Objective To explore the associations between fasting serum lipids and high-sensitivity C-reactive protein ( hsCRP).Methods Serum triglyceride ( TG),high-density lipoprotein cholesterol (HDL-C) and hsCRP were measured in residents of Chengdu,China.Subjects with potential factors which might influence lipids and hsCRP were excluded,580 subjects [ mean age ( 62.3 ± 6.6 ) years ; male:58.7％ ] were finally recruited by random sampling methods.Results There was a weak positive relationship between TG and hsCRP ( r =0.108,P =0.01 ) and a weak negative relationship between HDLC and hsCRP (r =- 0.197,P ＜ 0.001 ),this was also true in the sub-group with BMI ＜ 24 kg/m2 ( r =0.236,-0.140 respectively,all P ＜0.001 ).In subjects with BMI ＜24 kg/m2,the hsCRP concentration was significantly higher in subjects with higher TG or lower HDL-C ( all P ＜ 0.05 ).hsCRP increased in proportion with the degree of dyslipidemia.After adjusting for gender,age,TC,LDL-C,fasting blood glucose,systolic blood pressure,diastolic blood pressure,history of hypertension and diabetes,smoking and alcohol drinking,logistic regression analysis showed that the odds ratio for increased hsCRP was 1.970 in subjects with either increased TG or lower HDL-C (P =0.105) and 9.098 in subjects with both higher TG or lower HDL-C levels (P =0.031 ).However,the observed relationship between TG,HDL-C and hsCRP in subjects with BMI ＜ 24 kg/m2 could not be observed in subjects with subjects with BMI ＞ 24 kg/m2despite significant more cardiovascular risk factors in these subjects.Conclusions A weak positive correlation between TG and hsCRP as well as a weak negative correlation between HDL-C and hsCRP was evidenced in the whole cohort suggesting dyslipidemia might be related to enhanced inflammatory status.However,this relationship is not observed in subjects with BMI ＞ 24 kg/m2 despite existence of more cardiovascular risk factors in these subjects.

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.

Background It has been proven that ultrasonic destruction of microbubbles can enhance gene transfection efficiency into the noncardiac cells, but there are few reports about cardiac myocytes. Moreover, the exact mechanisms are not yet clear; whether the characteristic of microbubbles can affect the gene transfection efficiency or not is still controversial.This study was designed to investigate whether the ultrasound destruction of gene-loaded microbubbles could enhance the plasmids carried reporter gene transfection in primary cultured myocardial cell, and evaluate the effects of microbubbles characteristics on the transgene expression in cardiac myocytes.Methods The β-galactosidase plasmids attached to the two types of microbubbles, air-contained sonicated dextrose albumin (ASDA) and perfluoropropane-exposed sonicated dextrose albumin (PESDA) were prepared. The gene transfection into cardiac myocytes was performed in vitro by naked plasmids, ultrasound exposure, ultrasonic destruction of gene-loaded microbubbles and calcium phosphate precipitation, and then the gene expression and cell viability were analyzed.Results The ultrasonic destruction of gene-loaded microbubbles enhanced gene expression in cardiac myocytes compared with naked plasmid transfection ((51.95±2..41) U/g or (29.28±3.65) U/g vs. (0.84-0.21) U/g, P ＜0.01), and ultrasonic destruction PESDA resulted in more significant gene expression than ASDA ((51.95e2.41) U/g vs. (29.28±3.65)U/g, P ＜0.05). Ultrasonic destruction of microbubbles during calcium phosphate precipitation gene transfection enhanced 3-galactosidase activity nearly 8-fold compared with calcium phosphate precipitation gene transfection alone ((111.35±11.21) U/g protein vs. (14.13±2.58) U/g protein, P＜0.01). Even 6 hours after calcium phosphate precipitation gene transfection, ultrasound-mediated microbubbles destruction resulted in more intense gene expression ((35.63±7.65)U/g vs. (14.13±2.58) U/g, P＜0.05 ).Conclusions Ultrasonic destruction of microbubbles might be a promising method for the delivery of non-viral DNA into cardiac myocytes, and the gene tranfection is related to the characteristics of microbubbles.

