Abstract:Aim Atherosclerosis (As) primarily involves the systemic arteries. The luminal surface of the artery is directly exposed to blood and is susceptible to active blood substances. Exosomes contain a significant amount of components that are either beneficial or detrimental to cells. Thus, blood exosomes may contribute to As. The aim of this study was to investigate the contribution of exosome proteins to As. Methods Fifty-six subjects were recruited and divided into two comparison pairs:healthy subjects vs. As patients, and hypertension vs. hypertension＋As patients. Serum exosomes were decoded by protein mass spectrometry. Protein profile and function were analyzed by gene ontology (GO).A structure hierarchy tree was constructed to illustrate the proteins associated with GO terms, and protein-protein interaction analysis was performed to indicate the proteins involved in As. Results Five differentiated child terms appeared in both comparisons under the biological process GO terms of “response to stimulus” and “immune system process”. They are “positive regulation of innate immune response”, “immune response-activating signal transduction”, “activation of innate immune response”, “innate immune response-activating signal transduction” and “innate immune response activating cell surface receptor signaling pathway”. Two differentiated child terms emerged in both comparisons in the molecular function category of “binding”:“antigen binding” and “enzyme binding”. In addition, three differentiated proteins, PSMA6, PSMA7 and annexin A2, appeared in both comparisons. Conclusions The innate immune system contributes to AS development. PSMA6, PSMA7 and annexin A2 may be new target proteins for As prevention and treatment.

Abstract:Aim To improve the differentiation of bone marrow-derived mesenchymal stem cell (BMMSC) into cardiomyocyte-like cell; To observe the effect of intergrin-linked kinase (ILK) overexpression on the differentiation of BMMSC into cardiomyocyte like cell. Methods Swine BMMSC was isolated and transfected by recombinant adenoviral vectors containing both human wild-type ILK cDNA and humanized recombinant green fluorescent protein (GFP) (Ad-GFP-ILK). The differentiation of BMMSC into cardiomyocyte-like cell was induced with high concentration (50 mol/L) 5-azacytidine (5-AZA). Cells were divided into 4 groups:blank control group (N group), Ad-GFP transfection group (Ad group), 5-AZA inducing group (5-AZA group) and Ad-GFP-ILK transfection group (ILK group). Methyl thiazolyl tetrazolium (MTT) assay was used to detect the cell viability. Cardiac troponin I (cTnI) and α-actinin expressions were detected by immunocytochemistry after transfection for 2,4 weeks. Western blot was performed to assess the expressions of cTnI, gap junction protein connexin-43 (CX-43), caspase-3, and ILK after transfection for 4 weeks. Results MTT results showed that cell viabilities were significantly decreased in Ad group, 5-AZA group than those in N group, ILK group (P＜0.05), but there was no significant difference between Ad group and 5-AZA group, between N group and ILK group (P＞0.05). When the cells were cultured for 2 weeks, immunocytochemistry staining showed that 5-AZA group and ILK group began to express cardiac specific markers cTnI and α-actinin, while N group and Ad group had no obviously positive expression. Western blot results showed that the expression of ILK protein in ILK group was significantly higher than that in the other groups (P＜0.05). Compared with N group and Ad group, the expressions of cTnI in 5-AZA group and ILK group were significantly higher (P＜0.05), but there was no difference between 5-AZA group and ILK group, between N group and Ad group (P＞0.05). The expression trend of CX-43 in the 4 groups was the same as that of cTnI. Caspase-3 expressions in Ad group, 5-AZA group were significantly higher than those in other groups (P＜0.05). Conclusions ILK overexpression can promote the differentiation of BMMSC into cardiomyocyte-like cells, and the differentiation efficiency is not different from that of high concentration of 5-AZA stimulation in vitro. ILK overexpression has no effect on cell proliferation, and has a certain anti-apoptotic effect.

