Analysis of influence factors for spontaneous closure of atrial septal defect and ventricular septal defect in the northern of Xinjiang / 新乡医学院学报

Objective To analyse the risk factors for spontaneous closure of atrial septal defect(ASD) and ventricular septal defect(VSD) in children in the northern of Xinjiang.Methods Ninety-two ASD and sixty-five VSD children in Department of Pediatrics,the First Affiliated Hospital of Medical College,Shehezi University from January 2010 to May 2014 were selected as research subject.According to the spontaneous closure condition of children,the children with ASD were divided into ASD spontaneous closure group and ASD non spontaneous closure group;the children with VSD were divided into VSD spontaneous closure group and VSD non spontaneous closure group.The risk factors for spontaneous closure of ASD and VSD were analysed by single factor and multiple factor logistic regression analysis.Results In 92 ASD children,12 cases (13.04％) were spontaneous closure.In 65 VSD children,9 cases (13.85％) were spontaneous closure.Single factor analysis result showed that there was statistic difference in defect diameter,defect type and the age between spontaneous closure group and non spontaneous closure group in ASD and VSD children (P ＜ 0.05);but there was no statistic difference in defect number and complications between spontaneous closure group and non spontaneous closure group in ASD and VSD children (P ＞ 0.05).Multivariate logistic regression analysis showed that the defect diameter,defect type and the age were the independent risk factors for the spontaneous closure of ASD and VSD (P ＜ 0.05).Conclusion The age ＜ 2 years old,central ASD,perimembranous VSD and defect diameter ＜ 5 mm are important factors for promoting spontaneous closure of ASD and VSD.

Acanthopanax Senticosus Saponins induced tolerance to ischemia and its possible molecular mechanism in PC12 cells / 中华儿科杂志

<p><b>OBJECTIVE</b>To study the tolerance to ischemia induced by Acanthopanax Senticosus Saponins (ASE) in PC12 cells and the involved mechanism.</p><p><b>METHODS</b>An ischemic model was developed in PC12 cell line by treatment with oxygen-glucose deprivation. The effects of ASE pretreatment on tolerance of PC12 cells to ischemia were evaluated by MTT assay and analysis of cellular morphology. The expression of hypoxia-inducing factor (HIF)-1alpha, erythropoietin (EPO) after the pretreatment with ASE was detected by Western blotting. The DNA binding activities of HIF-1 in PC12 cells with the pretreatment of ASE were demonstrated by using electrophoretic mobility shift assay (EMSA).</p><p><b>RESULTS</b>In ischemia model, the viability of PC12 cells was decreased to (49.12 +/- 3.22)% after oxygen-glucose deprivation for 9 hours. However, ASE (50 microg/ml) pretreatment could remarkably increase the viability of PC12 cells by (67.97 +/- 2.92)%. There were significant differences between the experimental group and control group (F = 473.67, P < 0.01). The cellular morphology showed that PC12 cells exposed for 7 days to nerve growth factor (NGF) exhibited round, smooth cell bodies with normal processes and that processes formed extensive network. At 9 hour after ischemia, cell bodies of many PC12 cells were found shrinken, the processes were disrupted and network disappeared. However, pretreatment with ASE (50 microg/ml) could largely prevent the morphological damage to PC12 cells that would have caused by subsequent exposure to 9 h ischemic insult, many cellular bodies were intact and many processes and network of PC12 cells still existed. The expression of HIF-1alpha increased after pretreatment with ASE shown by Western blot. There were significant differences between the experimental group and control group (F = 167.18, P < 0.01). The DNA binding activities of HIF-1 in PC12 cells after pretreatment with ASE was significantly increased, and it could activate the expression of EPO (F = 128.37, P < 0.01).</p><p><b>CONCLUSIONS</b>The pretreatment with ASE could induce tolerance against ischemia in PC12 cells. The elevated expression and increased DNA binding activity of HIF-1alpha, the overexpression of its downstream target EPO may be the molecular mechanism in tolerance of PC12 cells to ischemia induced by ASE pretreatment.</p>

Ischemic Tolerance and Expression of Hypoxia Inducible Factor-1? in PC12 Cells Induced by Acanthopannx Senticosus Saponins / 实用儿科临床杂志

Objective To study ischemic tolerance induced by acanthopannx senticosus saponins(ASS) on ischemia in PC12 cells and involve expression of hypoxia inducible factor-1?(HIF-1?).Methods An ischemic model was developed in PC12 cell line with treatment of oxygen glucose deprivation(OGD).The protective effects of ASS pretreatment on ischemic tolerance of PC12 cells and whether protective effects of ASS could be inhibited by LY294002(PI3K inhibitor) were analyzed through MTT assay.The induction of phospho-glycogen synthesis kinase-3?(p-GSK-3?) and HIF-1? after pretreatment of ASS and possible blocking effects of LY294002 were detected by Western-blot.Results MTT results showed that after 9 h ischemia,the viability of PC12 cells decreased dramatically(P