Objective To investigated the effects of combined arsenic trioxide(ATO) and resveratrol(Res)on the viability of NB4 human leukemia cells. Methods NB4 human leukemia cell was used in this experiment.Cells were cultured in ATO (0,0.1875,0.3750,0.7500, 1.1250, 1.5000,2.2500,3.0000,5.0000 μmol/L) and Res (0, 1.5625,3.1250,6.2500, 12.5000, 18.7500,25.0000,37.5000,50.0000 μmol/L). Cell viabilities were measured by MTT in different treatment groups. Half inhibitory concentration(IC50) was calculated. The ratio of concentration of ATO and Res 1.5∶ 18,1.5∶ 25,1.5∶ 35 was added to cells, and the combination index(CI) was calculated. The level of ROS in control, ATO( 1.5000 μmol/L), Res(25.0000 μmol/L) and ATO(0.9000 μmol/L) + Res( 12.5000μmol/L) groups was measured by chemiluminescence assay. Results ①ATO( ≥0.7500 μmol/L) reduced the viability of NB4 cells in a concentration-dependent manner(P ＜ 0.05 ), and IC50 was (1.78 ± 0.11 )μmol/L. ②)Res (≥18.7500 μ mol/L) dose-dependently decreased the viability of NB4 cells (P ＜ 0.05 ), and IC50 was ( 18.71 ±0.18)μ mol/L. ③Combination of ATO and Res showed an antagonistic effect on NB4 cells viability. ④The ROS in Res group( 1670.55 ± 13.97) was significantly lower than that in control group(2345.88 ± 14.48,P ＜ 0.05). The ROS in ATO group (3092.42 ± 94.84) was significantly higher than that in control group(P ＜ 0.05). The ROS in ATO + Res group (1860.27 ± 15.99) was significantly lower than that in ATO group(P ＜ 0.05). Conclusions NB4 cell survival rate can be decreased by ATO and Res. The combination of arsenic trioxide and Res presents an antagonistic effect on NB4 cell viability, in part by reducing intracellular ROS formation.

Background Bone morphogenetic protein-6 (BMP-6) is closely correlated with tumor differentiation and skeletal metastasis. Estrogen is considered as a stimulant for the initiation and promotion of breast cancer. Previous studies demonstrated that 17β-estadiol (E2) can selectively increase the expression of BMP-6. This experiment is designed to detect the molecular mechanism of estrogen activating BMP-6 gene transcription in human estrogen receptor positive (ER+) breast cancer cell line MCF-7. Methods After the treatment of MCF-7 cells with E2 at different concentrations (10-11 mol/L, 10-9 mol/L, 10-7 mol/L), the BMP-6 expression level was examined through real-time polymerase chain reaction. Through restriction enzyme digestion, human BMP-6 1.2 kb long promoter, BMP-6 0.7 kb long promoter was cloned into pGL-3 basic vector; after the treatment with 10-7 mol/L E2, luciferase activities of the two promoters were detected. Site-directed mutagenesis was performed to obtain the mutant forms of estrogen response element half-site (1/2 ERE) element and Sp1 sites in the BMP-6 promoter, the activities of these mutant form promoters were detected following the methods mentioned above. Chromatin immunoprecipitation (ChIP) assay was also used to confirm the binding of estrogen receptor α (Erα) on BMP-6 promoter in the presence of E2. Results E2 dose dependently increased BMP-6 mRNA expression in human ER+ breast cancer cell line MCF-7. At a dose of 10-7 mol/L E2, human BMP-6 1.2 kb promoter activity was increased by 90% compared with the control group treated with ethanol (P<0.05). Both the 1/2 ERE response element mutant form and the Sp1 site mutant form of the BMP-6 promoter abolished the activation of the BMP-6 promoter's response to E2. Through ChIP assay, the binding of Erα on 1/2 ERE response element in BMP-6 promoter was further validated. Conclusion Estrogen induces BMP-6 expression in human ER+ breast cancer cell line MCF-7 through its receptor Erα binding on 1/2 ERE element in the BMP-6 promoter.

