Abstract:To date, translational medicine is very attractive and multifaceted in the field of science. Aiming at promoting clinical application achievements incrementally, it devotes to break through the inherent barriers between basic research and clinical practice. As well, it plays an important role in bridging the gap between laboratory research and drug development. Herein, we highlight the advances in current ischemic stroke related translational research tragedy, which covers the trends and opportunities in future studies. We also lay emphasis on the necessity of pushing forward stroke-related translational research in an emerging blueprint of neuroscience.

Abstract:Aim To observe the effects of hyperlipidemia on the microvascular blood flow volume and oxygen supply of the rabbit aortic wall. Methods Twenty male New Zealand rabbits were randomly divided into normal control group or high-fat diet group, 10 rabbits in each group, and were fed for 4 weeks. Blood and abdominal aorta samples were collected at the end of the study. The serum lipoprotein levels were measured by automatic biochemical analyzer, microvascular blood flow of the rabbit aortic wall was measured by color microspheres technology. Immunohistochemical staining was used to observe the microvessel density and the hypoxia condition in abdominal aorta wall. Hypoxia inducing factor-1α （HIF-1α） mRNA and protein expression of the arterial wall tissue were detected respectively by Western blot and Real-time fluorescent quantitative reverse transcription PCR （RT-qPCR）. Results Serum lipoprotein levels in high-fat diet group were increased significantly compared to normal control group （all P＜0.01）. Color microspheres test result showed the microvascular blood flow of the aortic wall in high-fat diet group was significantly higher than that in the normal control group ［58.56 ±6.21 μL/（min·g） vs. 39.17±4.47 μL/（min·g）, P＜0.01］, and the wall microvessel density in high-fat diet group was also significantly higher than that in the normal control group （5.1 ± 0.4 n/mm² vs. 2.7±0.7 n/mm², P＜0.01）, as HIF-1α expression also had no obvious changes in protein and mRNA levels （P>0.05）. Conclusion Hyperlipidemia increases the microvessel density and microvascular blood flow volume of the rabbit aortic wall, but does not affect the oxygen supply.

Abstract:Aim To explore the effect of autophagy intervention on endothelial cells endothelial nitric oxide synthase （eNOS） and endothelin-1 （ET-1） expression under low shear stress. Methods ApoE^－/－ mice were fed with high fat diet for 12 weeks. HE staining was used to detect the pathological changes of aortic sinus. Immunohistochemistry was applied to detect the protein expression of autophagy markers Beclin1, microtubule-associated protein 1 light chain 3 （LC3Ⅱ） and p62. Human umbilical vein endothelial cells （HUVEC） and separated New Zealand rabbits common carotid arteries were placed into an in vivo perfusion system with low shear stress （5 dyne/cm²） or normal shear stress （15 dyne/cm²） for 1 h, then the expression of Beclin1, LC3Ⅱ/LC3Ⅰ and p62 was measured using Western blot. After treated with 5 dyne/cm² for 1 h followed with or without rapamycin or 3-methyladenine （3-MA） for 30 min, the expression of eNOS and ET-1 in human vascular endothelial cells and common arteries of New Zealand rabbits was detected. Results The expression of Beclin1, LC3Ⅱ and p62 was significantly increased in atherosclerotic plaque. Compared with 15 dyne/cm² treatment group, the expression of Beclin1, LC3Ⅱ and p62 was significantly increased in 5 dyne/cm² treatment group （P<0.05）. The autophagy inducer rapamycin up-regulated the eNOS expression and inhibited the ET-1 expression in both 5 dyne/cm² treated HUVEC and common carotid arteries, whereas autophagy inhibitor 3-MA further inhibited eNOS expression and increased the ET-1 expression. Conclusion The inhibition of autophagy might contribute to the decreased expression of eNOS and the increased expression of ET-1 under low shear stress, which was improved by promoting autophagy.