Abstract:Aim To explore the role of Notch signaling pathway in platelet derived growth factor-AA (PDGF-AA) induced vascular smooth muscle cell (VSMC) proliferation and migration. Methods 1-2 months old Sprague Dawley (SD) male rats were used in present study. Rat abdominal aorta was gained by aseptic operation, after removing the outer membrane of vascular and the endothelium, smooth muscle cells (SMC) was acquired by block pasting method and identified by immunofluorescence assay for α-SM-actin staining. The experiment was divided into four groups:normal group (Control), γ-secretase inhibitor group (DAPT), PDGF-AA group (PDGF-AA), PDGF-AA combined γ-secretase group (PDGF-AA+DAPT). The expression of Jagged1, Jagged2, Notch1-4, HES1, HEY1 and HEY2 mRNA was detected by real-time quantitative polymerase chain reaction (real-time qPCR), cell proliferation activity was detected by CellTiter96 Aqueous One Solution kit, and the migration of SMC was detected by cell scratching assay. Results Notch signals including Jagged1, Jagged 2, and Notch1-3 were expressed in cultured SMC. PDGF-AA induced increased Jagged 2 mRNA expression 24 h post-stimulation ( P<0.01,n=4) and increased Jagged1 mRNA expression 48 h post-stimulation (P<0.01, n=4); Notch1 and 3 mRNA expression also significantly increased 72 h after PDGF-AA stimulation compared with 0 h group (P<0.01, n=4), whereas Notch2 mRNA were obviously decreased by PDGF-AA 48 h post-stimulation (P<0.01, n=4). PDGF-AA also significantly promoted the HES1 (P<0.05,n=4), HEY2 (P<0.05, n=4) and transcription factor Rbp-j kappa (P<0.05, n=4) mRNA expression in SMC, DAPT markedly inhibited PDGF-AA induced HES1, HEY2 mRNA expression (P<0.01, n=4), but DAPT further increased PDGF-AA induced Rbp-j kappa mRNA expression (P<0.05, n=4); PDGF-AA stimulation obviously promoted SMC proliferation (P<0.01, n=5) and reduced remaining scratches area (P<0.01, n=4), whereas the effects were significantly attenuated by DAPT (P<0.01,n=4). Conclusions PDGF-AA can directly affect the expressions of Notch signaling molecules in SMC, Notch signaling pathway is partly in responsible for PDGF-AA-induced SMC proliferation and migration.

Abstract:Aim To investigate the effect of cigarette smoke extracts (CSE) on protein S-nitrosylation in human umbilical vein endothelial cells (HUVEC). Methods The experiments performed in HUVEC. The levels of protein S-nitrosylation were analyzed by using immunofluorescence, and further confirmed by biotin switch method. Protein expression was analysed by Western blot. In addition, superoxide anion were also detected during the experiment. Results CSE (0.005%, 0.01%, 0.02% and 0.04%) reduced the levels of protein S-nitrosylation in dose-dependent manner.Sodium nitroprusside (SNP), nitrosoglutathione (GSNO), NONOate and apocnin restored the reduction of protein S-nitrosyation induced by CSE. Moreover, CSE increased levels of superoxide anion, which were inhibited by apocnin. Conclusion In HUVEC, CSE is able to reduce the protein S-nitrosylation level, which is associated with superoxide anion accumulation and nitric oxide (NO) pathway blockage.