Objective To investigate the expression changes of myeloid-related protein-8 (MRP-8) and myeloid-related protein-14 (MRP-14) in children with Kawasaki disease (KD) and to obtain laboratory diagnostic serum markers and new targets for its drug therapy.Methods A total of 46 patients with KD(KD group) were enrolled from Jul.2009 to Dec.2010 and divided into the coronary artery dilatation(CAD) group(n =15) and the normal coronary artery group(n =31) ;Meanwhile,25 febrile patients with acute respiratory tract infection but without disease in the circulatory,blood,immune systems formed the non-KD febrile group.Twenty healthy children from the out-patient department formed the healthy control group.Peripheral venous blood was collected in the acute and subacute stage of KD.Levels of MRP-8/MRP-14 were detected with enzyme-linked immunosorbnent assay (ELISA).Gene expressions of MRP-8,MRP-14 in leukocytes were analyzed by semi-quantitative reverse transcription-polymerase chain reaction(RTPCR).Results The serum levels of MRP-8/MRP-14 along with mRNA expressions of MRP-8 and MRP-14 in the leukocytes in the out-patient acute and subacute stage of KD were significantly higher than those in the non-KD febrile group and the healthy control group(all P ＜ 0.05) ;There was no significant difference between non-KD febrile group and healthy control group (P ＞ 0.05).The serum levels of MRP-8/MRP-14 along with mRNA expressions of MRP-8 and MRP-14 in leukocyte in actue stage of KD were significantly higher than those in subacute stage(all P ＜ 0.001).The serum levels of MRP-8/MRP-14 as well as mRNA expressions of MRP-8 and MRP-14 in the acute and the subacute stage of CAD group were significantly higher than those in the normal coronary artery group(P ＜ 0.05).Conclusions MRP-8/MRP-14 may probably play a role in the pathogenesis of KD and can be used as a diagnostic indicator for KD;MRP-8/MRP-14 may be involved in the formation of coronary artery lesion and can be used as an effective predictor for the coronary artery lesion.

Objective To evaluate the clinical characteristics of left ventricular fat replacement. Methods We identified 45 patients [28M/17F, mean age (51.9 ± 14. 7 )years] with left ventricular myocardial fat replacement ( CT value ≤ - 30 Hu) by cardiovascular CT. Results Among 45 patients, 25 patients[20M/5F, mean age (61.2 ± 10. 4) years] were diagnosed as coronary artery disease (CAD). There was 56% single-vessel disease, 20% double-vessel disease and 24% triple-vessel disease,true left ventricular aneurysm was detected in 3 patients and left ventricular thrombi in 1 patient, the dimension of left ventricle was (54. 5 ±9. 4) mm and the LVEF was (51.8 ± 13 ) % in CAD group. In this group, fat replacement occurred in the region of myocardial infarction and presented as curvilinear band in subendocardial region. The left ventricular wall thickness was lower than 5 mm in 21 cases. The location of fat replacement in CAD group is as follows: apical region in 18 patients, distal septal in 15 patients, distal anterior in 11 patients, mid-septal in 7 patients, mid-anterior in 7 patients and basal in 1 patients. The age of remaining 20 patients (8M/12F) without CAD were (57. 8 ± 13.3) years. In the group of non-CAD,dilated cardiomyopathy was diagnosed in 3 patients, atrial septal defect in 1 patient, rheumatic heart disease in 1 patient, there was no structural heart disease in the remaining 15 patients. The dimension of left ventricle was (51.1 ± 9. 1 ) mm and the LVEF was (59. 4 ± 13.9 )%. In non-CAD group, fat replacement mainly occurred in septal region, presented as curvilinear band in 17 patients and patch in 3 patients. The location of fat replacement in this group is as follows: mid-septal region in 11 patients, distal-septal in 10 patients and apical in 9 patients. The intramural fat replacement was detected in 14 patients: subendocardial fat replacement in 10 patients and both intramural and subendocardial fat replacement in 4 patients. Conclusions Left ventricular fat replacement could be documented in CAD patients, non-CAD cardiomypathy patients and in patients without structural heart disease. Left ventricular fat replacement often positioned in apical region in CAD patients as a consequence of infarct healing while mostly positioned in septal region in non-CAD patients, the definite clinical implication of left ventricular fat replacement in nonCAD patients remains to be clarified.