Abstract:Aim To investigate the effect of Neu-P11, a novel melatonin receptor agonist, on insulin sensitivity in sleep restricted rats as well as the underlying mechanism. Methods Method of rotating cage was adopted to establish SD rat models of sleep restriction. During the 8 days of sleep restriction, rats were injected intraperitoneally with Neu-P11 （20 mg/kg）, MLT （5 mg/kg）, saline respectively every day. Plasma glucose, fasting insulin, malondialdehyde （MDA） levels and enzyme activity of glutathione peroxidase （GSH-Px）, superoxide dismutase （SOD） were detected at the end of experiment, the proteins of JNK and phosphorylated JNK in muscles were measured by Western blot. Results Compared with control group, sleep restricted rats showed increased levels of plasma glucose, fasting insulin, but antioxidative potency decreased. However, in Neu-P11 and melatonin-treated sleep restricted rats, the levels of plasma glucose, fasting insulin and MDA decreased with an increase of SOD, GSH-Px activities. Neu-P11 or melatonin also down-regulated the levels of JNK and phosphorylated JNK which were increased by sleep restriction. These data suggest that glucose homeostasis and antioxidative potency of the chronic sleep restricted rats were protected by Neu-P11 and melatonin. Conclusions Neu-P11 could improve metabolic profiles and insulin resistant induced by sleep restriction, and the regulation of JNK and antioxidative potency may be the underlying mechanism.

Abstract:Aim To investigate the effects of angiotensin（1-7）［Ang（1-7）］ and angiotensinⅡ（AngⅡ） on scavenger receptor class B type Ⅰ（SR-BⅠ）, ATP-binding cassette transporter A1（ABCA1） and cholesterol efflux in THP-1 derived foam cells. Methods Human monocytic cell line （THP-1） were induced into macrophages by 100 nmol/L phorbol myristate acetate（PMA） for 48 h, and treated with oxidized low density lipoprotein （ox-LDL） to construct the foam cells, then were randomly allocated into five groups: control group, AngⅡ group,Ang（1-7） group,Ang（1-7）+AngⅡ group and AngⅡ+Ang（1-7）+A-779 group. The mRNA and protein expression of SR-BⅠ, ABCA1 were determined by RT-PCR and Western blot, the intracellular cholesterol efflux rate was detected by liquid scintillator. Results Compared with the control group, AngⅡ decreased SR-BⅠ and ABCA1 in both protein and mRNA, and inhibited the cholesterol efflux（P<0.05）. Those effects could be attenuated by cotreatment with Ang（1-7）（P<0.05）. However when incubated with A-799, an inhibitor of Ang（1-7）, the effects of Ang（1-7） on promoting the expression of SR-BⅠ, ABCA1 and the cholesterol efflux were significantly abolished（P<0.05）. Conclusion In THP-1 derived foam cells, Ang（1-7） via its specific receptor MAS attenuates the reduction of the expression of SR-BⅠ and ABCA1 induced by AngⅡ, and increases the cholesterol efflux.

