Aim To investigate the effect of flavonoids from Prinsepia utilis Royle( FPR) on the histomorphol-ogy of kidney in diabetic mice, and to investigate its protective mechanism. Methods Diabetic mice in-duced by alloxan were given FPR orally each day for four weeks. After the administration for two and four weeks, ten mice in each group were randomly sacri-ficed. The kidneys were removed and weighed. The extracted renal tissue was embedded with paraffin and sectioned, the sections were stained with Hematoxylin and Eosin(HE)、Periodic acid Schiff(PAS) and Go-mori, and then observed under the microscopy. 1mm3 of renal cortex fixed with glutaral in four centi-degree , and then the ultrastructure of each group was observed under the electron microscope respectively after four weeks′ treatment. Results Compared with the model control group, in the treatment group, observation un-der the microscopy showed that glomerular volume and mesangial cells reduced, FPR could relieve thickening of the glomerular basement membrane ( GBM ) , little inflammatory cells infiltrated in the interstitium,tubular epithelial cells almost became normal, renal tubule had little glucogen, fiber decreased in the interstitium of renal tubule. Observation under the electron micro-scope indicated that foot process in podocytes lined up in order, mitochondria of the renal tubule’ s epithelial cell almost recovered. Conclusion FPR can relieve the changes of renal pathology,improve renal function, and delay the progression of pathologic changes of kid-ney in diabetic mice partly through reducing the blood glucose and the blood lipid.

Objective:In oder to investigate the effect of Chuanmingshen violaceum polysaccharides ( CVP) and Solfated Chua-nmingshen violaceum polysaccharides ( SCVP) on immunosuppression induced by cyclophosphamide ( CY) in mice.Methods: CY were used to induce immunosuppression in mice;Spleen and thymus indexes were used to evaluate the immune organs indexes;the [3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltet-razolium bromide,MTT] method was used to detect the proliferation of spleen lymphocytes of each group;the concentrations of IFN-γand IL-2 were assayed by ELISA kit.Results: SCVP and CVP could resist immunosuppression by promoting lymphocyte proliferation, increasing the contents of IFN-γ and IL-2, promoting immune organs development in immunosuppressive mice induced by CY.Conclusion:SCVP and CVP exhibited the potential to used as immunopotentiator.

Objective To analyze the epidemiological and clinical characteristics of 5 patients with importing yellow fever ,and to explore the preventive and control strategies of infection in hospital .Methods The epidemiological and clinical characteristics of 5 cases of importing yellow fever in Infectious Disease Hospital of Fujian Medical University from March 18th to April 6th in 2016 were retrospectively reviewed and analyzed .Results Five patients were all from Angola Luanda .One of them was vaccinated before going aboard ,and the others were vaccinated 1—10 days before disease onset in Angola .All of them were bitten by mosquitoes ,and their onset date ranged from March 11th to March 27th ,before returned to Fujian .The main clinical symptoms were fever ,chilly ,shivering ,fatigue ,arthrodynia ,headache ,and liver and kidney injury .At manifestations ,two patients had positive nuclear acid of yellow fever virus in serum samples and 3 patients were positive in urine samples .All of these patients were negative for dengue virus and Zika virus testing ,meanwhile no plasmodium was found in blood smears .All patients were cured and discharged . Conclusions There is risk of yellow fever transmission in Fujian Province . Prevention and control of the disease should be focus on improving the ability of finding and coping with the importing cases .Vaccination and hygiene knowledge propagation should be given for those who are going to epidemic country/area .Emergency monitoring and control of mosquitoes are necessary .

