Objective To compare the efficacy and adverse effects of rubomycin plus aracytidine(DA) dripping in bone marrow with DA dripping in vein in the treatment of acute nonlyphocytic leukemia (ANLL). Methods 60 cases of previously untreated ANLL patients were randomly divided into two groups, group A(DA dripping in bone marrow) and group B (DA dripping in vein). the efficacy and adverse effects of both groups were compared. Results The complete remission (CR) rate was 70.0% and 33.3% in group A and group B, and the total response rate was 86.7% and 50.0%, respectively. Both were significant higher than those of group B (P0.05). Conlusions The treating outcome was better in group A than that in group B for ANLL, with higher cure remission rate and lower toxic reaction.

砄bjective: To determine the effects of interleukin 1 receptor antagonist( IL lra) on the production of IL 6 induced by IL 1? in human gingival fibroblasts(HGFs). Methods:HGFs at passage 5 were exposed to various concentrations of IL 1? with or without IL 1r? . IL 6 in the culture medium was measured with a sandwish ELISA assay. Results:IL 6(?g/L) produced by HGFs exposed to IL 1? at the concentrations (?g/L) of 0.1, 1.0, 10 and 100 were 207?40.29, 235?80.78, 370?40.62, 570?68.17 and 737.5?83.47 respectively. While that by HGFs exposed to IL 1? at 10 ?g/L with IL 1r?(?g/L) at 1, 10, 100 and 1 000 were 387.5?49.69, 312.5?26.81, 242.5?25.86 and 217.5?21.65 respectively. Conclusion: IL lra can inhibite the IL 1? induced IL 6 production in HGFs.

Objective Cell therapy is a possible effective way to treat myelination disorder diseases.Cell therapy needs to apply a method for culturing oligodendrocyte precursor cells.Therefore,this study was to develop a stable,efficient and economical method for obtaining human oligodendrocyte precursor cells (OPCs) in order to provide cell required for clinical treatment.And this will provide a new option for clinical applications.Methods Human OPCs were obtained through magnetic bead sorting and cultured in OPCs proliferation medium.For a short-time (2,4,6,8days) and long-time culture,morphology of OPCs was observed.The fourth generation of OPCs was analyzed for expression of OPCs specific markers O4,Soxl0 and platelet derived growth factor alpla receptors(PDGFαR) and the capacity to differentiate into oligodendrocytes by immunofluorescence staining.At the same time,the effects of B27 and N1 on OPCs growth state were inspected as well.Results For a short-time culture,OPCs had typical bipolar or tripolar morphology and proliferated in good condition.For a long-time culture,all 4 generations OPCs had typical bipolar or tripolar morphology;the fourth generation OPCs highly(＞ 90％) expressed 04,Sox10 and PDGFαR,after induction,OPCs could be differentiated into oligodendrocytes.After 4 generations of long-time culture,OPCs already maintained the original sharp,high purity and had the capacity to differentiate into oligodendrocytes.It was indicated that this culture system was suitable for human OPCs for a long-time culture.Conclusions Overall,using this culture system,isolated human OPCs not only can be stably cultured and proliferated in vitro,but also have the capacity to differentiate into oligodendrocytes.From this reproducible method,a large number of human OPCs can be stably obtained in vitro as convenient as possible.And this will provide a new option for clinical applications.This method uses fewer cytokines.Therefore,this method will provide stable,efficient and economical OPCs for cell therapy of myelination disorders or myelin damage diseases.