Abstract:Aim Lentiviral vectors targeting human lectin-like oxidized low density lipoprotein receptor-1 （LOX-1） gene with RNA interference （RNAi） were transfected into human umbilical vein endothelial cell （HUVEC）, and the protective mechanisms on the injury induced by oxidized low density lipoprotein （ox-LDL） were observed. Methods The LV-si-OLR1 optimal interference was selected from the small interfering RNA （siRNA） interference which validity had been verified and the virus titer was measured. HUVEC were transfected after 96 h. The expressions of mRNA and protein of LOX-1 were respectively detected by reverse transcription polymerase chain reaction （RT-PCR） and Western blot.72 h after transfection, HUVEC were cultured with ox-LDL, which final concentration was 150 mg/L. 24 h after cultured by ox-LDL, endothelial cells vigor were detected by methyl thiazolyl tetrazolium （MTT） method and the expression levels of nitric oxide （NO） were detected by nitrate reductase method the changes in the expression level of intercellular adhesion molecule-1 （ICAM-1）, monocyte chemotactic protein-1 （MCP-1）, RhoA, Rho kinase-1 （ROCK1）, Rho kinase-2 （ROCK2） were detected by Western blot in each group. Results The sequencing results confirmed that interference targeting human LOX-1 lentiviral vector was successfully constructed, which packaged lentiviral titer 6×10¹¹ TU/L. Compared the transfected with the non-transfected groups, the expression of LOX-1 mRNA and protein significantly decreased （P<0.01） Compared with the control group, ox-LDL treated group could decrease endothelial cells vigor and expression levels of NO, while increase the expression levels of ICAM-1, MCP-1, RhoA, ROCK1, ROCK2 （P<0.05） After suppressing the expression of LOX-1, compared with ox-LDL treated group, endothelial cells vigor and expression of NO were increased, while expressions of ICAM-1, MCP-1, RhoA, ROCK1, ROCK2 were restrained （P<0.05）. Conclusion RNA interference in the expression of LOX-1 could reduce endothelial cell injury by increasing endothelial cells vigor and expression of NO, while reducing expressions of ICAM-1, MCP-1 and the levels of Rho/Rho kinase activity, which provided experimental evidence for treating atherosclerosis for the use of targeting LOX-1 gene.

Abstract:Aim To investigate the role and significance of voltage dependent K⁺ channel（K_V） and ERK1/2 signal pathway in the pathological process of hypoxia hypercapnia pulmonary vasoconstriction （HHPV） in rats. Methods We made the second pulmonary artery rings of SD rats in vitro, and divided the rings randomly into: control group, hypoxia hypercapnia group, hypoxia hypercapnia+DMSO incubation group（HD group）, hypoxia hypercapnia+4-aminopyridione（4-AP） incubation group（4-AP group）, hypoxia hypercapnia+U0126 incubation group（U0126 group）, hypoxia hypercapnia+4-AP+U0126 incubation group（4-AP+U0126 group）. Under acute hypoxia hypercapnia condition, we observed the effects of the three stages of HHPV incubated by 4-AP or the combined application of 4-AP and U0126. At the same time, the values of rings’ tension changes were recorded . Results Under the acute hypoxia hypercapnia condition,we observed a biphasic pulmonary artery contractile response The second pulmonary artery rings were incubated by 4-AP which phase Ⅱ persistent vasoconstriction were enhanced compared with the HD group（P<0.05） U0126 can significantly relieve the phase Ⅱ persistent vasoconstriction created by 4-AP（P<0.05）. Conclusion The blocker of voltage dependent K⁺ channel-4-AP enhanced HHPV, U0126 can significantly relieve the phase Ⅱ persistent vasoconstriction created by 4-AP, which pointed out that the ERK1/2 signal pathway’s participation may be one of the important mechanisms of K_V’s regulation to the process of HHPV in rats.

Abstract:Aim To investigate the RELMɑ/FIZZ1 signal pathway in intervening atherosclerosis in experimental animals, and inspect its influences on angiogenesis. Methods 20 ApoE^－/－ mouse were fed with high fat diet for 12 weeks and randomly divided into 2 groups equally. The model group were fed with high fat diet and another group were fed with high-fat diet but were injected with RELMɑ/FIZZ1 for 2 weeks. 10 C57BL/6J mice were fed with normal diet for control The positive area of plaque were determined. The RELMɑ/FIZZ1 and CD34 positive response intensity at aorta vessel wall, and the capillary density in plaque were measured by immunohistochemical staining. Investigate the abnormally expressed genes and changed signal pathway via array hybridization. Results Compared to control group, model group atherosclerosis plaque formed in mouse arteriae. RELMɑ/FIZZ1 protein had obvious expression by immunohistochemistry in atherosclerotic plaque. Compared to model group, the correcting plaque area was significantly increased in RELMɑ/FIZZ1 group （31.58%±6.65% vs 24.16%±3.59%, P<0.01）. The RELMɑ/FIZZ1 and CD34 positive response intensity and the capillary density in RELMɑ/FIZZ1 group were higher than those in model group （P<0.01）. Array hybridization data analysis shows that 856 genes expressed difference significantly, which 391 genes raised while 465 genes lowered, and 22 signaling pathways are significantly different, including that 12 signaling pathways are activity raised while 10 signaling pathways are activity down. Conclusions RELMɑ/FIZZ1 could promote the progression of atherosclerosis plaque by stimulating angiogenesis. The mechanism has a close relationship with the significant expression of Atg9a and Gng8 genes, the regulation of actin cytoskeleton pathway （rno04810） and the activation of gap junction （rno04540） cell.

