cryⅢ gene,they were found in 75 6%,67 9%,58 4% and14 5% of the strains respectively,no cryⅠ Ⅴ gene was found,10cry gene combination types were concluded.The Bt isolates which contained cryⅠ genes were further characterized by additional PCR detection with specific primers of the cryⅠAc,cryⅠC and cryⅠE genes.20 Bt isolates which contained cryⅠAc,cryⅠC,cryⅡ and cryⅤ genes were found,among them the strain Bt\|15A3 is high toxic to Heliothis armigera,Spodoptera exigua and Plutella xylostella,and has potential developing and applying value.

Objective To investigate mutation and deletion of genes mecR1 and mecI in clinical methicillin-resistant staphylococci isolates and study the mutation and deletion have effect on gene mecA expression and drug resistance phenotype.Metheods PCR was used to detecte gene mecA and the regulatory genes mecR1 and mecI in staphylococci which were separated from clinical specimen in 2006,then the sequence of gene mecI was determined and compared with the sequence obtains from pre-MRSA strain N315(GI:BA000018).Results Gene mecA was detected in 60 strains of Staphylococcus aureus,58 strains of Staphylococcus epidermidis and 37 strains of Staphylococcus heamolyticus,but gene mecA in 6 strains of Staphylococcus epidermidis and 4 strains of Staphylococcus heamolyticus were only amplified by primer mecA2-F/R and not by primer mecA1-F/R.The percentage of gene mecR1 exist in Staphylococcus aureus was higher than Staphylococcus epidermidis and Staphylococcus heamolyticus,but the percentage of gene mecR1 exist in Staphylococcus epidermidis was not higher than Staphylococcus heamolyticus.The mutation and deletion of gene mecI were often seen,the wild type mecI was only detected in 14 strains,the point mutation of nucleotice 202 was detected in 36 strains.Conclusions Gene mecA expression in Staphylococcus aureus could be chiefly induced by mecR1,but which in coagulase-ngeative staphylococci could be other factors.The mutation and deletion of mecI were universal phenomenon in clinical strains,there could be a mechanism for overcoming the repressing of resistance caused by mecI in staphylococci.

Objective To construct a fusion protein that used for treatment of resistance and palindromia in leukemia and studied its biological activity. Methods IL-3 and LP gene fragments were amplified by PCR. After enzymatic digestion and T4 ligation, the fusion gene was cloned into expression vector pAYZ. The product was purified by exchange chromatography and anti-Etag affinity chromatography. IL3-G4SLP fusion protein was analyzed by SDS-PAGE and Western blot. Protein biological activity was detected by FACS. Results The fusion protein was expressed as soluble protein by E.Coli 16C9. The protein expression level was about 1 mg/L, its purity was over 95 %, and the expression level was about 1 mg/L. The fusion protein can combined specificely with CD123 on leukemia stem cells. Conclusion Fusion protein IL-3-G4S-LP can target on leukemia stem cells and maybe as a potential drug used for treatment of resistance and palindromia in leukemia.

In this paper,to evaluate the existence and extent of MRI artifacts caused by frequently used metallic dental materials and to compare the influence of different MRI sequences on artifacts. The artifact of Au-Pt-Pd alloy crown were the smallest and Au-Ag-Pd alloy crown, pure Titanium crown were smaller. But the artifact of Ni-Gr alloy crown were the largest.With the same scan sequences, the different metal materials can make different effects on MRI images with the different scan sequences, the MRI artifact is not obvious caused by the same metal materials. Artifacts produced by oral metallic materials related closely to the type of the materials.The high quality MRI can be gained by choosing proper metallic materials.

The tumor multidrug resistance reversal effect of NPB304, a novel taxane, was studied. MTT assay was used to determine the IC50 of chemotherapy drugs. Western blotting assay was applied to analyze the expression of P-glycoprotein (P-gp). The effect of compounds on the P-gp function and P-gp ATPase activity was determined by rhodamine 123 (Rh123) accumulation assay and analysis kit, respectively. Molecular docking was employed to predict the binding force between compounds and P-gp. Transmembrane transport of NPB304 was analyzed using MDCK II and MDR1-MDCK II cell model. NPB304 displayed multidrug resistance reversal effect on KBV cells and MCF-7/paclitaxel cells, NPB304 collaborative with P-glycoprotein (P-gp) inhibitors verapamil enhanced the reversal activity, specifically, 10 μmol x L(-1) verapamil in combination with paclitaxel reversed resistance by 56.5-fold, while combined with NPB304 increased the reversal fold; NPB304 synergistically increased Rh123 accumulation in the resistant cells when combined with verapamil, and NPB304 at 0-1 μmol x L(-1) enhanced the ATPase activity activated by verapamil was observed. NPB304 existed the hydrophobic interactions with the TM regions of P-gp, and the binding force between NPB304 and the A chain of the TM region was stronger. P-gp ATPase activity assay demonstrated NPB304 at lower concentrations (0-1.5 μmol x L(-1)) could activate the P-gp ATPase, playing a role on inhibition of P-gp function. However, NPB304 did not have an obvious feature of P-gp substrate. NPB304 exerted itself and synergy with verapamil activity on reversing tumor resistance via inhibiting the P-gp function.

Western blotting of autophagic markers LC3Ⅱ and p62 are widely used for estimating autophagic activity. To compare the regulation of various autophagy modulators on LC3Ⅱ and p62,HEK293 cells were treated separately with mTOR-dependent autophagy activator rapamycin or -independent autophagy activators trehalose, and autophagy inhibitors including 3-methyladenine (3-MA),bafilomycin A1 or E64d and pepstatin A that inhi-bited the initiation of autophagy,the fusion of autophagosome and lysosome,and the activities of lysosomal enzymes accordingly,and then LC3Ⅱ and p62 levels were assessed. Western blot results demonstrated that rapam-ycin enhanced the conversion of LC3I to LC3Ⅱ,promoted the degradation of p62 simultaneously,while trehalose merely increased the expression of LC3Ⅱ with no influence on the p62 level. Moreover,inhibition of autophagy commonly led to accumulation of LC3Ⅱ as well as blockage of p62 degradation in a concentration- and time-dependent manner. These results indicate that obvious differences exist in the regulation of LC3Ⅱ and p62 by various modulators although both are autophagic markers.