ObjectiveTo discuss the potential relationship of plaque burden (PB) and coronary remodeling in acute coronary syndrome (ACS) patients.MethodsNinety-one patients with ACS in Qingdao Municipal Hospital during January 2011 to June 2014 underwent the conventional coronary angiography and intravascular ultrasonography (IVUS). The remodeling of 60 cases were positive (remodeling index [RI]>1) and those of 31 cases were negative (RI<1). All 91 patients were included in this study, including 9 cases (PB<60%), 19 cases (60%≤PB<70%), 48 cases (70%≤PB<80%) and 15 cases (PB>80%). The difference of plaque cross-sectional area (P-CSA), lumen cross-sectional area (L-CSA), external elastic membrane cross-sectional area (EEM-CSA), average EEM-CSA, PB between positive remodeling andnegative remodeling were compared by independent-samplest test. ANOVA was used to compare P-CSA, L-CSA, EEM-CSA and RI among patients with different PB. The relevance of PB, P-CSA, EEM-CSA, L-CSA and RI were analyzed by Pearson correlation analysis.ResultsThere were no signifi cant differences in P-CSA, L-CSA, EEM-CSA and PB between patients with positive remodeling and negative remodeling. Average EEM-CSA of patients with negative remodeling were signifi cantly greater than that of patients with positive remodeling ([13.24±1.98] mm2vs [17.30±3.16] mm2,t=2.46,P<0.05). P-CSA, EEM-CSA and L-CSA had signifi cant differences (F=24.56, 28.97 and 7.14,P<0.001) while RI had not statistical signifi cant difference among patients with different PB. With the increase of PB, P-CSA and EEM-CSA increased (P-CSA: [6.01±1.68], [9.12±2.00], [11.42±2.05] and [14.05±4.00] mm2, EEM-CSA: [11.43±1.90], [13.64±2.93], [15.14±2.64] and [16.64±4.08] mm2), L-CSA reduced ([5.44±0.89], [4.52±0.99], [3.72±0.74] and [2.60±0.63] mm2). PB was positively correlated with P-CSA and EEM CSA (r=0.76, 0.50,P<0.001), but was negatively correlated with L-CSA (r=-0.74, P<0.001). RI had no relationship with PB, P-CSA, L-CSA and EEM-CSA.ConclusionsCoronary artery remodeling is a very complicated dynamic process. Except the PB, other factors probably affect the direction of remodeling. RI is not suitable as the index for the assessment of vascular remodeling.

Objective To discuss the feasibility of Monte Carlo N-particle transport code(MCNP)simulated calculation.Methods The calculation in water phantom was contrasted with the practical measurements and the reported values using the percent depth dose(PDD)curve and normal peak scatter factor.Results There Was no significant difference between calculated and measured results in the 10 cm×10 cm field(t＝-0.41,P>0.05),however,there were significant differences in the 5 cm×5 cm field(t=7.2,P<0.05)and in the 12 cm×12 cm field(t=-4.6,P<0.05).There was no significant difierence between the calculated results and the reported values(t=-1.91,P>0.05).In the same radiation field,the PDD decreased as the depth increased,but increased as the size of the radiation field increased at the same depth.PDD and normal peak scatter factor were both important parameters for calculation of prescribed dose.Conclusions It is possible to establish a set of accurate and comprehensive percent depth doses and normal peak scatter factor parameters so as to provide the basis of clinical use, quality assurance and quality control for radiotherapy.

Objective:To study the specific mechanism of LINC01018 involved in the pathogenesis of colon cancer.Methods:The expression of LINC01018 in colon cancer tissues and cells and normal colon tissues and cells were detected by real time fluorescence quantitative polymerase chain reaction (qRT-PCR). HT-29 cell line which overexpresses LINC01018 stably was established. RNA binding protein immunoprecipitation (RIP) assay was used to detect the interaction between LINC01018 and E2F1 protein. Dual luciferase assay was used to detect the regulatory effect of E2F1 on CDK6 promoter. The expression of E2F1 or CDK6 was up-regulated in HT-29 cell line which overexpresses LINC01018, then the proliferation, invasion and migration of HT-29 cells and the expression of CDK6 and matrix metalloproteinase-2 (MMP-2) in HT-29 cells were detected by cell counting method (CCK-8) assay, Transwell assay and Western blot.Results:The expression of LINC01018 was abnormally low in colon cancer tissues and cells. The result of RIP assay showed that LINC01018 interacted with E2F1 protein. The result of dual luciferase assay showed that E2F1 protein could enhance the efficiency of CDK6 promoter, and E2F1 had a positive regulatory effect on CDK6. Overexpression of LINC01018 could attenuate the positive regulatory effect of E2F1 on CDK6. Up-regulation of E2F1 or CDK6 expression could attenuate the effects of LINC01018 overexpression on the proliferation, invasion, migration and expression of CDK6 and MMP-2 in HT-29 cells.Conclusions:The expression of LINC01018 was abnormally low in colon cancer tissues and cells. LINC01018 may regulate the proliferation, invasion and migration of HT-29 cells through E2F1/CDK6/MMP-2 axis, and participate in the pathogenesis of colon cancer.