Abstract:Aim To investigate the effect of ox-LDL on platelet extracellular matrix metalloproteinase inducer（EMMPRIN，CD147） release. Methods Washed platelets were incubated with ox-LDL （final concentrations of 25 mg/L, 50 mg/L or 100 mg/L ox-LDL, respectively）, PBS （as control） or 100 mg/L native LDL in vitro, and the expressions of CD147 and alpha-granule membrane glycoprotein （CD62P） on platelets were detected by flow cytometry. Soluble CD147 from the platelets was assessed by an enzyme-linked immunosorbent assay. Laser scanning microscopy （LSM） and transmission electron microscopy （TEM） were used to visualize the morphological changes and granule release, respectively, from the platelets. In parallel, the expression of CD147 on the platelets pre-incubated with anti-LOX-1 antibody was detected by flow cytometry. Results The CD147 relative mean fluorescence intensity （rMFI） from the groups of 25 mg/L, 50 mg/L or 100 mg/L ox-LDL （1.01±0.06，1.18±0.07, 1.24±0.08, respectively） were higher than that from the control group （0.86±0.10, both P<0.01） or native LDL group （0.89±0.11, both P<0.01）. The CD147 rMFI（0.96±0.08，1.05±0.07） from the platelets incubated with ox-LDL （50 mg/L or 100 mg/L） prior to pre-incubation with anti-LOX-1 antibody decreased compared with the 50 mg/L or 100 mg/L ox-LDL-treated platelets, respectively （both P<0.001）. After exposure to ox-LDL, morphological changes and granule release in the platelets were visualized by LSM and TEM. Conclusion ox-LDL induces the release of platelet CD147 via binding to LOX-1.

Abstract:Aim To investigate the effects of RNA interference （RNAi） downregulating TLR4 of mice with isoproterenol （ISO） induced myocardial ischemic necrosis. Methods A myocardial ischemic necrosis model of mice was established by abdominal cavity injection of ISO for 3 days. The rats were divided into four groups: control group, myocardial ischemic group （MI group） and myocardial ischemic treated with negative plasmid group （PCN group）, myocardial ischemic treated with siRNA-TLR4 plasmid group （siRNA-TLR4 group）. Inhibition of TLR4 by siRNA-TLR4 plasmid was constructed. Pathological changes of myocardial ischemic were observed through myocardial tissue stained with HE. The expression level of TLR4 was detected by Western blot. The variation of cardiomyocytes apoptosis was measured with TUNEL.Results The expressions of protein of TLR4 in siRNA-TLR4 group were significantly decreased compared with those of control group, PCN group, and MI group. Compared to MI group and PCN group, myocardial ischemic necrosis was relieved in the siRNA-TLR4 group. And numbers of apoptosis cardiomyocytes in siRNA-TLR4 group were lower than those in MI group and PCN group （9.39%±2.61% vs. 61.44%±2.34% and 57.21%±4.40%）. Conclusions RNAi can inhibit TLR4 expression and ameliorat myocardial ischemic necrosis induced by ISO efficiently. It may be promising as a new treatment of acute myocardial ischemic necrosis.

