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Objective To investigate whether immunotherapy with dendritic cells (DC) transduced with glypican 3 (GPC3) (DC-GPC3) and cocultured with cytokine-induced killer cells (CIK) (DCIK-GPC3) is capable of inhibiting hepatocellular carcinoma (HCC) in vivo. Methods The hepatocarcinoma cell-bearing mouse models were established and divided randomly into four groups (A, B, C, D) for the injection of normal saline (NS), CIK, DC-CIK, and DCIK-GPC 3, respectively. Changes of tumor size, tumor inhibitory rate and cell apoptosis were compared between four groups. Results After treatment, the tumor volumes and weights were significantly decreased in D group compared with those of A, B and C groups (P<0.01). The inhibition rate was significantly increased in D group compared with that of B group and C group (P<0.01). The apoptotic rate was significantly increased in D group compared with that of A group, B group and C group (P<0.01). Conclusion DCIK-GPC3 can significantly inhibit tumor growth in vivo.
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Objective To investigate whether immunotherapy with dendritic cells (DC) transduced with glypican 3 (GPC3) (DC-GPC3) and cocultured with cytokine-induced killer cells (CIK) (DCIK-GPC3) is capable of inhibiting hepatocellular carcinoma (HCC) in vivo. Methods The hepatocarcinoma cell-bearing mouse models were established and divided randomly into four groups (A, B, C, D) for the injection of normal saline (NS), CIK, DC-CIK, and DCIK-GPC 3, respectively. Changes of tumor size, tumor inhibitory rate and cell apoptosis were compared between four groups. Results After treatment, the tumor volumes and weights were significantly decreased in D group compared with those of A, B and C groups (P<0.01). The inhibition rate was significantly increased in D group compared with that of B group and C group (P<0.01). The apoptotic rate was significantly increased in D group compared with that of A group, B group and C group (P<0.01). Conclusion DCIK-GPC3 can significantly inhibit tumor growth in vivo.
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AlM: To silent hypoxia inducible factor-1α ( HlF-1α) gene in malignant melanoma of the choroid cell by small interference RNA ( siRNA ) and investigate its effect on the expression of matrix metalloproteinase-2 ( MMP-2 ) in the choroid cell line human uveal melanoma cell (OCM-1) in hypoxia environment.METHODS:OCM-1 cells cultured on culture flask were divided into normal group and hypoxia group. Hypoxia group were divided into five groups: simple hypoxic group, and interference group, and negative control group, and positive control group, and liposome group. Normal group cells were cultured on DMEM culture flask with 10% FBS, 100U/mL penicillin, 100μg/mL streptomycin as well as high concentration of glucose. The cells were maintained at 37℃ in a humidified 5% CO2 incubator. Cells in good condition were selected for experiment. For hypoxia group, chemical hypoxia inducer CoCl2 was added into nutrient medium at the concentration of 100μmol/L to simulate hypoxia microenvironment. We designed and synthesised siRNA ( siRNA + negative control+positive control ) , the target sequences of the HlF-1α to transfect hypoxic malignant melanoma of the choroid cell. SiRNA including HlF-1α siRNA, β-actin siRNA and negative control group synthesized in vitro transfected hypoxic OCM - 1 cell through Lipofectamine2000. The expression of HlF-1α, MMP-2 gene and the protein were detected by RT-PCR and Western blot. RESULTS: Compared with the normal group, the expression of HlF-1α mRNA was not obviously changed (P>0. 05), but the expression of HlF-1α protein and MMP- 2 mRNA protein was significantly higher ( P0. 05).CONCLUSlON: Hypoxia status may upregulate the HlF-1α in OCM-1 cells by increasing the expression of protein. Hypoxia can also inactivate MMP-2, resulting in upregulation of MMP-2 RNA and the expression of its protein. The expression of HlF-1α and MMP-2 mRNA can be down-upregulated by transfecting OCM-1 with HlF-1α siRNA.