Objective To investigate the role of SIRT1/autophagy pathway in mediating the regulatory effect of lncRNA SOX2OT on 5-fluorouracil(5-FU)resistance in cholangiocarcinoma cells.Methods HCCC-9810 cells were used to construct a 5-FU-resistant cell model(HCCC-9810/5-FU cells),and the expression levels of lncRNA SOX2OT and SIRT1 mRNA and the protein expressions of SIRT1,Beclin1,LC3 and P62 were detected with qRT-PCR and Western blotting.The effects of transfection with a SOX2OT mimic on drug resistance and cell migration of HCCC-9810/5-FU cells were detected using CCK-8 assay and wound healing assay,and the changes in expressions of SOX2OT,SIRT1,Beclin1,LC3 and P62 were detected.Rescue experiment was performed by co-transfection of HCCC-9810/5-FU cells with both a SOX2OT-overexpressing plasmid and si-SIRT1 to confirm the role of SIRT1 in SOX2OT-mediated regulation of 5-FU resistance.A RNA pulldown assay was used to verify the targeted binding between SOX2OT and SIRT1.Results The proliferation of HCCC-9810 cells was significantly inhibited after treatment with different concentrations of 5-FU(P<0.05).The 5-FU-resistant cells showed significantly increased protein expressions of SIRT1,Beclin1 and p62,an increased LC3Ⅱ/LC3Ⅰ ratio,and enhanced expressions of SIRT1 mRNA and SOX2OT(P<0.05).Transfection of the resistant cells with SOX2OT mimic significantly enhanced cell migration and increased the protein expressions of SIRT1,Beclin1 and p62,the LC3Ⅱ/LC3Ⅰratio,and expression levels of SIRT1 mRNA and SOX2OT(P<0.05),and these changes were obviously attenuated by SIRT1 knockdown,which also resulted in lowered 5-FU resistance of the cells without significantly affecting the expression level of SOX2OT(P>0.05).RNA pulldown assay suggested that SOX2OT could directly bind to SIRT1.Conclusion LncRNA SOX2OT enhances 5-FU resistance in HCCC-9810 cells by promoting autophagy through up-regulating SIRT1 expression.

Objective To investigate the role of SIRT1/autophagy pathway in mediating the regulatory effect of lncRNA SOX2OT on 5-fluorouracil(5-FU)resistance in cholangiocarcinoma cells.Methods HCCC-9810 cells were used to construct a 5-FU-resistant cell model(HCCC-9810/5-FU cells),and the expression levels of lncRNA SOX2OT and SIRT1 mRNA and the protein expressions of SIRT1,Beclin1,LC3 and P62 were detected with qRT-PCR and Western blotting.The effects of transfection with a SOX2OT mimic on drug resistance and cell migration of HCCC-9810/5-FU cells were detected using CCK-8 assay and wound healing assay,and the changes in expressions of SOX2OT,SIRT1,Beclin1,LC3 and P62 were detected.Rescue experiment was performed by co-transfection of HCCC-9810/5-FU cells with both a SOX2OT-overexpressing plasmid and si-SIRT1 to confirm the role of SIRT1 in SOX2OT-mediated regulation of 5-FU resistance.A RNA pulldown assay was used to verify the targeted binding between SOX2OT and SIRT1.Results The proliferation of HCCC-9810 cells was significantly inhibited after treatment with different concentrations of 5-FU(P<0.05).The 5-FU-resistant cells showed significantly increased protein expressions of SIRT1,Beclin1 and p62,an increased LC3Ⅱ/LC3Ⅰ ratio,and enhanced expressions of SIRT1 mRNA and SOX2OT(P<0.05).Transfection of the resistant cells with SOX2OT mimic significantly enhanced cell migration and increased the protein expressions of SIRT1,Beclin1 and p62,the LC3Ⅱ/LC3Ⅰratio,and expression levels of SIRT1 mRNA and SOX2OT(P<0.05),and these changes were obviously attenuated by SIRT1 knockdown,which also resulted in lowered 5-FU resistance of the cells without significantly affecting the expression level of SOX2OT(P>0.05).RNA pulldown assay suggested that SOX2OT could directly bind to SIRT1.Conclusion LncRNA SOX2OT enhances 5-FU resistance in HCCC-9810 cells by promoting autophagy through up-regulating SIRT1 expression.