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随着直肠癌外科治疗理念的更新和多学科协作模式的不断完善,直肠癌患者生活质量及生存期有了很大提高.但直肠癌术后局部复发仍是影响患者生存期的重要因素.直肠癌局部复发是指直肠癌根治术后直肠癌原发区域再发肿瘤,常累及吻合口、淋巴血管和盆腔毗邻器官.术后局部复发除与肿瘤本身生物学特征相关外,还与患者术前肿瘤的分期有关.约5%~12%的直肠癌患者就诊时肿瘤已侵及邻近组织或器官. 相似文献
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目的 观察ERK2信号转导通路在血小板源生长因子(PDGF-BB)诱导血管平滑肌细胞(VSMC)增殖、迁移和表达转化生长因子(TGF)-β1中的作用.方法 将原代培养的大鼠VSMC分为4组:(1)对照组;(2)PDGF刺激组;(3)Ad-LacZ组;(4)Adanti-ERK2组.用Westernblot检测细胞磷酸化ERK2蛋白水平;噻唑蓝(MTT)比色法测定细胞增殖率;流式细胞仪检测细胞细胞周期;Boyden小室测定细胞的跨膜迁移能力;酶联免疫吸附试验(ELISA)法检测细胞培养液上清中TGF-β1的浓度.结果 Adanti-ERK2组和对照组细胞增殖率、S期细胞百分比及跨膜迁移细胞数目明显低于PDGF刺激组和Ad-LacZ组(细胞增殖率:2.75%、0.00%比64.45%、61.88%;s期细胞百分比:14.18%、13.58%比38.14%、32.99%;跨膜迁移细胞数:8.2±3.2、6.3±2.6比24.8±6.1、23.3±5.8,均P<0.05);(2)Adanti-ERK2组和对照组细胞培养上清液中TGF-β1含量明显低于PDGF刺激组和Ad-LacZ组(P<0.05);而Adanti-ERK2组明显高于对照组(P<0.05).结论 ERK2信号转导通路参与调控PDGF-BB诱导的VSMC增殖、迁移和基因表达.反义ERK2基因预先转染阻断ERK信号转导能显著抑制PDGF-BB刺激的VSMC增殖、迁移,阻断细胞周期由G1期进入S期,并且部分下调TGF-β1的合成分泌. 相似文献
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直肠前突和直肠内脱垂是引起出口梗阻型便秘(obstructed defecation syndrome,ODS)常见病因。经肛门吻合器直肠部分切除术(stapled transanal rectal resection,STARR)是近年来国际上治疗ODS的最常用术式。常规STARR需要使用两把PPH吻合器,且操作较复杂、学习曲线较长、切除组织容积有限。 Naldini等[1]报道了一种外径为36 mm、吻合腔容积大于35 cm3、钉高4.2 mm且具备4个可视开窗的圆形吻合器,将其应用于ODS和脱垂痔的治疗,疗效显著,并将该技术命名为TST STARR+。2013年4月至2014年5月,武汉大学中南医院结直肠肛门外科运用该技术治疗ODS患者100例,疗效满意,现报道如下。 相似文献
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目的 探讨结缔组织生长因子(CTGF)对肾小管上皮细胞向间充质细胞转化的影响.方法 体外培养的人肾小管上皮细胞(HK-2),按是否用CTGF处理将其分为实验组和对照组.直接免疫荧光法、间接免疫化学检测培养72 h后肾小管上皮细胞E-cadherin、波形蛋白、α-平滑肌肌动蛋白((α-SMA)、细胞外信号调节激酶2(ERK2)的表达;Western blot方法 在72 h检测E-cadherin、波形蛋白和ERK2的表达;Boyden小室在1、3、5 d检测细胞迁移能力的变化.结果 (1)实验组上皮细胞表型标志蛋白E-cadherin随着时间的延长而表达递减,波形蛋白表达渐增,ERK2表达上调;(2)在第1天,实验组与对照组细胞迁移能力差异无统计学意义,第3天实验组迁移至滤膜下面细胞多于对照组,第5天实验组细胞迁移数明显高于对照组[(45.0±1.1):(14.0±1.2),P<0.05].结论 在体外,人肾小管上皮细胞由CTGF刺激表现出向间充质细胞转化的特性,并且ERK2信号转导通路可能参与了对这一过程的调控效应. 相似文献
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Objective To investigate the role of connective tissue growth factor ( CTGF) in epithelial mesenchymal transition of HK-2 cells in vitro.Methods HK-2 cells were randomly divided into two groups; (1) control group including cells cultured in DMEM medium supplemented with 10% fetal bovine serum only; and (2) experimental group including cells cultured in DMEM medium supplemented with 10% fetal bovine serum and recombinant CTGF at a final concentration of 5 p-g/L The cells were collected at 72 h time points.Direct immunoiluorescence staining and immunohistochemistry were used to evaluate the E-cadherin,Vimentin,α-SMA and ERK2 in cells.Western-blotting was used to detect the E-cadherin,Vimentin and ERK2 protein expression.Boyden Chamber was used to detect the migration of tubular endothelium at 1 d,3 d and S d.Results There were less E-cadherin but more Vimentin expressed in cells of the experimental group.The presence of α-SMA was detected at 48 h with peak at 72 h in the cells of the experimental group.On the first day,the cellular migration in the two groups showed no difference.However,after 3 days,the transformed cells migrated surpassed the control group with peak at the 5th day [ (45.0±1.1) : (14.0±1.2),P < 0.05 ) ].Conclusion Connective tissue growth factor induces mesenchymal transformation of HK-2 cells,in which the ERK2 signaling pathway may play an important role. 相似文献