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Objective To evaluate the clinical effect in the treatment of the young patients(≤45 years old) with acute myocardial infarction(AMI)underwent emergent percutaneous transluminal coronary angioplasty(PTCA) combined with Lipo-PGE_1.Methods 39 patients with AMI(paroxysm within 12 hours),were underwent emergent PTCA(coronary stem performed in some patients),including 18 cases which were treated combined with Lipo-PGE_1 in the mean time.And the clinical efficacy and the results of short-period follow-up were recorded.Results The in- farctive vasculars were re-open in 37 patients(23 cares were routinely placed translunrinal srents),and the successful rate was 94.9 %.Those who also used Lipo-PGE_1 were re-open in 17 patients.The successful rate was 94.4 %,their ST segments on EKG 30 minutes after operations reduced significantly than that of patients who did not use Lipo- PGE_1,their cardial functions were also improved significantly 24 hours after operations and no side effects on blood pressure and heart rate were observed.Conclusion The emergent PTCA combined with Lipo-PGE_1 for acute my- ocardial infarction can protect the cardial function and show a better early therapy effect.
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<p><b>BACKGROUND</b>Both real-time three-dimensional echocardiography (RT3DE) and myocardial contrast echocardiography (MCE) are novel imaging techniques. The purpose of this study was to confirm the feasibility and accuracy of RT3DE combined with MCE for quantitative evaluation of myocardial perfusion defects.</p><p><b>METHODS</b>Thirteen dogs underwent ligation of the left anterior descending artery (LAD, n = 6) or distal branch of the left circumflex artery (LCX, n = 7) under general anaesthesia. Three to four ml of a perfluoropropane (C3F8) microbubble contrast agent was injected intravenously to assess the resulting myocardial perfusion defects with a commercially available Philips SONOS-7500 ultrasound system. After removal of the dog hearts, Evans blue dye was injected via the left and right coronary arteries to stain the myocardium at risk. In vitro anatomic measurements of myocardial mass after removal of the animals' hearts were used as controls.</p><p><b>RESULTS</b>Left ventricular (LV) mass determined by RT3DE ranged 36.7 - 68.9 g [mean, (54.6 +/- 9.6) g] before coronary artery ligation, and correlated highly (r = 0.99) with in vitro measurement of LV mass [range, 38.9 - 71.1 g; mean, (55.6 +/- 9.3) g]. There was no significant difference between RT3DE and in vitro measurements of LV mass [range, 36.7 - 68.9 g; mean, (51.3 +/- 12.5) g. Or range, 38.9 - 71.1 g; mean, (53.7 +/- 12.3) g, respectively] and under-perfused mass [range, 0 - 21.4 g; mean, (12.0 +/- 6.9) g. Or range, 0 - 19.8 g; mean, (10.8 +/- 6.3) g, respectively] after the LAD ligation (P > 0.05). Likewise, no significant difference was present between RT3DE and in vitro measurements of LV mass [range, 50.1 - 65.4 g; mean, (57.5 +/- 5.9) g. Or range, 51.5 - 65.8 g; mean, (57.3 +/- 6.4) g, respectively] and under-perfused mass [range, 0 - 25.6 g; mean, (13.3 +/- 9.6) g. Or range, 0 - 22.7 g; mean, (12.8 +/- 8.1) g, respectively] after the LCX ligation (P > 0.05). For all the animals with coronary ligation, LV mass measured by RT3DE ranged 35.9 - 68.6 g [mean, (54.8 +/- 10.0) g] and there was no significant difference between RT3DE and in vitro measurements of LV mass and under-perfused mass (P > 0.05, r = 0.99). Further, the under-perfused mass derived from RT3DE [range, 0 - 25.6 g; mean, (12.7 +/- 8.2) g] correlated strongly with the in vitro measurements [range, 0 - 22.7 g; mean, (11.9 +/- 7.2) g] (r = 0.96).</p><p><b>CONCLUSION</b>RT3DE with MCE is a rapid and accurate method for estimating LV myocardial mass and quantifying perfusion defects.</p>