To construct a recombinant fowl adenovirus 4(FAdV-4)expressing the Cap protein of goose astrovirus genotype 2(GoAstV-2),the expression cassette of Cap gene was inserted into the natural 1 966 bp deletion region of the FAdV-4 genome in the infectious clone p15A-cm-FAdV4-HNJZ.The resulted recombinant plasmid p15A-cm-FAdV4-HNJZ-Cap/GoAstV-2 was linearized with restriction enzyme and transfected into chicken hepatoma cell line(LMH)to rescue the recombinant FAdV-4 expressing the Cap protein of GoAstV-2,rF Ad V4-Cap/GoAstV-2.After 15 passages in LMH cells,the recombinant rFAdV4-Cap/GoAstV-2 was identified by PCR using primers flanking the insertion site of the Cap gene expression cassette and using viral genome DNA extracted from rFAdV4-Cap/GoAstV-2 infected LMH cells as template.LMH cells were in-fected with 15th passage rFAdV4-Cap/GoAstV-2 and indirect immunofluorescence was performed with a polyclonal antibody against Cap protein as the primary antibody.Western blot was carried out with lysates of rFAdV4-Cap/GoAstV-2 infected LMH cells.The in vitro replication dynamic of the 15th passage of the rFAdV4-Cap/GoAstV-2 was also investigated in LMH cells.The results demonstrated that the Cap gene of GoAstV-2 was presented in the genome of the recombinant vi-rus rF AdV4-Cap/Go Ast V-2,and could be expressed stably.The prepared recombinant virus in this study will lay a foundation for developing inactivated bivalent vaccine candidate against co-in-fection of FAdV-4 and GoAstV-2 in goose.

To construct a recombinant fowl adenovirus 4(FAdV-4)expressing the Cap protein of goose astrovirus genotype 2(GoAstV-2),the expression cassette of Cap gene was inserted into the natural 1 966 bp deletion region of the FAdV-4 genome in the infectious clone p15A-cm-FAdV4-HNJZ.The resulted recombinant plasmid p15A-cm-FAdV4-HNJZ-Cap/GoAstV-2 was linearized with restriction enzyme and transfected into chicken hepatoma cell line(LMH)to rescue the recombinant FAdV-4 expressing the Cap protein of GoAstV-2,rF Ad V4-Cap/GoAstV-2.After 15 passages in LMH cells,the recombinant rFAdV4-Cap/GoAstV-2 was identified by PCR using primers flanking the insertion site of the Cap gene expression cassette and using viral genome DNA extracted from rFAdV4-Cap/GoAstV-2 infected LMH cells as template.LMH cells were in-fected with 15th passage rFAdV4-Cap/GoAstV-2 and indirect immunofluorescence was performed with a polyclonal antibody against Cap protein as the primary antibody.Western blot was carried out with lysates of rFAdV4-Cap/GoAstV-2 infected LMH cells.The in vitro replication dynamic of the 15th passage of the rFAdV4-Cap/GoAstV-2 was also investigated in LMH cells.The results demonstrated that the Cap gene of GoAstV-2 was presented in the genome of the recombinant vi-rus rF AdV4-Cap/Go Ast V-2,and could be expressed stably.The prepared recombinant virus in this study will lay a foundation for developing inactivated bivalent vaccine candidate against co-in-fection of FAdV-4 and GoAstV-2 in goose.

A 57-year-old male patient received oral sorafenib 400 mg twice daily for pulmonary metastases after operation of thyroid carcinoma. About 3 and a half months of treatment,the patient experienced dizziness,pain in the anterior region of the heart and blood pressure of 180 / 105 mmHg(before treatment it was 120 / 75 mmHg). He received oral metoprolol administration(initial dose of 25 mg twice daily,gradually increased to 200 mg twice daily). About one and a half months later,he received sustained release capsules of isosorbide mononitrate 50 mg once daily because of the intermittent attack of precordial pain. Angina pectoris still occurred frequently. He underwent percutaneous coronary intervention twice(a total of 2 stents implantation). Hypertension and angina pectoris were still poorly controlled. On month 19 of sorafenib treatment,the dose of drug was reduced to 400 mg once daily. His blood pressure was 135 / 85 mmHg but angina still occurred intermittently. On month 22,sorafenib was stopped. Two months later,the patient's blood pressure declined to 130 / 80 mmHg,and the frequency of angina pectoris decreased. Four months after the termination of sorafenib,his blood pressure was 120 / 75 mmHg and no episode of angina pectoris occurred.

A 57-year-old male patient received oral sorafenib 400 mg twice daily for pulmonary metastases after operation of thyroid carcinoma. About 3 and a half months of treatment,the patient experienced dizziness,pain in the anterior region of the heart and blood pressure of 180 / 105 mmHg(before treatment it was 120 / 75 mmHg). He received oral metoprolol administration(initial dose of 25 mg twice daily,gradually increased to 200 mg twice daily). About one and a half months later,he received sustained release capsules of isosorbide mononitrate 50 mg once daily because of the intermittent attack of precordial pain. Angina pectoris still occurred frequently. He underwent percutaneous coronary intervention twice(a total of 2 stents implantation). Hypertension and angina pectoris were still poorly controlled. On month 19 of sorafenib treatment,the dose of drug was reduced to 400 mg once daily. His blood pressure was 135 / 85 mmHg but angina still occurred intermittently. On month 22,sorafenib was stopped. Two months later,the patient's blood pressure declined to 130 / 80 mmHg,and the frequency of angina pectoris decreased. Four months after the termination of sorafenib,his blood pressure was 120 / 75 mmHg and no episode of angina pectoris occurred.

HepG2 cells were pre-incubated with insulin (Ins 0,1,0. 1,0.01 μol/L) and dexamethasone ( Dex 0,3,0. 3,0.03 μol/L) alone or together for 24 h to induce insulin resistance (IR) in vitro, the resistant level was estimated by glucose consumption, the optimal model of insulin resitance was chosen, and at the same time its lasting time of resistance was determined. In order to investigate the effects and mechanisms of mifepristone on in sulin-resistant HepG2 cells induced by insulin and dexamethasone, mifepristone and pioglitazone were adminis tered 24 h after the optimal model of insulin-resistant HepG2 cells was established. The glucose consumption, in tracellular concentrations of glucose, glycogen, ATP, and free fatty acid (FFA) in each group were detected. The expression of InsR-mRNA and GR-mRNA was detected by semi-quantitative reverse transcription and polymerase chain reaction (SqRT-PCR). Results revealed that pretreatment with insulin (0. 1 μmol/L) and dexamethasone (0.3 (μol/L) for 24 h caused optimal insulin resistance of HepG2 cells which lasted for 36 h. Compared with control group, the glucose consumption, intracellular glucose, glycogen, ATP contents and the level of InsR-mRNA in model cells decreased while FFAs concentrations and GR-mRNA increased. However, the tendency of insulin resistant HepG2 cells was obviously attenuated by pioglitazone at the concentration of 0. 2 mmol/L and mifepris tone at 200μmol/L and 20 μol/L while mifepristone at 2 μol/L had no effect on insulin-resistant cells. The findings indicated that mifepristone at 200 μol/L and 20 μol/L improved the insulin resistance via modulating intracellular glucolipid metabolism and the expression of InsR-mRNA and GR-mRNA.