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We report a rare but serious case of upper gastrointestinal hemorrhage from hepatic artery pseudoaneurysm. Clinical Presentation and Intervention: An 11-year-old child with a history of hepatic trauma 6 months before was admitted for hematemesis and melena. Repeat ultrasound examination showed a 3.6 _ 2.8 cm anechoic area with clear border in the right hepatic lobe. Selective angiography confirmed the presence of a pseudoaneurysm of the right hepatic artery. Transcatheter arterial embolization was used to successfully treat the pseudoaneurysm. This report shows that hepatic artery pseudoaneurysm should be considered as a possible cause of upper gastrointestinal hemorrhagefollowing known hepatic injury. A high index of suspicion, repeated Doppler ultrasound and timely selective angiography are required for diagnosis. Embolotherapy is the treatment of choice
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Objective: To elucidate the relationship between Notch3 expression and chemosensitivity of human colon carcinoma cell line SW620 to topotecan. Methods: Notch3 siRNA was transfected into SW620 cells, and the expression of Notch3 in SW620 cells was examined by Western blotting. After transfected with Notch3 siRNA for different time peri-ods, SW620 cells were further treated with topotecan, and the proliferation of SW620 cells was detected by MTT assay; the apoptosis of SW620 cells was detected by Hoechst 33342 staining and flow cytometry. Caspase-3 activation in SW620 cells was examined by caspase-3 activation kit. Results: Notch3 siRNA transfection remarkably inhibited Notch3 protein expression in SW620 cells. The IC_(50) of topotecan in Notch3 siRNA-transfected group was significantly decreased compared with that in the Ctrl siRNA group (P <0.05). Silence of Notch3 expression in SW620 cells by Notch3 siRNA remarkably promoted apoptosis (P < 0.05) and caspase-3 activation (P < 0.05) of SW620 cells induced by topotecan. Conclusion: Notch3 down-regulation by siRNA in SW620 cells can enhance the chemosensitivity cells to topotecan.
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Objective To construct the recombinant retroviruses vector PCLNRX-ICN and to explore over-activation Notch1 on the growth of human colon carcinoma cells HT-29.MethodsICN(intracellular domain of Noctch1) genes were inserted into retrovirus expression vector pCLNRX.The expression vector pCLNRX-ICN and packaging vector pCL-10A1 were co-transfected into 293 package cells.The recombinant retroviruses were used to infect HT-29 cells.After being infected,proliferation of HT-29 cells was observed by MTT assay.The expression of c-Myc and ?-catenin detected by RT-PCR and Western Blot.ResultsRecombinant retrovirus vector pCLNRX-ICN was successfully constructed.Overactivation of Notch1 by over-expressing exogenous ICN significantly inhibited the growth of HT-29 cells,and down-regulated ?-catenin,a key regulator of Wnt signaling,in protein level but not in mRNA levels.However,the mRNA or protein levels of c-Myc were not affected by overactivation of Notch1.ConclusionOver-activated Notch1 signaling could inhibit the growth of HT-29 cells partly through down-regulation of Wnt signaling independent of c-Myc inhibition.
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Objective To explore the regulatory function of over-expression of NOTCH-1 in TNF?-induced apoptosis of gastric carcinoma carcinoma BGC-823 cells.Methods BGC-823 cells were infected with retrovirus recombined with intracellular domain of NOTCH-1.The cell clones,into which objective genes had been transfected,were obtained after screening with G-418.Before and after incubation with TNF?,MTT assay,flow cytometry,Western blot and EMSA were used to detect cell growth,apoptosis,expressions of NOTCH-1,NF-?B and caspase-3 activity.Results There was stronger expression of NOTCH-1 and its target gene HES-1 in the cells transfected with NOTCH-1 gene than that of control.After TNF? treatment,the rates of killing and apoptosis in NOTCH-1-transfected cells were all lower than those in control cells.Moreover,we showed over-expression of NOTCH-1 suppressed caspase-3 activation induced by TNF?.However,TNF?-induced activation of NF-?B was not affected by over-expression of NOTCH-1.Conclusion Over-expression of NOTCH-1 significantly protects BGC-823 cells from apoptosis and growth suppression induced by TNF?.This effect is mediated,at least in part,through inhibition of caspase-3 activation independent of NF-?B.
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Objective:To construct pEGFP-C1-Smad4 expression vector and to observe the influence of Smad4 over-expression on the proliferation of human gastric cancer SGC7901 cells and its relationship with nuclear factor kappa B (NF-?B). Methods:Recombinant expression vector pEGFP-C1-Smad4 was constructed and was used to transfect human gastric cancer SGC7901 cells. EGFP expression in transfected cells was detected by fluoroscopy. Smad4 and NF-?B expression in transfectant was examined by Western blotting. Effect of Smad4 over-expression on activation of NF-?B and proliferation of transfected SGC7901 cells were examined by electrophoretic mobility shift assay (EMSA) and MTT assay,respectively. Results:Expression of EGFP in transfected SGC7901 cells was observed under fluorescence microscope. Smad4 was over-expressed in transfected SGC7901 cells,accompanied by down-regulation of NF-?B p65 expression in the tranfectants. EMSA and MTT demonstrated that Smad4 over-expression significantly inhibited the activation of NF-?B and the proliferation of SGC7901 cells (P