Objective: To explore the impact of different atorvastatin doses on platelet function and highreactivity in patients with acute ST-elevation myocardial infarction (STEMI) after emergent percutaneouscoronary intervention (PCI) therapy.
Methods:A total of 120 STEMI patients with emergent PCI therapy were randomly divided into 2 groups:Standard group, the patients received atorvastatin 20 mg/day and Intensive group, the patientsreceived atorvastatin 40 mg/day, all patients were treated for 7 days. n=60 in each group. Blood lipids and biochemistry were examined before PCI and 7 days after atorvastatin treatment respectively;platelet fibrin clot strength induced by ADP (MAADP), AA and ADP induced platelet inhibition rate were measured by thrombelastography (TEG) test.
Results: With 7 days treatment, compared with Standard group, Intensive group showed decreased MAADP (38.40±17.40) mm vs (45.70±14.50) mm, P<0.05. On day 7 of atorvastatin treatment, compared with Standard group, Intensive group had reduced occurrence rate of high ADP reactivity (18.3%vs 31.7%), P<0.05. The occurrence rate of high AA reactivity was similar between 2 groups (13.3%vs 18.3%), P>0.05. The patients were followed-up for 3 months and the end point events including unstable angina, non-fatal MI, in-stent restenosis, in-stent thrombosis, and cardiovascular death or target vessel revascularization were similar between 2 groups, P>0.05.
Conclusion: Early stage and short term administration of high dose atorvastatin could obviously inhibit platelet activity in STEMI patients after emergent PCI;such intensive atorvastatin treatment had no reduction on end point events in 3 months follow-up period.

Objective To investigate the effects of different doses of atorvastatin on plasma endothelin and platelet function in acute ST-segment elevation myocardial infarction (STEMI) patients after emergency percutaneous coronary intervention (PCI).Methods A total of 120 patients with acute STEMI treated with emergency PCI were enrolled and randomly divided into 20 mg of atorvastatin treatment group (standard group,n =60),and 40 mg of atorvastatin treatment group (intensive group,n =60).The blood C reactive protein (CRP),blood lipid profiles,plasma endothelin (ET) were measured before atorvastatin treatment and after 7 days of treatment,respectively.The platelet fibrin clot strength induced by ADP (MAADP) was determined by thrombelastography (TEG).Results Seven days after of atorvastatin treatment,the level of plasma ET in intensive group was significantly lower than that in standard group [(0.49 ± 0.21) pmol/L vs (0.63 ± 0.58) pmol/L,P ＜ 0.05].Moreover,the MAADP in intensive group was significantly decreased compared with the standard group [(38.4 ± 17.4) mm vs (45.7 ± 14.5) mm,P ＜ 0.05].There was a positive correlation between the ET level and MAADP in intensive group after treatment (r =0.378,P ＜ 0.05).However,no significantly differences could be viewed in the CRP and LDL-C levels between the two groups (P ＞ 0.05).Conclusion In patients with acute STEMI,early administration of 40 mg atorvastatin after emergency PCI could significantly reduce the vascular endothelial injury,improve endothelial function,and reduce the residual platelet activity.

Objective To investigate the effects of insulin-like growth factor-1 (IGF-1) and oxidized low density lipoprotein (oxLDL) on expression of phosphatase PHLPP1 in vascular smooth muscle cells (VSMCs).Methods Rabbit aortic VSMCs were cultured.VSMCs proliferation ability was determined by measuring cell number and mitochondrial dehydrogenase (MD) activity with MTT assay.Western blot was used to detect the protein expression of phosphatase PHLPP 1.Results IGF-1 (100μg/L) increased cell number and MD activity to 3.02 and 3.59 times of that in control group.oxLDL(50μg/ ml) elevated the above two parameters to 2.03 and 2.91 times respectively.Western blot showed that IGF-1 and oxLDL inhibited the expression of PHLPP 1 to 39.27% and 40.26% of the control group (P＜0.01).Conclusion IGF-1 and oxLDL may enhance the proliferation of VSMCs by decreasing the expression of phosphatase PHLPP1 .

A model of acute lung injury was reproduced by intravenous injection of endotoxin (700?g / kg) to rabbits. It had been found that the rabbits were in the state of shock, with leukopenia and thrombocytopenia, increased 6 -keto-PGF1? and TXB2, decreased serum ACE and increased permeability of the pulmonary capillaries. Granulocyte sequestration and disturbance in pulmonary microcirculation were found in lungs. A series of changes in epithelial and endothelial cells were also found in both lungs. It was obviously proved that PGE1 had some therapeutic effects in acute lung injury induced by E. coli endotoxin.

Objective To study the difference of the constructed doses between electronic portal imaging device (EPID) and dynalogs files of linac for in vivo phantom dosimetry.Methods Twelve pelvic patients treated with volumetric modulated arc therapy (VMAT) plans were selected and the information of each plan was copied to theCheese phantom to recalculate the doses before delivered on Varian RapidArc Linac.TheCheese phantom was placed on the isocenter and the electronic portal image (EPI) formed by the EPID was sent to EPIgray software to reconstruct the actual delivered doses.Meanwhile,dynalogs files were respectively imported to the Mobius software to reconstruct the actual delivered doses too.The point dose in the center of each VMAT plan (the center of the effective sensitive volume of ionization chamber) was measured by the A1SL ionization chamber.At the same time,the dose of sensitive volume of ionization chamber from treatment planning systcm (TPS) was recorded.Results The relative deviation between the dose from TPS and the measurement results by the ionization chamber was 1.13％.The difference between the reconstructed doses of EPID-based or the dynalogs file-based with the measurement results by the ionization chamber was not statistically significant (P ＞ 0.05).Conclusions The two methods of dose reconstruction can provide reference for in vivo dosimetry of VMAT.