Abstract:Aim By transfection of small interfering RNA (siRNA) to silence RAW264.7 derived foam cells’ neurite outgrowth inhibitor-B receptor (NgBR) expression, to study the effect of NgBR on reverse cholesterol transport (RCT) of foam cells, explore new methods to prevent atherosclerosis from RCT pathway and provide new ideas for clinical prevention and treatment of coronary heart disease. Methods Using oxidized low density lipoprotein (ox-LDL) to induce the RAW264.7 cells to form foam cells, and using the oil red O staining to identify them. Then the foam cells were divided into 4 groups:blank control group, siRNA negative control group, NgBR-siRNA1 transfection group (siNgBR-1 group) and NgBR-siRNA2 transfection group (siNgBR-2 group). Whereafter siRNA was used to silence NgBR expression in RAW264.7 cells, and the interference efficiency was identified by real-time PCR and Western blot. Then real-time PCR was applied to detect mRNA content of liver X receptor alpha (LXRα), ATP-binding cassette transporter A1 (ABCA1), ATP-binding transporter G1 (ABCG1) in cells of each group, and corresponding protein content of each group cells were detected by Western blot, and the intracellular cholesterol efflux was determined by liquid scintillation counter. Results Ox-LDL induced foam cells formation successfully. Compared with other groups, NgBR mRNA and protein were significantly decreased in siNgBR-1 and siNgBR-2 group (P＜0.05), mRNA and protein expressions of ABCA1, LXRα, and ABCG1 were significantly inhibited (P＜0.05), and the cholesterol efflux was significantly reduced in siNgBR-1 and siNgBR-2 group (P＜0.05). Conclusion NgBR can increase the expression of LXRα and its downstream genes as ABCA1 and ABCG1 related to RCT regulation of macrophage derived foam cells, thereby weaken or avoid the occurrence and development of atherosclerosis, and provide the theoretical basis for clinical prevention and treatment of coronary heart disease.

Abstract:Aim To investigate the effect of nanobacteria on the injury of human umbilical vein endothelial cell (HUVEC) and the secretion of superoxide dismutase (SOD). Methods HUVECs were treated with the different concentration nanobacteria, and the cell viability was tested by methyl thiazolyl tetrazolium (MTT) analysis. HUVECs were attacked with a concentration of 0.5 Mcfarland of nanobacteria. The lactate dehydrogenase (LDH), malondialdehyde (MDA) and SOD levels were detected in the supernatant of culture medium at 0,6, 2,4, 48 and 72 h, respectively. Results Compared with the control group, the cell viabilities were significantly decreased by treatment with nanobacteria (the absorbance values were 0.1,0.005 and 0.02) for 48 and 72 h (P＜0.05). Compared with the control group, the concentrations of LDH and SOD in cell culture solution were significantly increased in nanobacteria treatment group (P＜0.05), while the content of MDA was not significantly changed (P＞0.05). Conclusion Nanobacteria can injure HUVEC, and increase the activity of SOD in HUVEC.

Abstract:Aim To observe the protective effect of pioglitazone (PIO) on myocardial cell membrane in hyperlipemia rats with myocardial ischemia/reperfusion. Methods Establish hyperlipemia rat model and conduct intragastric administration with PIO. 4 weeks later, myocardial ischemia/reperfusion model was made on the basis of hyperlipemia. Then the myocardial cell membrane was separated through low temperature and high speed centrifugal preparation and the level of cholesterol(C), phospholipid (P) and the value of C/P and the activity of phospholipase A₂(PLA₂), the Na⁺-K⁺-ATPase, Mg²⁺-ATPase and Ca²⁺-ATPase were detected. Results ① At the end of the 4^th week, the levels of serum triglycerides (TG), total cholesterol (TC) and high density lipoprotein cholesterol (HDLC) were significantly higher in hyperlipemia group than in control group (P＜0.05). At the 8^th week, the levels of serum TG,TC were significantly lower in HL+PIO group than in HL group(P＜0.01 and P＜0.05). ② Myocardial membrane phospholipids in HL group were lower than in control group and HL+PIO group (P＜0.01 and P＜0.05). ③ The values of C/P in HL group were higher than in control group (P＜0.01) and HL+PIO group (P＜0.01). ④ The activity of PLA₂ were higher in HL group(P＜0.05)and HL+PIO group(P＜0.05) than in control group. ⑤ Compared with the control group, the activity of Na⁺-K⁺-ATPase in HL group and Mg²⁺-ATPase in HL+PIO group differed respectively. Conclusion Pioglitazone protected myocardial cell membrane through maintaining the value of C/P, the activity of PLA₂ and the activity of ion pump.

