ABSTRACT
Objective To investigate the predisposing locations of active hemorrhage in patients with esophageal variceal bleeding. Methods Data of 823 patients with acute esophageal and gastric variceal hemorrhage receiving emergency gastroscopy diagnosed from January 2003 to December 2013 were retrospectively studied. The location and site of active hemorrhage or stigmata were analyzed and its relationship with active hemorrhage was discussed. Results A total of 372(45. 2%,372/823) patients with active bleeding and stigmata were found under emergency endoscopy. Among 372 patients, 190 got accurate hemorrhage and stigmata location and site description. Bleeding or stigmata in 58(30. 5%) patients was 28-32 cm from incisor in group A, and that in 132 (69. 5%) patients was more than 35 cm in group B ( χ2＝57. 642, P＜0. 000 1). In 190 cases, the proportion of bleeding or stigmata at 3:00 point was the highest (37%,70/132), followed by those at 12:00 point(30%,58/132),6:00 point(24%,45/132),and 9:00 point (9%,17/132). The change trend of the percentage of each point in group A and group B was the same as that in all cases. The percentage of almost all points in group B was significantly higher than that in group A except that at 9:00 point ( P＜0. 000 1).Conclusion Esophageal variceal bleeding in cirrhosis is more common at 3:00 point, 6:00 point and 12:00 point of esophagus, and the high risk area is 35 cm below the incisors.
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Objective To explore the mechanism and way for CT10 regulator of kinase like (CRKL) involving in drug resistance in leukemia cells. Methods The four major proteins included Ras protein, signal transducer and activator of transcripton 5 (STAT5) protein, phosphoinositide 3-kinase (PI3K) protein and paxillin protein in leukemia which involved in signal transduction pathway of CRKL. The expressions of those proteins were detected by Western-blot and immunofluorescent staining and confocal laser scanning microscopy. Results Compared with K562/S cells, the expressions of Ras(41.52±15.47 vs. 23.74±8.67) and PI3K (35.60±12.48 vs. 10.09±0.005) protein were up-regulated in K562/ADM cells (t=3.01,6.13;both P<0.05), while there were no significant changes in the expressions of paxillin (20.10±11.89 vs. 23.11±12.40) and STAT5 protein (25.72±14.46 vs. 17.58±9.21) between K562/S cells and K562/ADM cells(t=0. 18,1.43;both P>0. 0S). Conclusions Ras and PI3K protein may play a role in the multidrug resistance of K562 cell line, while paxillin and STAT5 protein may be not involved in the formation of resistant in K562 cells.
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Objective To investigate the role of CRKL activity in leukemia cells with muhidrug resistance and find new factor related to multidrug resistance. Methods By flow cytometry, CRKL activity was compared in K562, HL-60 cells and its resistance cells. The change of CRKL activity was observed in sensitive cells treated with and withdrawal daunorubicin. Results With the comparison of K562, HL-60 sensitive cells, in K562, HL-60 resistant cell lines, the level of CRKL phosphorylation in K562, HL-60 resistance cells treated with daunombicin 72 hours increased markedly. The level of CRKL phosphorylation was time-dependent with chemotherapy drugs, not change of CRKL activity was found in Jurkat ceils.Conclusion The level of CRKL activity is new factor related to muhidrug resistance in leukemia cells.
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Objective To construct a lentiviral vector carrying CRKL gene RNA interfering( RNAi ).Methods The CRKL RNAi was selected and subcloned into the lentiviral vector,pGCL-GFP(including U6 promotor and green fluorescent protein),generating the lentiviral vector LV-shCRKL.The corrected CRKL was confirmed by endoenzyme digestion ,sequencing.Recombinant lentiviruses were produced by 293T cells following the eo-transfection of LV-shCRKL,with the packaging plasmids pHelper1.0 and pHelper2.0.The virus titer was detected by GFP expressions in 293T cells.Results Plasmid LV-shCRKL carried the correct sequence.The recombinant lentiviruse LV-shCRKL could be produced by co-transfection of LV-shCRKL to 293T cells.Conclusion The recombinant lentiviruse vector LV-shCRKL is constructed successful.