Objective To examine the influence of gender difference on the reperfusion delay in patients with ST-elevation myocardial infarction (STEMI).Methods A total of consecutive 325 patients with STEMI were analyzed admitted in the 306 Hospital of PLA from Jan.2011 to Dec.2015.Patients were divided into two groups:male group (n=268) and female group (n=57).The clinical data and the time intervals including symptom onset to first medical contact (So-to-FMC),transfer delay (FMC-to-D),FMC to balloon dilatation (FMC-to-B),activation delay and door to balloon (D-to-B) time were compared between different gender groups,and the prognosis was observed.Results The overall median of pre-hospital delay was 125 minutes.The median of prehospital delay time (male 119.5min vs.female 160.0min) and So-to-FMC time (male 69.5min vs.female 100.0min) were longer in female than in male patients,but no statistical difference existed (P＞0.05) between the two groups in pre-hospital delay,So-to-FMC,FMC-to-B,D-to-B and total ischemia time.Compared with male patients,female patients were more likely to have additional comorbidities,such as hypertension and diabetes mellitus,and lower rate of smoking (P＜0.05).However,the incidence of major adverse cardiac and cerebrovascular events (MACCE) showed no significant difference between female and male patients at 30-day (male 5.22％ vs.female 5.26％) and I-year (male 10.82％ vs.female 8.77％) follow-up (P＞0.05).Conclusion The influence of gender on reperfusion delay is gradually weakening.

Objective To investigate the expression of centromere protein F(CENPF)in pancreatic ductal adenocarcinoma(PDAC)and its relationship with the clinicopathological features and prognosis of patients.Methods Based on Gene Expression Omnibus(GEO)from National Center for Biotechnology Information(NCBI),using GEO2R,Venn diagram,Cytoscape,MCODE and GEPIA software to screen out the suspected differential gene CENPF in PDAC;based on the Cancer Genome Atlas(TCGA)and the Genotype-Tissue Expression(GTEx),using NCBI,GEPIA,Ualcan,Oncomine,TIMER software and Kaplan-Meier on-line survival analysis tool to analyze its possible molecular mechanism from the level of messenger RNA(mRNA).In all,surgical specimens of 121 PDAC cases diagnosed at the pathology department of the First Affiliated Hospital of Fujian Medical Univer-sity were analyzed from the histoprotein level to analyze the relationship between CENPF and clinicopathological features and prognosis of PDAC.Results CENPF gene was abnormally expressed in various human cancers,and there was a difference in expression between pancreatic ductal adenocarcinoma and normal pancreatic tissue(P＜0.05),and it was related to the grading(P＜0.05)and prognosis(P=0.038)of pancreatic ductal adenocarcinoma.Immunohistochemistry showed that the expression of CENPF was correlated with nerve invasion(P=0.036),TNM stage(P=0.041),lymph node metastasis(P=0.023),degree of differentiation(P=0.020)and overall survival of pancreatic ductal adenocarcinoma(Log-rank=18.608,P=0.000016),and CENPF expression(HR=2.654,95％CI=1.373-5.131,P=0.004)was an independent risk factor for the prognosis of PDAC patients.CENPF combined with other key module genes in PDAC was mainly enriched in exosomes,extracellular mechanisms,and was related to serine endopeptidase activity and metalloendopeptidase activity.The action pathway of CENPF single gene in pancreatic ductal adenocarcinoma was mainly related to cell cycle,P53 pathway,ubiquitin-mediated proteolysis,and played a joint role with P53 and MDM2 in PDAC.Immune infiltration studies showed that CENPF expression was negatively correlated with CD4+T lymphocyte infiltration and positively correlated with dendritic cell infiltration(both P＜0.05).Conclusion CEN-PF may be involved in the progression of PDAC,and high expression of CENPF indicates a poorer prognosis.Our research is expected to provide more scientific evidence for the prevention and treatment of PDAC.