Background The non-operation treatment of intra-abdominal trauma guided contrast enhanced ultrasound (CEUS) is one of the hottest research topic. Gelatin/thrombin/calcium (GTC) was developed as a novel haemostatic agent for non-operable intra-abdominal trauma. We hypothesized that GTC can achieve haemostasis (without the use of pressure)within a short time in a large wound model by percutaneous injection under CEUS guidance.Methods Forty Wister rats received large liver injuries by haemostatic clamp and were randomly divided into four groups, according to the haemostatic agent used. These included normal saline (NS) group A, lyophilising thrombin powder (LTP) group B, GTC group C, and absorbable α-cyanoacrylate (ACNA) group D. Each injury site was treated with one of the above materials and total bleeding time was recorded. All liver wounds were evaluated using CEUS at three periods: pre-injury, injury and post-treatment. The liver wounds were also evaluated by histology 3, 6, and 9 days after injury and the extents of abdominal adhesions were recorded.Results The sensitivity of CEUS (100%) in detecting blunt traumatic liver lesions was significantly higher than conventional ultrasound (42.5%). Bleeding times at the injury site in the GTC group C ((129.3±14.0) seconds) and ACNA group D ((5.2±1.0) seconds) were significantly shorter than those in the NS group A ((369.5±48.8) seconds, P ＜0.01) and LTP group B ((324.7±52.22) seconds, P ＜0.01). The LTP group B showed no significant difference compared with the NS group A. Gross examination of liver tissue revealed that there were fewer intra-abdominal adhesions in the GTC group C (10%) than in the ACNA group D (100%). Histopathologic examination showed that GTC was completely absorbed after nine days.Conclusions GTC, delivered by percutaneous injection under CEUS, may achieve haemostasis (without the use of pressure) within a short time in a large wound model. GTC is absorbable and may prevent intra-abdominal adhesions.Therefore, it may be the optimal choice for first aid treatment of large abdominal wounds in the setting of blunt trauma.

Objective To determine the prevalence and to identify risk factors of peri-procedure electrical storm (ES) in patients with acute myocardial infarction (AMI) underwent emergency percutaneous coronary intervention (PCI).Methods The clinical data of 228 AMI patients underwent emergency PCI were retrospectively analyzed and patients were divided into ES group (n = 39) and non-ES (n = 189) group.ES was referred to spontaneous ventricular tachycardia or ventricular fibrillation occurring twice or more within 24 h and requiring emergency treatment including anti-arrhythm medicine and/or cardioversion or defibrillation.Results ES was diagnosed in 39 out of 228 patients (17.1%) during peri-procedure stage.The incidence of ES in patients with various infarct related arteries (IRA) was as follows:55.6% with left main artery (LM),23.7% with right coronary artery (RCA),12.4% with anterior descending branch (LAD) and 0 with left circumflex artery (LCX).Older age,lager diameter of IRA,higher concentration of CK-MB and cTnT,higher incidence of reporfusion arrhythmia (RA),lower grade of TIMI after PCI and higher mortality were associated with increased risks of ES (The P value was 0.043,0.012,0.036,0.018,0.001,0.049,respectively).Gender,systolic pressure,diastolic pressure,random blood glucose level,white blood count and concentration of hs-CRP were similar between ES and non-ES patients.Logistic analysis showed that the diameter of IRA (OR 2.381,95% CI 1.127-5.028,P = 0.023),TIMI grade of IRA after PCI (OR 4.744,95% CI 1.773-12.691,P = 0.002) and RA (OR 12.680,95% CI 4.360-36.879,P =0.000)were the independent risk factors of per-procedure ES in AMI patients underwent emergency PCI.Conclusions The AMI patients with LM as IRA had the highest incidence of ES during emergency PCI and the diameter of IRA,TIMI grade of IRA after PCI and RA were independent risk factors for the development of ES during peri-PCI stage.