Abstract:Aim To investigate the role of aldehyde dehydrogenase-2 (ALDH-2) in the oxidized low density lipoprotein(ox-LDL) induced endothelial progenitor cells (EPC) apoptosis and its molecular mechanism. Methods EPC isolated from peripheral circulation of healthy adults were cultured, challenged with blank, 10 mg/L ox-LDL and 1 μmol/L Alda-1 (a ALDH-2 specific activator) pretreatment plus 10 mg/L ox-LDL and used to evaluate apoptotic rate with DAPI stain, reactive oxygen species (ROS) level with DCFH-DA, mitochondrial membrane potentials with JC-1, caspase-3 signal pathway with Western blot. Results The apoptotic rate of the blank group, ox-LDL treatment group and Alda-1 pretreatment plus ox-LDL treatment group were respectively 4.9%±0.4%, 17.9%±2.9% and 7.5%±0.8%,the difference was significant(P＜0.05, n=6). The proportion of EPC lost which their mitochondrial membrane potentials were respectively 3.6%±0.7%, 28.5%±5.3% and 12.4%±1.3% in the blank group, ox-LDL treatment group and Alda-1 pretreatment plus ox-LDL treatment group, the difference was significant(P＜0.05, n=6). The ROS levels were respectively 319.7%±23.5% and 152.7%±9.4% in ox-LDL treatment group and Alda-1 pretreatment plus ox-LDL treatment group compared to the blank group (P＜0.05, n=6). The Western blot results showed that ox-LDL increased caspase-3 expression, but the pretreatment of Alda-1 reduced the ox-LDL induced caspase-3 expression(P＜0.05, n=6). Conclusion ALDH-2 could reduce ROS level in EPC, stabilize mitochondrial membrane potentials of EPC and reduce EPC apoptosis. Otherwise these are related to caspase-3.

Abstract:Aim To observe the effects of curcumin on blood lipid, endothelial function and oxidative stress of acute hyperlipidemia model rats, and to investigate the relationship between antioxidative effect and the expression of nuclear factor E-2-related 2(Nrf2). Methods Fourty healthy male Sprague Dawley rats were randomly divided into normal control group, hyperlipidemia model group, high-dose curcumin group (250 mg/(kg·d)), low-dose curcumin group (125 mg/(kg·d)) and atorvastatin intervention group (2.1 mg/(kg·d)). The rats in normal control group and hyperlipidemia model group were gavaged with corn oil, rats in other groups were gavaged with high dose curcumin, low dose curcumin and atorvastatin respectively for 10 days. The acute hyperlipidemia model was established by intraperitoneal injection of yolk emulsion 1 hour after the last gavage. Serum total cholesterol(TC), triglyceride(TG), low density lipoprotein cholesterol(LDLC), oxygenized low density lipoprotein (ox-LDL), nitric oxide(NO), superoxide dismutase (SOD) activity were measured 24 hours after intraperitoneal injection, while malondialdehyde (MDA) content and pathological examination of aorta tissue were determined. Results Compared with the normal control group, the serum TC, TG, LDLC and ox-LDL increased in the rats of model group; SOD activity and NO content reduced, MDA content and expression of Nrf2 in the aorta tissue increased. Compared with the model group, serum TC, TG, ox-LDL and MDA content of aorta tissue was obviously decreased in high-dose curcumin group, low-dose curcumin group and atorvastatin intervention group, serum SOD activity, NO level and Nrf2 expression in aorta tissue increased. Conclusion Curcumin may play the role of endothelial protection through improving the antioxidant capacity of the aorta by lowering blood lipid and inducing the expression of Nrf2.