ObjectiveTo perform a predictive analysis of the quality marker（Q-Marker） for the anticoagulant activity of Kunning granules. MethodThe chemical components of Kunning granules were analyzed by ultra high performance liquid chromatography-quadrupole-time of flight tandem mass spectrometry（UHPLC-Q-TOF-MS/MS） on a Waters ACQUITY UPLC HSS T3 column（2.1 mm×100 mm， 1.8 μm） with the mobile phase of acetonitrile（A）-25 mmol∙L^-1 ammonium acetate aqueous solution（B） for gradient elution （0-5 min， 5%-22%A； 5-10 min， 22%-30%A； 10-15 min， 30%-95%A； 15-20 min， 95%-5%A； 20-30 min， 5%A）， flow rate of 0.2 mL∙min^-1， column temperature at 30 ℃， injection volume of 1 μL， electrospray ionization（ESI）， positive and negative ion detection modes. Interaction analysis between the targets of chemical components and the targets of abnormal uterine bleeding（AUB） was performed by network pharmacology， and the key components were screened through network topology analysis. The fingerprints of 10 batches of Kunning granules were established by high performance liquid chromatography（HPLC）， the anticoagulant activity of the granules was determined by blood coagulation method and fibrinogen plate method， and the spectrum-effective relationship was established. The components co-occurring in the topological analysis and spectrum-effective relationship were selected as Q-Markers， and their anticoagulant activities were verified and confirmed. ResultA total of 475 chemical components were identified from Kunning Granule， of which 22 key components such as salvianolic acid B， paeoniflorin， naringin and neohesperidin， were the potential material basis for the treatment of AUB. The spectrum-effective analysis showed that peaks 7（paeoniflorin）， 9（naringin）， 10（neohesperidin） and 11（salvianolic acid B） were the optimal principal components， and in vitro activity test showed that these four components could better characterize their anticoagulant activity. ConclusionSalvianolic acid B， paeoniflorin， neohesperidin and naringin may be Q-Markers for the anticoagulant activity of Kunning granules.

OBJECTIVE To study the effect and potential mechanism of eriodictyol on non-alcoholic fatty liver disease （NAFLD）. METHODS Sixteen C57BL/6J mice were randomly divided into control group， NAFLD model group， and eriodictyol low-dose and high-dose groups （50， 100 mg/kg）， with 4 mice in each group. Except for control group， the other groups were fed with high fat diet to induce NAFLD model. After four weeks of preprocessing， they were given relevant medicine intraperitoneally （0.01 mL/g）， once a day， for 6 consecutive weeks. The body weight and liver weight of mice were measured， and the pathological damage of liver tissue in mice was observed. The levels of aspartate aminotransferase （AST）， alanine aminotransferase（ALT）， and triglycerides （TG） in serum， as well as the protein expressions of nuclear factor-erythroid 2-related factor 2 （Nrf2） and heme oxygenase-1 （HO-1） in liver tissue were determined. In vitro NAFLD model was established by using 0.5 mmol/L oleic acid （OA） in HepG2 cells. Normal control group， NAFLD model group and eriodictyol low-， medium- and high-concentration groups （50， 100， 150 μmol/L） were set up. HepG2 cells in drug groups were treated with eriodictyol for 24 h at the time of modeling. The lipid deposition was observed in cells， and the levels of TG， malondialdehyde （MDA） and reactive oxygen species （ROS） as well as the phosphorylation levels of the mitogen-activated protein kinase （MAPK） signal pathway related proteins [extracellular signal-regulated kinase （ERK）， c- Jun N-terminal kinase （JNK）] and the protein expressions of Nrf2 and HO-1 were all determined. RESULTS In the in vivo experiment， compared with the NAFLD model group， the body weight， liver weight， the serum levels of AST， ALT and TG were all decreased significantly in eriodictyol low- and high-dose groups （except for serum level of AST in eriodictyol low-dose group） （P＜0.01）； liver lipid deposition was reduced significantly and the protein expressions of Nrf2 and HO-1 in liver tissues were further up-regulated （P＜0.01）. In the in vitro experiment， compared with the NAFLD model group， the lipid deposition in hepatocytes was reduced in eriodictyol low-， medium- and high-concentration groups （P＜0.01）， and the levels of ROS， MDA and TG were down-regulated （P＜0.05 or P＜0.01）； the phosphorylation levels of ERK and JNK were significantly down-regulated （P＜0.01）， while the protein expressions of Nrf2 and HO-1 were up-regulated significantly （P＜0.01）. CONCLUSIONS Eriodictyol can inhibit MAPK signaling pathway and activate Nrf2/HO-1 signaling pathway to alleviate NAFLD.