Abstract:Aim To study the effect of fluvastatin on cardiac remodeling and cardiac function， and to investigate the effect of matrix metalloproteinase-9 （MMP-9） and MMP-10. Methods 36 Wistar rats were randomly divided into acute myocardial infarction （AMI） group,AMI+fluvastatin group and the sham-operated group. AMI was established by ligation of the anterior descending coronary artery in rats, fluvastatin was fed to AMI+ fluvastatin group by 20 mg/（kg·d） for 6 weeks. After 6 weeks treatment, then the hemodynamic parameters and mass index of left ventricular and the expression of MMP-9 and MMP-10 were detected. Results Compared with the sham-operated group, left ventricular systolic pressure（LVSP） and the maximal rate of rise and fall （±dp/dt_max） of left ventricular pressure in the AMI group and AMI+fluvastatin group were all decreased（P<0.05）, moreover,these indexes decreased significantly in AMI group than those in AMI+fluvastatin group（P<0.05）. Compared with the sham-operated group, left ventricular end-diastolic diameter （LVEDD）, left ventricular end systolic diameter （LVESD）, left ventricular mass index （LVMI）, MMP-9, MMP-10 were significantly increased in the AMI group and AMI+fluvastatin group moreover,these indexes decreased in AMI+ fluvastatin group than those in AMI group（P< 0.05）. Conclusion Fluvastatin could prevent the cardiac remodeling， the mechanisms may be by reducing the levels of MMP-9 and MMP-10.

Abstract:Aim To observe the effect of Shenshao oral lotion on serum lipids and vasoactive substances in atherosclerotic rats. Methods Atherosclerotic rats model were established by high fat feed and intraperitoneal injection of vitamin D3. 60 male SD rats were divided into six groups randomly: normal feed group, atherosclerotic model group, low dose of Shenshao oral lotion group, middle dose of Shenshao oral lotion group and high dose of Shenshao oral lotion group, simvastatin control group. Pathomorphology change of aorta of the rats was observed through light microscope. Serum lipids and vasoactive substances level of rats in each groups were examined after 12 weeks feed and Shenshao oral lotion were given for 4 weeks. Results The pathological change of aorta of the rats in high dose of Shenshao oral lotion group was alleviated compared with that in atherosclerotic model group. Compared with atherosclerotic model groups, the serum level of total cholesterol, triglyceride, low density lipoprotein cholesterol, endothelin, angiotensinⅡ, thromboxane B2 were lower and the serum level of high density lipoprotein cholesterol, nitric oxide synthase were higher in high dose Shenshao oral lotion group and simvastatin control group（P<0.05）. Conclusions Shenshao oral lotion could modulate blood lipids and vasoactive substances concentration in experimental rats, which may be one of the mechanism of Shenshao oral lotion to prevent atherosclerosis.

Abstract:Aim To investigate the effect of bezafibrate on reversing cholesterol transport from macrophage to feces in vivo, serum lipid profiles of mice were tested after bezafibrate administration. The ³H-cholesterol contents in serum, liver and feces in mice were measured to explore the effect of bezafibrate on reversing cholesterol transport from macrophage to feces in vivo. Methods 28 male C57BL/6 mice were randomly divided into four groups and treated with ordinary diet or plus different dosage （0.1%, 0.25% and 0.5%） of bezafibrate for 4 weeks, then these mice were injected intraperitoneally with ³H-cholesterol-labeled and cholesterol-loaded RAW264.7 macrophages （0.5 mL/mice, the amount of cells achieve 5.0×10⁶）. Serum lipid profiles were determined by enzymatic method. Serum and liver tissues were harvested at 24 h, feces were collected. And all samples were analyzed for the appearance of ³H-tracer （as the percentage of the total injected counts）. Results Bezafibrate （0.1%, 0.25% and 0.5%） dose-dependently and increased the level of high density lipoprotein cholesterol （HDLC） and reduced the level of triglyceride （TG）. After 24 hours of being intrapentoneally injected, the serum ³H-cholesterol levels in the mice treated with different dosage of bezafibrate （0.1%, 0.25% and 0.5%） were significantly higher by 100%, 131% and 110% compared with those in the control （P＜0.05）, the liver ³H-cholesterol levels in the mice treated with different dosage of bezafibrate （0.1%, 0.25% and 0.5%） were significantly higher 86.4%, 52.3%, 51.6% compared with those in the control （P＜0.05）, the feces ³H-cholesterol levels in the mice treated with different dosage of bezafibrate （0.1%, 0.25% and 0.5%） were significantly higher by 110%, 140% and 160% compared with those in the control （P＜0.05）. Conclusions Bezafibrate significantly and dose-dependently reduces the level of TG and increases the level of HDLC, bezafibrate promotes cholesterol reverse transport in vivo, accelerates clearance of cholesterol via feces, so it will be in favor of the prevention of atherosclerosis.