Abstract:Aim To observe the effect of cobalt dichloride (CoCl₂) preconditioning on the cerebral infarction volume percentage and the expressions of stroma cell-derived faetor-1α (SDF-1α)/chemokine receptor 4 (CXCR4) in rats; To investigate the protective effect of SDF-1α/CXCR4 biological axis in the brain of the hypoxic ischemic environment. Methods The 168 adult male SD rats were randomly divided into hypoxia preconditioning group (n＝84) and model group (n＝84). According to the time of reperfusion after ischemia, each group was divided into 6 subgroups:6 h, 24 h, 3 d, 5 d, 7 d and 14 d subgroup. The focal cerebral ischemia model was prepared by modified Longa method. The pathological change of brain tissue was observed after hypoxia and ischemia. The change of cerebral infarction volume percentage was observed by triphenyl tetrazolium chloride (TTC) staining after reperfusion in two groups. The expressions of SDF-1α and CXCR4 in cerebral cortex were detected by immunohistochemistry at each time point. Results TTC staining showed that visible infarction focus occured at 6 h and cerebral infarction volume tended to be stable at 24 h in the hypoxia preconditioning group and the model group. There was no significant difference in cerebral infarction volume percentage among 24 h, 3 d, 5 d, 7 d, 14 d in two groups (P＞0.05). Cerebral infarction volume percentage in the hypoxia preconditioning group was significantly less than that in the model group at each time point (P＜0.05). The results of immunohistochemistry showed that the expressions of SDF-1α and CXCR4 increased significantly in the two groups at 6 h, and the expressions were the highest at 7 d, followed by a gradual decrease, and the expression was still in existence at 14 d. The number of SDF-1α and CXCR4 positive cells in the cortex of hypoxia preconditioning group was significantly higher than that in model group (P＜0.05). Conclusion Cobalt dichloride preconditioning can reduce cerebral infarct volume, which may increase the expressions of SDF-1α and CXCR4, induce brain hypoxia tolerance, promote the migration of mesenchymal stem cells to ischemic tissue, and play a protective role in the brain.

Abstract:Aim To explore preliminarily the change of migration ability of human umbilical vein endothelial cell (HUVEC) after injury and its relationship with vascular endothelial cadherin (VE-cad) and p120 catenin (p120ctn). Methods HUVEC was cultured in MEM culture medium, and was divided into control group and injury group. The change of HUVEC migration ability was detected by Transwell experiment. Expression levels of P120ctn and VE-cad protein were determined by Western blot. Location expression change of VE-cad was detected by immunofluorescence assay.Mutual combination of P120ctn and VE-cad was detected by Co-immunoprecipitation. Results Transwell experiment showed that the migration ability of HUVEC was the strongest in the 6 and 8 h after injury (P＜0.05). Western blot results showed that p120ctn and VE-cad expression levels of HUVEC were significantly up-regulated in the 6 and 8 h after injury.Immunofluorescence assay showed that VE-cad was localized from cell membrane into cytoplasm after HUVEC was injured.Co-immunoprecipitation confirmed that P120ctn could be mutually combined with VE-cad. Conclusion The migration ability of HUVEC is enhanced after injury stimulation, and its mechanism may be related to that elevated p120ctn carries VE-cad from cell membrane into cytoplasm, which leads to loss of VE-cad expression on the membrane.

Abstract:Aim To investigate the role of Ghrelin in diabetic vascular calcification. Methods Thirty cases of diabetic foot amputation patients from the Affiliated Hospital of Jiangsu University were enrolled. The tibial artery stenosis of patients were divided into three groups according to Doppler ultrasound:mild stenosis group (stenosis＜50%)(n=10), moderate stenosis (50%≤stenosis＜70%)(n=10) and severe stenosis / occlusion group (70%≤stenosis≤ 100%)(n=10). Serum and clinical related indicators detection, HE staining, Von Kossa calcium staining, vascular calcium content, alkaline phosphatase(ALP)activity assay and Western blot assay were performed. Results Consistent with ultrasound results of diabetic amputee tibial artery, HE staining and Von Kossa staining showed:there were a lot of diffuse black membrane calcium in the tibial arteries of three groups; but compared with mild stenosis group and moderate stenosis group, there were a lot of spotty black calcium deposition (hard hyperechoic plaque in ultrasound) in the tibial artery atherosclerotic plaques of severe stenosis / occlusion group. Quantitative tests showed the ALP activity and calcium content of tibial artery increased significantly in severe stenosis group, they were 2.44 times and 2.39 times for mild stenosis group respectively, but compared with mild stenosis group,there was no statistically significant difference in the moderate stenosis group. Western blot assay showed the expression of osteoprotegerin(OPG) were reduced, while the expression of receptor activator of nuclear factor kappa B ligand(RANKL) was up-regulated. According to Pearson correlation analysis we observed a negative correlation between tibial artery calcium content and Ghrelin (r=－0.64, P<0.001) as well as between Ghrelin and sRANKL (r=－0.85, P<0.001),while OPG was positively correlated with Ghrelin (r=0.85,P<0.001). Conclusion With the extent of vascular calcification in diabetic patients worsing, the expression of Ghrelin and OPG were down-regulated, while the expression of RANKL was up-regulated, suggesting serum Ghrelin, OPG/sRANKL levels may have an early-warning value.