Objective Acute lung injury induced by variety causes can be reduced by mesenchymal stem cells.Some studies have shown that mesenchymal stem cell-derived exosomes have similar features with mesenchymal stem cell,but its role in acute lung injury is less studied.The study was to investigate the protective role and underlying mechanisms of bone marrow mesenchymal stem cell-derived exosomes (BMSC-DEs) on smoke inhalation injury (SⅡ) in rats.Methods Thirty Wistar rats were randomly divided into 3 equal groups:normal control group,smoke inhalation injury (SⅡ) model group and bone marrow mesenchymal stem cell-derived exosomes (BMSC-DEs) treated group.12 h after establishing the SⅡ model,BMSC-DEs treated group was injected with 0.5 mL BMSC-DEs (derived from 4× 106 BMSCs),and normal control group and SⅡ model group were injected with equivalent volume of normal saline.7 days later,samples were collected.The histopathologic changes of lung were observed after HE staining;BCA was used to test the amounts of total protein in bronchoalveolar lavage fluid (BALF);Enzyme linked immunosorbent assay was used to test the levels of tumor necrosis factor-α (TNF-α) and keratinocyte growth factor (KGF) in the lung tissue;Immunohistochemical was used to test the levels of pulmonary surfactant protein C(SP-C).Results The BALF levels of total protein of SⅡ group was significantly higher than those of normal control group (P＜0.01) and BMSC-DEs groups(P＜0.05);Compared with normal group [(0.164±0.021) ng/L],the levels of tumor necrosis factor-α of SII and BMSC-DEs groups [(0.355±0.106)、(0.234±0.024) ng/L] (P＜ 0.05) were significantly higher,and SⅡ group was higher than that of BMSC-DEs group(P＜0.01);Compared with normal group,the KGF protein expression level in lung tissue of SⅡ group was significantly lower (P＜0.05),but BMSC-DEs group was higher (P＜0.05).BMSC-DEs group was higher than SⅡ group (P＜0.01);Immunohistochemistry showed that the SP-C expression level in lung tissue of SⅡ group was significantly lower than those of other groups (P＜0.05).There was no statistically difference between BMSC-DEs group and control group (P＞0.05).Conclusion BMSC-DEs has a protective effect of smoke inhalation injury rats,the underlying mechanism may be related to BMSC-DEs to reduce inflammation and promote restoration of the alveolar epithelial type Ⅱ.

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.

Objective Novel stents loaded with antibody against CD105 were analyzed for their potential to limit coronary neointima formation and to accelerate endothelialization by attracting activated endothelial cell. Methods Thirty Stents coated with antibody against CD105, thirty unloaded polymer, and thirty bare metal stents were deployed in 90 coronary arteries of 30 minipigs. Oral aspirin (300 mg before operation and 100 mg post operation) and clopidogrel (300 mg before operation and 75 mg post operation) were orally administrated. Coronary artery quantitative analysis was completed by coronary arteriography,the vascular endothelium changes were observed under scanning electron microscope and the vascular morphological changes were observed under light microscope 7 and 14 days after operation. Results Complete procedural and angiographic success was achieved in all 30 minipigs. There were no major adverse cardiac and cerebrovascular events. At 7 days, there was no difference for mean neointimal area and percent rea stenosis among various groups. At 14 days, endothelialization scores were significantly higher in the CD10S antibody-loaded stents and bare metal stents group than in sirolimus-eluting stents group (1.78 ± 0.49, 1. 50±0. 67 vs. 1. 08±0. 29, all P < 0. 05 ), mean percent area stenosis in the CD105 antibody-loaded stents, sirolimus-eluting stents group were less than that in bare metal stents group [ (23. 8± 4) % , (24. 2±2)% vs. (38.0 ±3)% , all P <0.05] ,mean angiographic late luminal loss in the CD105 antibody-loaded stents, sirolimus-eluting stents group were less than that in bare metal stents group [ (0. 29±0. 28) mm, (0. 28±0. 02) mm vs. (0.41±0. 01) mm, all P < 0. 05 ]. There was no difference for mean percent area stenosis in the CD105 antibody-loaded stents and sirolimus-eluting stents group. The mean neointimal area in the CD105 antibody-loaded stents,and sirolimus-elutingstents group were less than that in bare metal stents group [(0.88±0.08) mm2, (0. 89 ±0. 12mm)2 vs. ( 1. 00 ±0. 14) mm2 , all P<0.05] and there was no difference for the mean neointimal area in the CD105 antibody-loaded stents and sirolimus-eluting stents group. At 7 and 14 days, there was no difference for the injury score and the inflammation score among various groups, scanning electron microscopy evidenced enhanced endothelial coverage on CD105 antibody-loaded stents compared to sirolimus-eluting stents group. Conclusion Stent coated with antibody against CD105 could effectively reduce in-stent restenosis and accelerate endothelialization in th eminipigs.