Abstract:Aim To investigate the expression of vascular endothelial growth factor （VEGF） and transforming growth factor-β1 （TGF-β1） on diabetic atherosclerosis in rats and the mechanism and protective effects of simvastatin.Methods SD rats were randomized into normal control group （n＝8）, normal intervention group （n＝8）, model group （n＝18） and model intervention group （n＝16）. Intervention groups were perfused with simvastatin at 20 mg/（kg·d）, and the control groups were given distilled water ［20 mL/（kg·d）］ instead. The diabetic atherosclerosis model was established by streptozotocin （STZ）＋vitamin D3 （VitD3）＋high-fat and high-cholesterol diet. The contents of fasting plasma glucose （FPG）, total cholesterol （TC）, triglyceride （TG）, low density lipoprotein （LDL）, high density lipoprotein （HDL）, fasting insulin （FINS） were detected, and insulin resistance homeostasis （HOMA-IR） was calculated. Plasma VEGF and plasma TGF-β1 were measured by enzyme-linked immunosorbent assay （ELISA）. The expression of VEGF on aortic was evaluated by immunohistochemical method. Results Compared with normal control group, TGF-β1 was significantly increased in intervention group （P<0.01）, and FPG, TC, TG, LDL, HDL, FINS, VEGF and TGF-β1 were significantly increased in model group （P<0.01, P<0.05）. Compared with model group, FPG, TC, TG, LDL, HDL and VEGF were significantly decreased （P<0.01, P<0.05）, and TGF-β1 was significantly higher in intervention group （P<0.01）. In correlation analysis, VEGF showed a negative correlation with body weight and FINS, and had a positive correlation with TC, TG, LDL, FPG and HOMA-IR. TGF-β1 showed a negative correlation with TC, LDL and FPG. In a stepwise multiple regression analysis, FPG and TC were independent risk factors for plasma VEGF level. Conclusions VEGF and TGF-β1 may participate in the occurrence of diabetic atherosclerosis. Simvastatin can decrease the level of VEGF and increase the expression of TGF-β1, and has a significant protective effect on diabetic atherosclerosis.

Abstract:Aim To study the effect of serum interleukin-18 （IL-18） in human acute myocardial infarction and its possible mechanism in the process of plaque rupture. Methods Serum levels of IL-18 and MMP-9 proteins were determined using commercially available enzyme-linked immunoassays in each group: acute myocardial infarction （AMI） group, stable angina pectoris （SAP） group and heathy control group （n＝20, respectively）. Flow cytometry was applied to assess extracellular matrix metalloproteinase inducer （EMMPRIN） expression on the surface of monocytes of each group. In vitro experiment, quantitative real-time polymerase chain reaction （QRT-PCR） and Western blot were performed to compare EMMPRIN expression of monocytes cultured in presence and absence of IL-18. Results In patients with AMI, serum level of IL-18 and MMP-9 and expression of EMMPRIN on monocytes markedly increased compared with patiens with SAP and heathy control group. Furthermore, increased level of IL-18 was positively associated with elevated expression of EMMPRIN on monocytes in AMI group （r²＝0.57, P<0.001）. The data proved that expression of EMMPRIN was enhanced in monocytes cultured in presence of IL-18 （P<0.05）. Conclusion IL-18 stimulates monocytes to express EMMPRIN, which may induce secretion of MMP-9, contributing to atherosclerotic plaque instability and rupture.