Abstract:Aim To investigate the gender differences in the levels of nitric oxide in prehypertension and its correlation with the number and function of circulating endothelial progenitor cells. Methods Eighty consecutive population, 46.4±4.3 years old, were divided into four groups:normotensive premenopausal women (n=21), prehypertensive premenopausal women (n=20), normotensive men (n=19) and prehypertensive men (n=20). The nitric oxide (NO), granulocyte-macrophage colony stimulating factor (GM-CSF) and vascular endothelial growth factor (VEGF) levels in plasma and secreted by circulating EPCs were measured in the four groups. Results The distribution of plasma NO level, the NO secretion by cultured EPCs in normotensive and prehypertensive premenopausal women were significantly higher than those in normotensive and prehypertensive men (P＜0.05). The plasma NO level or NO secretion by EPC in normotensive men was also higher than that in prehypertensive men (P＜0.05). However, the plasma NO level or NO secretion by EPC in normotensive premenopausal women was almost equal to that of prehypertensive premenopausal women (P＞0.05). The plasma NO level or NO secretion by EPC was related to the number or activity of circulating EPC. No significant difference was found in plasma VEGF or GM-CSF level in the four groups (P＞0.05). Conclusions The plasma NO level and NO secretion of circulating EPC were preserved in prehypertensive premenopausal women, which was correlated with the number and activity of circulating EPC.

Abstract:Aim To explore the influence of brachial-ankle pulse wave velocity (baPWV) on the urine protein.Methods A total of 5440 participants who were aged over 40 without previous stroke, transient ischemic attack (TIA) and myocardial infarction were randomly selected from serving and retired workers of Tangshan Kailuan Company in 2006-2007 health examination, among which 5012 participants with integrated data were recruited into the study. Urine protein and baPWV were detected. Grouped baPWV using quartile group. The influence of baPWV on urine protein was analyzed by Logistic regression. Results Compared with the first quartile group, baPWV was a risk factor for positive urine protein, OR values were 0.778 (95%CI was 0.463～1.309), 1.323 (95%CI was 0.834～2.096) and 3.172 (95%CI was 2.122～4.741); and adjustment for age, sex, TC, TG, HDLC, LDLC, DBP, SBP, FBG, smoking, and drinking, similar results were obtained, OR values were 0.663 (95%CI was 0.424～1.036), 0.977 (95%CI was 0.640～1.491) and 1.682 (95%CI was 1.073～2.637). Conclusion The increase of baPWV was correlated with urine protein. The increase of baPWV was a risk factor for positive urine protein.

Abstract:Aim To explore the relationship between platelet-derived growth factor-D(PDGF-D) (rs3809021 and rs7950273)genetic polymorphisms and the risk of coronary heart disease(CHD). Methods A total of 158 cases confirmed by coronary Arteriograghy(CAG) were included in CHD group and 120 healthy subjects confirmed by CAG or coronary CTA were included in control group. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) techniques and gene sequencing analysis was used to analyze the polymorphism of rs3809021 and rs7950273 of PDGF-D gene and to compare its relationship with coronary artery disease between the two groups. The severity of CHD was evaluated by the number of stenotic coronary arteries and the Gensini scores respectively. Results The distributions of PDGF-D gene rs3809021 polymorphism was not significantly different between case of CHD and control group(P＞0.05),but the PDGF-D gene rs7950273 polymorphism was significantly different(P＜0.05). However, there was no statistical difference with the severity of CHD in CHD cases (P＞ 0.05). Conclusion PDGF-D gene rs7950273 allele is an important genetic susceptibility gene for CHD. It is associated with CHD, but is no associated with the severity of CHD.

