaction mechanisms of combined therapy,the transplantation tumor models of A549 lung adenocarcinoma were established.When the largest diameter of tumor reached 1.0cm,all nude mice were randomly divided into 4 groups:Endostar group,radiotherapy group,radiotherapy plus Endostar(combined treatment)group,and control group(n=6 in each group).The largest diameter and the vertical diameter of tumor were measured at different time points.At the 16th day,mice were executed,and the tumors were applied to analysis of rate of tumor cell apoptosis,and the expression levels of basic fibroblast growth factor(bFGF)mRNA were detected by reverse transcription-polymerase chain reaction(RT-PCR)and those of vascular endothelial growth factor(VEGF)by immunohistochemistry.The results demonstrated that the rate of tumor inhibition in combined treatment group was higher than that in other groups.And the rate of tumor cell apoptosis in combined treatment group was also higher than that in other groups.Meanwhile,the levels of bFGF mRNA and VEGF expression in combined treatment group were lower than those in other groups.It was concluded that Endostar obviously enhanced the curative effectiveness of radiotherapy on lung adenocarcinoma A549 in mice.The underlying mechanisms may involve the down-regulation of bFGF mRNA and VEGF expression to inhibit angiogenesis by Endostar and the cooperative effect of Endostar and radiotherapy to synergistically promote tumor cell apoptosis.And Endostar inhibits angiogenesis by down-regulating the expression of bFGF mRNA and VEGF.