Abstract:Aim To explore the association of the functional －509C/T polymorphism in the promoter region of the transforming growth factor-β1 （TGF-β1） gene with coronary heart disease （CHD） and its conventional risk factors including body mass index （BMI）, lipid levels of plasma, and blood glucose in Chongqing Han population. Methods The －509C/T polymorphism of TGF-β1 was genotyped by polymerase chain reaction-restriction fragment length polymorphism methods and DNA sequence technology in 457 CHD patients and 413 controls. The sample was characterized for relevant clinical and biochemical parameters. Results The －509C/T polymorphism of TGF-β1 was significantly associated with the risk of CHD in females for the additive and dominant genetic models （adjusted OR＝1.515, 95%CI＝1.045～2.196, P_additive＝0.028 adjusted OR＝1.937, 95%CI＝1.008～3.719, P_dominant＝0.047）, but not in male for all genetic models （P>0.05）. Female individuals with TT genotype had a 2.36-fold increased risk of developing CHD （adjusted 95%CI＝1.11～5.03, P＝0.026）. In female CHD patients, both CT and TT genotype carriers were related to the decreased high density lipoprotein cholesterol （HDLC） levels and increased levels of total cholesterol （TC）, low density lipoprotein cholesterol （LDLC） and body mass index （BMI） compared with CC genotype carriers, especially in TT genotype carriers reached statistical significance （all P＜0.05）. Conclusions The functional －509C/T polymorphism in the TGF-β1 promoter region was associated with the susceptibility to CHD in Chongqing Han women. Our data show that TGF-β1 polymorphism－509C/T is associated with lipid levels, BMI and CHD in Chongqing Han women. Female individuals with TT genotype have significantly increased the risk of developing CHD.

Abstract:Aim To observe the effects of different atorvastatin doses on contrast induced acute kidney injury （CI-AKI） in patients undergoing coronary angiography （CAG） or percutaneous coronary intervention （PCI）. Methods 106 cases were randomized into 2 groups: one group received 20 mg atorvastatin at night and another group received 40 mg atorvastatin at night, all patients received drug treatment for 3 days before CAG or PCI all patients admitted to hospital within 24 hours completed routine inspections and examinations of heart ultrasound and renal vascular ultrasound and improved renal function in 48 hours after CAG or PCI and the preoperative, and postoperative modification of diet in renal disease （MDRD） method were used to estimate glomerular filtration rate （eGFR） all patients were taken 5 mL middle segment urine three times in the morning before CAG, 2 hours and 48 hours after operation, and neutrophil gelatinase-associated lipocalin （NGAL） was detected with latex enhanced immunoturbidimetric. Results （1）The value of serum creatinine （SCr） （77.44±23.14 mmol/L vs 94.24±36.14 mmol/L, P＝0.014）, uric acid （313.05±110.84 μmol/L vs 354.00±100.66 μmol/L, P＝0.060） and eGFR （92.24±24.74 vs 75.31±31.34, P＝0.009） after CAG or PCI were different between the two groups. （2）The value of 2 h NGAL （33.13±20.44 μg/L vs 50.67±46.95 μg/L, P＝0.013）, 48 h NGAL （27.56±18.64 μg/L vs 58.38±56.81 μg/L, P＝0.001） after CAG or PCI had statistically significant differences between the two groups. （3）The occurrence of CI-AKI was as follows: the 20 mg/d atorvastatin group had 11 cases, the incidence was 20.75%, and the 40 mg/d atorvastatin group had 5 cases, the incidence was 9.43%, there was statistical significance （P＝0.04）. Conclusion Compared with 20 mg/d atorvastatin, 40 mg/d atorvastatin for 3 days before CAG or PCI can reduce the occurrence of CI-AKI.

