Objective Alprostadil can improve the clinical efficacy of the treatment of hepatitis B cirrhosis, but little literature is available about its effect on serum inflammatory factors in patients with hepatitis B cirrhosis.This study aimed to investigate the effect of alprostadil on serum inflammatory factors and liver function of the patients with hepatitis B cirrhosis and its possible action mechanisms.Methods We equally randomized 162 cases of hepatitis B cirrhosis admitted to our hospital from August 2014 to July 2015 into a control and an observation group, the former treated by conventional antiviral, liver-protecting and supportive therapies, and the latter with alprostadil in addition, both for 4 weeks.Then, we obtained the serum inflammatory factors, the contents of serum interleukin-6 (IL-6), high sensitive C reactive protein (hs-CRP) and tumor necrosis factor alpha (TNF-α) as well as such liver function indexes as glutamic-pyruvic transaminase (ALT), total bilirubin (TBil) and prothrombin activity (PTA), and compared them between the two groups before and after treatment.Results After 4 weeks of treatment, the effectiveness rate was significantly higher in the observation than in the control group (82.72% vs 62.96%, P<0.05).Compared with the baseline, the patients in the observation group showed significant improvement after treatment in serum IL-6 ([275.62±43.39] vs [97.15±19.73] pg/mL, P<0.05), hs-CRP ([425.54±55.58] vs [50.23±6.69] ng/L, P<0.05), TNF-α ([321.74±80.73] vs [85.45±13.61] pg/mL, P<0.05), ALT ([139.54±37.36] vs [96.13±23.62] μmol/L, P<0.05), TBil ([395.39±41.13] vs [271.55±25.12] μmol/L, P<0.05), and PTA ([38.50±4.19] vs [68.36±8.11]%), and the improvement was significantly better than in the control group (P<0.05).Conclusion Alprostadil helps alleviate the inflammatory condition, improve the liver function, and promote clinical efficacy in patients with hepatitis B cirrhosis.

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 observe clinical efficacy and safety of Danning tablets combined with endoscopic ligation in the treatment of esophageal varices in patients with nonalcoholic fatty liver cirrhosis(NFLC). METHODS:A total of 70 NFLC patients with esophageal varices in our hospital during Sept. 2015-Sept. 2016 were divided into control group and observation group by simple random sampling method,with 35 cases in each group. Both groups received endoscopic ligation. Control group was given Somatostatin for injection with intravenous pump at the speed of 250 μg/h for 72 h after surgery,and Pantoprazole sodium enteric-coated capsules 40 mg,qd. Observation group was additionally given Danning tablets 1 g,tid,on the basis of control group. Both groups were given medicine for consecutive 4 weeks.The situation of ligation and clinical efficacies were observed in 2 groups,and the grading of esophageal varices before and after treatment,the occurrence of re-bleeding events and ADR were observed. RESULTS:The patients of 2 groups completed ligation successfully,there was no statistical significance in the times of ligation between 2 groups(P>0.05). Total response rate of observation group was 91.43%,which was significantly higher than 74.29% of control group,with statistical significance(P<0.05).Before treatment,there was no statistical significance in the grading of esophageal varices between 2 groups(P>0.05). One month and three months after treatment,the grading of esophageal varices in 2 groups were significantly better than before treatment,and observation group was significantly better than control group,with statistical significance(P<0.05). There was no statistical significance of 2 groups between 3 months after treatment and one month after treatment(P>0.05).Total incidence of re-bleeding events in observation group was 14.29% within 3-month follow-up,which was significantly lower than 40.00% of control group,with statistical significance(P<0.05). There was no statistical significance in the total incidence of ADR between 2 groups(P>0.05). CONCLUSIONS:Danning tablets combined with endoscopic ligation show significant therapeutic efficacy for esophageal varices of NFLC,significantly mitigate the degree of esophageal varices and reduce the incidence of re-bleeding without increasing the occurrence of ADR.

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.

The UL49.5 gene of most herpesviruses is conserved and encodes glycoprotein N. However, the UL49.5 protein of duck enteritis virus (DEV) (pUL49.5) has not been reported. In the current study, the DEV pUL49.5 gene was first subjected to molecular characterization. To verify the predicted intracellular localization of gene expression, the recombinant plasmid pEGFP-C1/pUL49.5 was constructed and used to transfect duck embryo fibroblasts. Next, the recombinant plasmid pDsRed1-N1/glycoprotein M (gM) was produced and used for co-transfection with the pEGFP-C1/pUL49.5 plasmid to determine whether DEV pUL49.5 and gM (a conserved protein in herpesviruses) colocalize. DEV pUL49.5 was thought to be an envelope glycoprotein with a signal peptide and two transmembrane domains. This protein was also predicted to localize in the cytoplasm and endoplasmic reticulum with a probability of 66.7%. Images taken by a fluorescence microscope at different time points revealed that the DEV pUL49.5 and gM proteins were both expressed in the cytoplasm. Overlap of the two different fluorescence signals appeared 12 h after transfection and continued to persist until the end of the experiment. These data indicate a possible interaction between DEV pUL49.5 and gM.
Animals ; Ducks/virology ; Genes, Viral/genetics ; Mardivirus/*genetics ; Membrane Glycoproteins/*genetics ; Microscopy, Fluorescence ; Phylogeny ; Polymerase Chain Reaction/veterinary ; Viral Envelope Proteins/*genetics