Objective To study the influence of different starting time of hyperbaric oxygen(HBO) therapy on severe brain injury patients.Methods 60 cases of acute cerebral infarction patients were divided into 2 groups,namel 48 hours to 7 days group(group A) and 8 days to 15 days group(group B) after injury.Fugl-Meyer assemment and modified Barthel index were employed to assess the patients before and after HBO for 30 days in the 2 groups.Results After 30 days of HBO therapy the Fug-Meyer assemment and modified Barthel index in the A group were better than those of B group,there were significant differences between the 2 groups(P

Objective To evaluate the expression of epidermal growth factor-like domain 7 (Egfl7) in atherosclerotic plaques and effects of its small interference RNA (siRNA) on angiogenesis gene expression in human endothelial cell line (HUVEC). MethodsEgfl7 expression in atheroscleroticplaquesweredetectedinhumaniliacarteryandmousearteriaeusing immunohistochemistry and immunofluorescence stainings.The siRNA targeting Egfl7 was transfected into HUVEC by lipofectamine with non-transfected cells and unconcerned siRNA as controls.At 0 h,12 h,24 h and 48 h after intervention,the levels of mRNA and protein of Egf17,vascular endothelial growth factor(VEGF),platelet derived growth factor-A (PDGF-A),platelet derived growth factor-B (PDGF-B),vascular cell adhesion molecule(VCAM) and intercellular adhesion molecule (ICAM)were measured by RT-PCR and Western blotting,respectively. ResultsThe expressions of Egfl7 in human iliac artery and mouse arteriae were increased.The expressions of Egfl7 in HUVEC at the levels of mRNA were[(0.14±0.02),(0.09±0.01),(0.02±0.01)]and the levels of protein[(0.71±0.11),(0.39±0.09),(0.07±0.01)]at 12 h,24 h and 48 h after siRNA intervention,respectively,which were decreased as compared with 0 h intervention [(0.31 ±0.05) and (0.93±0.08) ].Other genes such as VEGF,PDGF-A and PDGF-B were reduced or silenced at the levels of protein and mRNA in HUVEC with siRNA longer interventions(all P＜0.05).ConclusionsThe expression of Egfl7 in atherosclerotic plaques is increased.The siRNA inhibiting Egfl7 gene expression results in silence of other factors involved in angiogenesis.

Objective To study the molecular mechanism of atherosclerosis induced by intravascular pressure.Methods Technic aortic coarctation (TAC) was performed in ApoE-/-mice (n＝8) and control littermate (n＝8) mice.HE staining was performed in the vessels upstream and downstream of the mice models.In vitro,hypoxia inducible factor-1a (HIF-1α),heme oxygenase,reactive oxygen species and phosphorylated AMP activated protein kinase (AMPK) were analyzed in different intravascular pressure with a myograph system that allowed independent variation of flow and pressure.Results After one month of TAC,ApoE/ mice in a normal chow diet developed occlusive plaque and accelerated atherosclerotic lesions exclusively in upstream high-pressure vessel segments.In vitro,HIF-1α was increased,heme oxygenase was higher over(2.7 ±0.6) fold,reactive oxygen species and phosphorylated AMPK were also enhanced in high intravascular pressure perfused vessel segments as compared with low intravascular pressure perfused vessel segments (all P＜0.05).Conclusions Intravascular pressure elevation can activate hypoxia and metabolism-associated pathways in the arterial wall,and predispose atherosclerosis accelerated.