Abstract:Aim To assess the relationship between brachial-ankle pulse wave velocity （baPWV） and left ventricular diastolic function of hospitalized patients in department of cardiology. Methods 652 patients in department of cardiology were enrolled in the study. The informations of clinical and ultrasonic cardiography were collected. Brachial-ankle pulse wave velocity was measured noninvasively. Results BaPWV increased with the decline of left ventricular diastolic function in four groups and there was statistical significance （P<0.001）. BaPWV was significantly negatively correlated with E/A ratio （r＝－0.257, P<0.001）, and was significantly positively correlated with E/E′ ratio （r＝0.249, P<0.001）. Multiple Logistic regression analysis showed baPWV≥1400 cm/s was a danger factor to left ventricular diastolic disfunction, the RR values were 1.93 （95%CI was 1.09～3.44, P＝0.03）. Conclusions BaPWV is correlated with left ventricular diastolic disfunction, and it can be a screening method for high risk group with left ventricular diastolic disfunction.

Abstract:Aim To explore the impact of ideal cardiovascular health behaviors and health factors on the detection rate of the right subclavian artery plaques. Methods Subject with previous stroke, transient ischemic attack （TIA）, myocardial infarction were excluded from the study. A total of 5852 employees （the retired employers from Tangshan Kailuan company） aged 40 years and over were included through stratified random sampling. Inforrmation was obtained from the unified questionnaire, measurements of blood biochemistry and right subclavian artery ultrasonography. Results （1）The right subclavian artery plaques detection rate were 41.8%, 35.8%, 33.4%, 31.4%, 29.7% and 25.2% in the group of with less than 2, 2, 3, 4, 5 and greater than 5 components of ideal cardiovascular health behaviors and health factors,respectively. （2）Compared to less than 2 components of ideal cardiovascular health behaviors and health factors, the detection risk （OR） values in the group with 2, 3, 4, 5 and greater than 5 components of ideal cardiovascular health behaviors and health factors were 0.78, 0.70, 0.64, 0.59, 0.47, respectively. Conclusions Increasing ideal cardiovascular health behaviors and factors are negatively linked with the detection rate of the right subclavian artery plaques. The ideal cardiovascular health behaviors and health factors can prevent the right subclavian artery plaques.

Abstract:Macrophage,an important component of the immune system,plays a crucial role in atherosclerosis and related cardiovascular diseases. Conventional wisdom holds that macrophages are derived from blood mononuclear phagocytic system and not renewable, but recent studies have shown that tissue macrophage can proliferate and has played a key role. Cell cycle regulators, bone growth factors and oxidized low density lipoprotein are closely related with macrophages in atherosclerosis. This article briefly reviews regulation of macrophage proliferation in atherosclerosis.

Abstract:Atherosclerosis （As） is a pathological and physiological process triggered by lipid deposition in arterial wall, and is highly correlated with chronic inflammatory reaction mediated by macrophages. In early stage of atherosclerosis, macrophage limits disease progression by phagocytizing modified lipoproteins, cellular debris and dead cells. As the disease progresses, macrophages apoptosis increases and efferocytosis defective causes the secondary necrosis and inflammatory reaction, thus promotes the formation of unstable plaques. Macrophage proliferation and apoptosis are closely related to atherosclerosis. Therefore, this article focuses on macrophage proliferation and apoptosis on atherosclerosis, providing the theoretical basis for atherosclerosis prevention and control.

Abstract:Daintain/AIF-1 is an inflammatory polypeptide factor/allograft inflammatory factor 1 derived from macrophages, which can activate macrophages, promote the proliferation and migration of vascular smooth muscle cells. Lately, extensive progress has been made in the understanding of mechanisms of atherosclerosis and coronary heart disease （CHD）. Daintain/AIF-1 plays an important role in the process of occurrence and development of atherosclerosis and possibly allows early prognostic assessment of atherosclerosis to therapy.