BACKGROUND:We have found that oriented fibers can guide the alignment of smooth muscle cells in our previous experiments. Thus, we designed the experiment to prepare wel aligned polymeric fibers using electrospinning technology, aiming at guiding the growth of esophageal smooth muscle cells to maintain cellmorphology and biological function. OBJECTIVE:Using electrospinning technology, to fabricate isotropic and directed nano-fibrous scaffolds made of polycaprolacton, gelatin and silk fibroin. METHODS:Polycaprolacton/silk fibroin fibers at a ratio of 4:1 were prepared with proper parameters, including solution concentration, voltage and injection speed, under the self-made spinning system. The polycaprolacton/gelatin sheets with mass ratio of 2:1, 1:1 and 1:2, respectively, were also fabricated under suitable process parameters. Using the rol er col ector instead of the metal plate, polycaprolacton/gelatin nano-fibrous scaffold with good alignment of fibers was manufactured. RESULTS AND CONCLUSION:The isotropic polycaprolacton/silk fibroin scaffold with fiber diameter of (535.9±126.7) nm was prepared under conditions of solution concentration (0.08 g/mL), injection speed (1.6 mL/h) and voltage (22.5 kV), and these fibers were uniform with no beads. The isotropic polycaprolacton/gelatin scaffold with fiber diameter of (257.9±117.8) nm was prepared under conditions of solution concentration (0.10 g/mL), injection speed (0.8 mL/h) and voltage (22.5 kV). Using the rol er col ector instead of the previous metal plate, polycaprolacton/gelatin (w:w, 1:2) nano-fibrous scaffold with good alignment of fibers was manufactured. The process parameters were 3 000 r/min of rol ing speed, 0.8 mL/h of injection speed and 15 kV of voltage.

This paper is to test the physical precision of SGS-I?-knife treatment system. The total positional precision and?-treatement planning system (?-TPS) planning misdose are tested by film and ionization chamber. The precision of head target location is less than 0.88mm. The body target is less than 1.52mm. The error of single target point between the measured and the predicted doses is less than 0.52% and the error of multi target points is less than 3%. The isodose distribution (on axial plane) from the film is consistent with the predicted one. So, SGS-I?-knife can meet clinical requirements.

An on-line solid phase extraction-high performance liquid chromatography ( SPE-HPLC ) system was applied in the plasma pharmacokinetic study of highly active anti-cancer compound tyrosine kinase inhibitors (TEB-415) in mouse. The on-line SPE-HPLC method associated with Ultimate3000 system which was applied to the determination of the blood drug level of TEB-415 in mouse plasma. C18 column ( Venusil MP, 150 mm × 4. 6 mm, 5μm) was used as analytical column and the mobile phase consisted of acetonitrile-5 mmol/L monopotassium phosphate buffer ( pH 3 . 5 ) at a flow rate of 1 . 0 mL/min was used as the isocratic elution. An MF Ph-1 column (10 mm×4 mm, 5 μm) was used as on-line SPE column, and water and water-acetonitrile were used as the washing solvent and elution solvent respectively. The detection wavelength was set at 262 nm. The pharmacokinetic parameters were calculated by WinNonlin 5. 2 software. The linear range of the calibration curve was between 100 and 20000 μg/L, and the limit of qualification was 20 μg/L. The extraction recovery was between 90 . 5% and 94 . 6%. The RSD of intra-day and inter-day precision was less than 3. 5%. The accuracy of short-term stability, freeze-thaw stability and long-term stability were between 91. 49% and 101. 96%. After oral medication, the mean peak time (Tmax) of TEB-415 in mice was 5. 29 h, and the mean maximum concentration ( Cmax) was 3403μg/L. The area under the curve ( AUC) of TEB-415 was 24600 μg/L·h. This drug's mean half-life was 3. 84 h, and its mean retention time (MRT) was 6. 56 h. These parameters suggested that TEB-415 had appropriate rate of absorption and elimination with preferable bioavailability.

Objective To investigate the feasibility and clinical effect of immediate ureterovesical reimplantation after ureteral rupture during laparoscopic hysterectomy. Methods From August 2010 to December 2015, 5 cases of ureteral rupture during the operation of laparoscopic hysterectomy were treated with immediate ureterovesical reimplantation under laparoscopy. Results All operations were successfully performed without transversion to open surgery. No patients with urinary leakage occurred. The mean follow-up were 21 months (range 3-60 months) . No cases with ureteral stricture were observed. Slight urine reflux was found in two patients, of whom obvious hydronephrosis and renal damage were not found. Conclusion Immediate ureterovesical reimplantation under laparoscopy is a feasible, safe and minimal invasive method for treatment of ureteral ruputure during laparoscopic hysterectomy.

