Objective:To study the curative effect of hydrotalcite combined with omeprazole in the treatment of gastric ulcer with gastric bleeding. Methods:Seventy-six patients with gastric ulcer and bleeding in the stomach were selected and randomly divided into two groups. Thirty-two patients in the control group were treated with omeprazole alone while 44 patients in the observation group were treated with hydrotalcite combined with omeprazole. The therapeutic effects were compared between the two groups. Results:The total effective rate in the observation group was 100% while that was 87. 5% in the control group,and the difference between the two groups was statistically significant(P<0. 05). The comprehensive score of symptoms of the patients in the observation group was(4. 2 ± 1. 2)while that was(6. 2 ± 1. 4)in the control group,and the difference was significant(P<0. 01). The abdominal pain,abdominal distention and belching remission time in the observation group were slightly shorter than those in the control group(P<0. 05)and the time of hematemesis and hemafecia remission was significantly shorter than that in the control group(P<0. 05). After the 3-month treatment,the re-bleeding rate in the observation group was 6. 82%,which was slightly better than that in the control group,and the difference had no statistical significance(P<0. 05). The incidence of adverse reactions in the observation group was 9. 09% while that was 6. 25% in the control group,and there was no significant difference between the two groups(P>0. 05). Conclusion:Hydro-talcite combined with omeprazole in the treatment of gastric ulcer with gastric bleeding is effective and safe.

Objective To select the aptamer to an extracellular soluble fragment of recombinant human TGF-? receptor Ⅱ (TGF-? RⅡ) in order to antagonize TGF-? effectively by using systematic evolution of ligants by exponential enrichment (SELEX). Methods Initial random RNA library was transcripted in vitro from ssDNA 5′-TAATACGACTCACTATAGGGAGGACGATGCGG-N60-CAGACGACTCCCCGA-3′; rhTGF-? RⅡ was used as target protein. Totally,selection of 8 times was carried out in SELEX experiment. Membrane binding assay was performed to detect the evolution of enriched RNA library; Electrophoretic mobility shift assay (EMSA) was done to determine the affinity between the selected nucleic acid sequence and TGF-? RⅡ. Results Evolution of the enriched RNA library along the increased affinity to TGF-? RⅡ was observed with the development of selection. Two types of dominant sequences were isolated and named as sequence A and sequence B. In membrane binding assay,both sequences A and B showed obvious affinity to TGF-? RⅡ. However,no retarded bands were seen in EMSA. Conclusion The affinity of sequences A and B to TGF-? RⅡ is beyond satisfaction. However,possible sequences with improved affinity to TGF-? RⅡ can be selected by post-SELEX on the basis of candidate sequences A and B.

Objective To evaluate the effect and mechanism of IL‐6 induced Gefitinib resistance in non small cell lung cancer (NSCLC) .Methods The sensitivity of cells to Gefitinib ,the invasion ability of cells and the expression of phosphorylated p‐mTOR was assessed by MTT assay ,Transwell assay and Western blot ,respectively .PC‐9psb388 stable over expressing human recombi‐nant IL‐6(hrIL‐6) cell line was established by transfecting PC‐9 cells with a lentivirus psb388 expressing IL‐6 and stable transfecta‐nts over‐expressing IL‐6 in human lung cancer cell line PC‐9 .The sensitivity of cells to Gefitinib ,the invasion ability ,expression of p‐mTOR were then detected .PC‐9/PC‐9psb388 xenografts were established and the expression of p‐mTOR and IL‐6 in tumor sec‐tions were then detected .Results The sensitivity of PC‐9 cells to Gefitinib was reduced by IL‐6 ,the invasion ability of PC‐9 cells and the expression of p‐mTOR was significantly increased with IL‐6 treatment .The sensitivity of PC‐9 cells to Gefitinib was promi‐nent higher in PC‐9psb388 cells ,while the invasion ability of PC‐9psb388 cells and the expression of p‐mTOR was higher than PC‐9 cells .The sensitivity to Gefitinib was improved and expression of p‐mTOR reduced in rapamycin‐treated PC‐9psb388 cells and IL‐6 stimulated PC‐9 cells .Tumor volume of PC‐9psb388 xenografts was significantly higher than that of PC‐9 cells .The expression of p‐mTOR and IL‐6 in tumor sections of PC‐9psb388 group were higher than that of PC‐9 group .Conclusion IL‐6 could elevate the expression of p‐mTOR to induce Gefitinib resistance in non small cell lung cancer (NSCLC) .

Objective: To explore the synergistic effect of silibinin combined with crizotinib on anaplastic lymphoma kinase positive (ALK+ ) non-small cell lung cancer (NSCLC) cells and its mechanism. Methods: H2228 and H3122 cells were treated with silibinin, crizotinib alone or in combination. Cell proliferation was measured by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and colony formation assay. Migration or invasion ability was tested by wound healing assay or transwell assay, respectively. Expressions of E-Cadherin and vimentin protein were examined by immunofluorescence staining. The protein expressions of ALK, p-ALK, E-Cadherin and Vimentin were detected by western blotting.The anti-cancer effect of silibinin combined with crizotinib in vivo was determined by subcutaneously injecting 2×10⁶ H2228 cells into immunodeficient nude mice. Results: The result of MTT assay showed that the cell viability of H2228 or H3122 treated with 100 μmol/L silibinin was (88.38±4.10)% or (72.27±3.62)%, respectively, marginally decreased compared with that of the control. The 50% inhibitory concentration (IC₅₀) of H2228 cells treated with crizotinib alone or combined with 100 μmol/L silibinin was (917.10±7.75) nmol/L or (238.73±7.67) nmol/L, respectively. The IC₅₀ of H3122 cells treated with crizotinib alone or combined with 100 μmol/L silibinin was (472.50±15.70) nmol/L or (206.10±12.01) nmol/L, respectively. The IC_50s of H2228 and H3122 cells were significantly decreased by combined treatment of crizotinib and silibinin compared to crizotinib treatment alone (P<0.01). When compared with the control group, colony forming ratios of H2228 cells were (83.34±2.72)% in 100 μmol/L silibinin treatment group, (69.42±3.06)% in 400 nmol/L crizotinib treatment group and (27.32±1.42)% in combined treatment group. When compared with the control group, colony forming ratios of H3122 cells were (84.45±5.67)% in 100 μmol/L silibinin treatment group, (45.02±5.83)% in 400 nmol/L crizotinib treatment group and (17.43±3.83)% in combined treatment group. Silibinin combined with crizotinib treatment significantly inhibited the colony formation ability of H2228 and H3122 cells (P<0.01). Migration and invasion results showed that combined treatment of crizotinib and silibinin markedly inhibited the migration and invasion ability of H2228 cells (P<0.01). Western blot results indicated that treated with silibinin alone or in combination of crozitinib for 48 hours, the protein level of E-cadherin in H2228 cells was upregulated, while the expressions of p-ALK and vimentin were downregulated, without obvious alteration of ALK protein expression. In the xenograft model, the mean tumor weight was (9.40±2.58)g in crizotinib treatment group and (4.58±1.07)g in the combined treatment group. The inhibitory effect of tumor growth in vivo of combined treatment was significantly superior to that of crizotinib treatment alone (P<0.05). Conclusion Silibinin enhances the inhibitory effect of crizotinib on ALK positive NSCLC cells, which may be associated with suppression of ALK activity and mesenchymal-epithelial transition.