老年胃癌患者的临床心理特点及护理对策

目的 探讨老年胃癌患者的临床心理特征并寻找合理的护理对策,以减轻胃癌患者的痛苦.方法 对我院2009年1月至2011年1收治的40例老年胃癌患者采用终腹近端胃切除术的治疗方式,适宜的护理手段,观察临床心理特点.结果 达到根除效果在80％左右,姑息性的低于10％,手术后产生并发症的超过30％,经过术后的有效护理,使得老年患者的心理充分缓解,降低了死亡率.结论 不同心理特点的老年胃癌患者通过相应的护理对策有效降低了并发症,提高了手术的根治性,取得了良好的效果.     

特发性肠系膜静脉硬化性肠炎1 例及文献回顾

特发性肠系膜静脉硬化性肠炎在临床上十分罕见,通常以反复腹痛、腹胀、呕吐等肠梗阻症状多见,极 易误诊。患者肠系膜断层扫描可见其典型的肠管周围沿血管走行的条索状高密度影,并可见血管钙化影,M-NBI肠 镜可见蜂窝状的毛细血管网消失,微血管结构紊乱,血管密度增加。     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

GW4064激活FXR受体下调肝星状细胞Ⅰ型胶原及TGFβ1的表达

目的探讨法尼酯衍生物X受体(FXR)配体GW4064对TNF-α作用后HSC-T6细胞系I型胶原及TGFβ1表达的影响。方法 TNF-α作用于HSC-T6后,应用实时荧光定量PCR法和Westernblot法检测FXR、I型胶原及TGFβ1表达的变化;再运用GW4064作用已被TNF-α作用的HSC-T6,再次应用实时荧光定量PCR法和Westernblot法检测FXR、I型胶原及TGFβ1表达的变化。结果 TNF-α能使HSC-T6表达FXR减少,而I型胶原及TGFβ1表达增加;GW4064作用HSC-T6后则明显增加FXR表达,从而减少I型胶原及TGFβ1表达。结论 GW4064通过激活FXR抑制HSC表达I型胶原及TGFβ1,为FXR配体治疗肝纤维化提供实验依据。     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

TPARM对人结直肠癌细胞株SW480增殖、凋亡、侵袭及迁移的影响

目的 探讨四肽重复结构域(TTC)12,也被称为TPARM,其表达对人结肠癌细胞SW480增殖、凋亡、侵袭及迁移的影响。方法 将人结肠癌SW480细胞株分为3组：NC组、TPARM-siRNA组和Scr-siRNA组。采用实时荧光定量聚合酶链反应(qPCR)法和Western印迹法检测各组TPARM mRNA和蛋白表达。细胞计数试剂盒(CCK)8法、平板克隆法测定各组TPARM表达对SW480细胞增殖的影响。Western印迹法检测TPARM表达对各组周期相关蛋白及凋亡相关蛋白的表达。流式细胞术检测各组TPARM表达对SW480细胞凋亡的影响。Transwell小室侵袭实验和划痕实验观察TPARM表达对SW480细胞侵袭、迁移能力的影响。结果 与NC组、Scr-siRNA组比较,转染TPARM-siRNA后,SW480细胞中TPARM mRNA及蛋白表达水平均明显降低(P<0.05)。分别与NC组和Scr-siRNA组比较,TPARM-siRNA转染组SW480细胞增殖明显减少(P<0.05),周期蛋白依赖性激酶(CDK)2、CDK4、CDK6的蛋白表达明显下降(P<...