Objective To investigate the effects of bufalin in reversing hepatocyte growth factor ( HGF)?induced resistance to afatinib in H1975 lung cancer cells, and explore its possible mechanism. Methods The afatinib?resistant H1975 lung cancer cells ( H1975AR) were induced by exogenous HGF and transfected with recombinant adenoviral vector Ad?HGF?GFP. The cytostatic effects of bufalin, afatinib and bufalin plus afatinib on H1975AR cells were evaluated by MTT assay. The impact of combined therapy with bufalin and afatinib on invasion of H1975AR cells was determined by transwell migration assay. The concentrations of HGF in the culture supernatants of H1975/Vec and H1975/HGF cells were determined by ELISA. The expression of EGFR, cMET and EMT signal pathway?related proteins in H1975AR cells treated with bufalin, afatinib and bufalin plus afatinib were detected by Western blot. Results The results of MTT assay showed that afatinib did not inhibit the growth of H1975 cells, but after 72 h of the combined treatment with bufalin and afatinib and in the presence of HGF, the growth rate of H1975 cells was (38.67±8.76)%, significantly lower than the growth rate of (63.45±12.65)% in the H1975 cells treated with HGF alone (P<0.05) . The results of transwell migration assay showed that in the presence of HGF, afatinib plus bufalin combination therapy markedly decreased the number of invaded H1975 cells through the Matrigel chamber (48.98±11.43), significantly lower than the 118.92±37.29 of afatinib?treated or the 88.84±19.53 of bufalin?treated cells (P<0.05 for all). The result of ELISA showed that H1975/HGF cells secreted high levels of HGF, and afatinib and bufalin had no effect on the HGF secretion in H1975/HGF cells. The results of Western blot analysis showed that the expression of p?EGFR, p?cMet, p?AKT, p?ERK, vimentin and snail in H1975AR cells treated with bufalin puls afatinb was down?regulated markedly, and the expression of E?cadherin was up?regulated markedly. Conclusions Combination of bufalin and afatinib strongly inhibits the growth of H1975AR lung cancer cells and decreases their invasion ability. The possible mechanism of combined treatment with bufalin and afatinib may be related to the blocking of cMet/PI3K/AKT and cMet/MAPK/ERK pathways and inhibiting of epithelial?mesenchymal transition.

Objective To investigate the effects of bufalin in reversing hepatocyte growth factor ( HGF)?induced resistance to afatinib in H1975 lung cancer cells, and explore its possible mechanism. Methods The afatinib?resistant H1975 lung cancer cells ( H1975AR) were induced by exogenous HGF and transfected with recombinant adenoviral vector Ad?HGF?GFP. The cytostatic effects of bufalin, afatinib and bufalin plus afatinib on H1975AR cells were evaluated by MTT assay. The impact of combined therapy with bufalin and afatinib on invasion of H1975AR cells was determined by transwell migration assay. The concentrations of HGF in the culture supernatants of H1975/Vec and H1975/HGF cells were determined by ELISA. The expression of EGFR, cMET and EMT signal pathway?related proteins in H1975AR cells treated with bufalin, afatinib and bufalin plus afatinib were detected by Western blot. Results The results of MTT assay showed that afatinib did not inhibit the growth of H1975 cells, but after 72 h of the combined treatment with bufalin and afatinib and in the presence of HGF, the growth rate of H1975 cells was (38.67±8.76)%, significantly lower than the growth rate of (63.45±12.65)% in the H1975 cells treated with HGF alone (P<0.05) . The results of transwell migration assay showed that in the presence of HGF, afatinib plus bufalin combination therapy markedly decreased the number of invaded H1975 cells through the Matrigel chamber (48.98±11.43), significantly lower than the 118.92±37.29 of afatinib?treated or the 88.84±19.53 of bufalin?treated cells (P<0.05 for all). The result of ELISA showed that H1975/HGF cells secreted high levels of HGF, and afatinib and bufalin had no effect on the HGF secretion in H1975/HGF cells. The results of Western blot analysis showed that the expression of p?EGFR, p?cMet, p?AKT, p?ERK, vimentin and snail in H1975AR cells treated with bufalin puls afatinb was down?regulated markedly, and the expression of E?cadherin was up?regulated markedly. Conclusions Combination of bufalin and afatinib strongly inhibits the growth of H1975AR lung cancer cells and decreases their invasion ability. The possible mechanism of combined treatment with bufalin and afatinib may be related to the blocking of cMet/PI3K/AKT and cMet/MAPK/ERK pathways and inhibiting of epithelial?mesenchymal transition.

