Epigenetics refers to the heritable changes in gene expression without an alteration in the DNA sequence of the genome.Epigenetic mechanism involves DNA methylation,histone modification,chromatin remodeling,non-coding RNA regulation and so on.Many experimental investigations indicate that the abnormalities in epigenetic regulation during cardiac development may be responsible for the progression of congenital cardiac disease.Based on the four aspects of epigenetic regulation above,this review mainly discusses the advances of epigenetic mechanism of congenital heart disease.

Objective To study the distribution and drug resistance of pathogens in neonatal septicemia in order to provide clinical guidance for antibiotic usage.Methods This retrospective study analyzed blood culture and clinical data from 83 confirmed neonatal septicemia patients and the blood collection cultures were analyzed.Results A total of 84 strains were isolated from 83 cases of blood specimens,Gram positive bacteria,Gram negative bacteria and fungi were 38(45.2%),41(48.8%),5(6.0%),respectively.Gram positive bacteria was mainly coagulase negative staphylococcus and staphylococcus aureus,which were 13(15.5%) and 8(9.5%) respectively.Gram negative bacteria was mainly Escherichia coli and Klebsiella pneumonia,which were 25(29.8%) and 9(10.7%) respectively.Gram positive bacteria were found high resistance to penicillin G,amoxicillin clavulanate potassium,oxacillin and clindamycin,from 34.2% to 73.7%,but they were sensitive to vancomycin,teicoplanin and linezolid.Gram negative bacteria were found high resistance to ampicillin(82.9%),the constituent ratio of the extended spectrum βlactamases(ESBLs) was 34.1%,carbapenem resistant strains was not found.All fungi were sensitive to azoles.Conclusion Gram negative bacteria are the major pathogens in neonatal septicemia,with high infection rate of Escherichia coli and high constituent ratio of the ESBLs,and antimicrobial agents should be chosen according to blood culture and antimicrobial susceptibility results.

Objective To investigate the effects of puerarin on the expression of human umbilical vein endothelial cells (HUVECs) tissue factor (TF) and tissue factor pathway inhibitor (TFPI) induced by oxidized low-density lipoprotein (ox-LDL).Methods After HUVECs were incubated with different concentrations of puerarin and 50 mg/L ox-LDL,the expression of TF and TFPI mRNA and protein were detected by real-time fluorescent quantitative PCR and Western blot respectively.Results Compared with control,treatment with ox-LDL caused the augment of TF mRNA and protein expression (P<0.01),and the decrease of TFPI mRNA and protein expression.However,50,100,and 200 μmol/L puerarin blunted the augment of TF mRNA and protein expression and weakened the inhibition of TFPI mRNA and protein expression induced by ox-LDL(P<0.01).Conclusions Puerarin reduces HUVECs TF and TFPI mRNA and protein induced by ox-LDL.

AIM: To explore the role of phosphatidylinositiol 3-kinase/protein kinase B/endothelial nitric oxide synthase (PI3K/Akt/eNOS) signaling pathways in the inhibitory effects of puerarin on oxidized low-density lipoprotein (ox-LDL)-induced tissue factor (TF) expression in vascular endothelial cells.METHODS: The mRNA expression of TF was detected by real-time fluorescent quantitative PCR.The protein levels of TF and Akt was determined by Western blot.The content of the nitric oxide (NO) was measured by nitrate reduction method.RESULTS: Compared with control group, incubating endothelial cells with ox-LDL significantly induced TF expression at mRNA and protein levels and the dephosphorylation of Akt protein, and decreased NO production.Incubation of the endothelial cells with puerarin for 1 h and then treatment of the cells with ox-LDL decreased the TF expression at mRNA and protein levels, increased Akt protein phosphorylation and intracellular NO content.Co-incubation of the endothelial cells with PI3K inhibitor LY294002 and puerarin for 1 h and then treatment of the cells with ox-LDL augmented the TF expression at mRNA and protein levels and the Akt protein dephosphorylation, and decreased NO production.Co-incubation of the endothelial cells with eNOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) and puerarin significantly decreased the inhibitory effect of puerarin on ox-LDL-induced TF expression at mRNA and protein levels in the endothelial cells, and reduced Akt protein phosphorylation and NO production.CONCLUSION: Puerarin inhibits ox-LDL-induced TF expression at mRNA and protein levels in the human umbilical vein endothelial cells via activation of PI3K/Akt/eNOS signaling pathway.

Educational reform of pathophysiology oriented to clinical application is to pass the physician qualifica -tion examination .One of essential approach is to implement pathophysiology teaching with the translational medical philosophy and promote the harmonious development of physician -patient relationship with the utilization of the de-velopment and changes of disease in the teaching process .In that way, the pathophysiology in basic and clinical medicine is worthy of the name of “bridge”, and ultimately achieves the goal of “the transformation and develop-ment of the cultivation of clinical application talents”.