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Objective To investigate the role of connective tissue growth factor ( CTGF) in epithelial mesenchymal transition of HK-2 cells in vitro.Methods HK-2 cells were randomly divided into two groups; (1) control group including cells cultured in DMEM medium supplemented with 10% fetal bovine serum only; and (2) experimental group including cells cultured in DMEM medium supplemented with 10% fetal bovine serum and recombinant CTGF at a final concentration of 5 p-g/L The cells were collected at 72 h time points.Direct immunoiluorescence staining and immunohistochemistry were used to evaluate the E-cadherin,Vimentin,α-SMA and ERK2 in cells.Western-blotting was used to detect the E-cadherin,Vimentin and ERK2 protein expression.Boyden Chamber was used to detect the migration of tubular endothelium at 1 d,3 d and S d.Results There were less E-cadherin but more Vimentin expressed in cells of the experimental group.The presence of α-SMA was detected at 48 h with peak at 72 h in the cells of the experimental group.On the first day,the cellular migration in the two groups showed no difference.However,after 3 days,the transformed cells migrated surpassed the control group with peak at the 5th day [ (45.0±1.1) : (14.0±1.2),P < 0.05 ) ].Conclusion Connective tissue growth factor induces mesenchymal transformation of HK-2 cells,in which the ERK2 signaling pathway may play an important role. 相似文献
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Objective To investigate the role of connective tissue growth factor ( CTGF) in epithelial mesenchymal transition of HK-2 cells in vitro.Methods HK-2 cells were randomly divided into two groups; (1) control group including cells cultured in DMEM medium supplemented with 10% fetal bovine serum only; and (2) experimental group including cells cultured in DMEM medium supplemented with 10% fetal bovine serum and recombinant CTGF at a final concentration of 5 p-g/L The cells were collected at 72 h time points.Direct immunoiluorescence staining and immunohistochemistry were used to evaluate the E-cadherin,Vimentin,α-SMA and ERK2 in cells.Western-blotting was used to detect the E-cadherin,Vimentin and ERK2 protein expression.Boyden Chamber was used to detect the migration of tubular endothelium at 1 d,3 d and S d.Results There were less E-cadherin but more Vimentin expressed in cells of the experimental group.The presence of α-SMA was detected at 48 h with peak at 72 h in the cells of the experimental group.On the first day,the cellular migration in the two groups showed no difference.However,after 3 days,the transformed cells migrated surpassed the control group with peak at the 5th day [ (45.0±1.1) : (14.0±1.2),P < 0.05 ) ].Conclusion Connective tissue growth factor induces mesenchymal transformation of HK-2 cells,in which the ERK2 signaling pathway may play an important role. 相似文献
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