OBJECTIVETo investigate the effects of bufalin in reversing hepatocyte growth factor (HGF)-induced resistance to afatinib in H1975 lung cancer cells, and explore its possible mechanism.

METHODSThe afatinib-resistant H1975 lung cancer cells (H1975AR) were induced by exogenous HGF and transfected with recombinant adenoviral vector Ad-HGF-GFP. The cytostatic effects of bufalin, afatinib and bufalin plus afatinib on H1975AR cells were evaluated by MTT assay. The impact of combined therapy with bufalin and afatinib on invasion of H1975AR cells was determined by transwell migration assay. The concentrations of HGF in the culture supernatants of H1975/Vec and H1975/HGF cells were determined by ELISA. The expression of EGFR, cMET and EMT signal pathway-related proteins in H1975AR cells treated with bufalin, afatinib and bufalin plus afatinib were detected by Western blot.

RESULTSThe results of MTT assay showed that afatinib did not inhibit the growth of H1975 cells, but after 72 h of the combined treatment with bufalin and afatinib and in the presence of HGF, the growth rate of H1975 cells was (38.67 ± 8.76)%, significantly lower than the growth rate of (63.45 ± 12.65)% in the H1975 cells treated with HGF alone (P < 0.05). The results of transwell migration assay showed that in the presence of HGF, afatinib plus bufalin combination therapy markedly decreased the number of invaded H1975 cells through the Matrigel chamber (48.98 ± 11.43), significantly lower than the 118.92 ± 37.29 of afatinib-treated or the 88.84 ± 19.53 of bufalin-treated cells (P < 0.05 for all). The result of ELISA showed that H1975/HGF cells secreted high levels of HGF, and afatinib and bufalin had no effect on the HGF secretion in H1975/HGF cells. The results of Western blot analysis showed that the expression of p-EGFR, p-cMet, p-AKT, p-ERK, vimentin and snail in H1975AR cells treated with bufalin puls afatinb was down-regulated markedly, and the expression of E-cadherin was up-regulated markedly.

CONCLUSIONSCombination of bufalin and afatinib strongly inhibits the growth of H1975AR lung cancer cells and decreases their invasion ability. The possible mechanism of combined treatment with bufalin and afatinib may be related to the blocking of cMet/PI3K/AKT and cMet/MAPK/ERK pathways and inhibiting of epithelial-mesenchymal transition.

Antineoplastic Agents ; pharmacology ; Antineoplastic Combined Chemotherapy Protocols ; pharmacology ; Bufanolides ; pharmacology ; Cadherins ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Coloring Agents ; Drug Resistance, Neoplasm ; drug effects ; Epithelial-Mesenchymal Transition ; drug effects ; Hepatocyte Growth Factor ; pharmacology ; Humans ; Lung Neoplasms ; drug therapy ; metabolism ; pathology ; MAP Kinase Signaling System ; Neoplasm Proteins ; metabolism ; Phosphatidylinositol 3-Kinases ; Quinazolines ; pharmacology ; Receptor, Epidermal Growth Factor ; Signal Transduction ; Tetrazolium Salts ; Thiazoles