Abstract:Aim To investigate the application value of high resolution magnetic resonance imaging (HR-MRI) including 3D T1-VISTA sequence for intracranial artery wall imaging in patients with type 2 diabetes mellitus (T2DM) complicated with ischemic stroke. Methods High definition magnetic resonance imaging data of 95 patients with ischemic stroke or transient ischemic attack were collected in our hospital. Some cases were excluded, because the poor image quality or scanning level tilt which might lead to unsatisfactory data measurement, and a total of 46 patients were included in the final analysis of the image data. The patients were divided into two groups:17 cases in T2DM group, 29 cases in non-T2DM group. The vessel wall parameters of the right middle cerebral artery (MCA), left MCA, and basilar artery (BA) were measured. Results HR-MRI could clearly show the intracranial arterial wall. MCA plaques were mostly located in the inferior wall of vessel. BA plaques were mostly located in the left wall of vessel, next to the abdominal wall. 3D T1-VISTA could clearly show the existence of small plaques. In comparison between T2DM group and non-T2DM group, the differences of luminal area (LA) (P＝0.003), wall area/luminal area (WA/LA) ratio (P＝0.018) in right MCA and WA/LA ratio (P＝0.015) in left MCA were statistically significant. Conclusions HR-MRI can clearly show the intracranial arterial wall detail in patients with T2DM complicated with ischemic stroke. It can find the wall thickening caused by atherosclerosis, and identify the plaque or thrombosis of responsible vessel in cerebral infarction. HR-MRI can early detect the intracranial vascular lesions.

Abstract:Aim To investigate the value of serum cardiac myosin binding protein-C (cMyBP-C) in the diagnosis of patients with acute myocardial infarction(AMI). Methods Sixty-two patients with AMI were selected as case group in the department of cardiology from March 2014 to November 2015, and sixty persons of normal physical examination were selected as control group. Enzyme-linked immunosorbent assay (ELISA) method was used for determining the concentrations of serum cMyBP-C. The concentration differences of cMyBP-C, cardiac troponin I(cTnⅠ), creatine kinase(CK-MB) and myoglobin(Myo) between AMI group and control group were compared. Correlations between cMyBP-C and cTnⅠ, CK-MB, Myo were analysed in AMI group. The concentration differences of serum cMyBP-C and cTnⅠ were also compared between the control group and AMI patients with the onset time of less than 4 h. The concentration differences of serum cMyBP-C and cTnⅠ were compared between 12 h after PCI and admission. Results In AMI group, the concentrations of serum cMyBP-C, cTnⅠ, CK-MB and Myo were higher than those of control group(P<0.05). Correlation analysis showed that the level of cMyBP-C had positive correlation with those of cTnⅠ,CK-MB and Myo in AMI group(r=0.876, P<0.05; r=0.632, P<0.05 and r=0.903, P<0.05 respectively). For AMI patients with the onset time of less than 4 h, the level of serum cMyBP-C was higher than that of the control group(P<0.05), but there was not significant difference when comparing the level of serum cTnⅠ and that of the control group(P>0.05). After 12 h of emergency PCI, the level of cMyBP-C was lower than that on admission, but the level of cTnⅠ was higher than that on admission (P<0.05). Conclusions The concentrations of serum cMyBP-C, cTnⅠ, CK-MB and Myo in AMI patients were significantly higher than those of control group on admission and the concentration of serum cMyBP-C had positive correlation with those of cTnⅠ, CK-MB and Myo. cMyBP-C started to rise in 4 h. These suggest that cMyBP-C can be used as early biochemical marker in the diagnosis of AMI. The level of serum cMyBP-C decreased obviously after 12 h undergoing emergency PCI in AMI patients. This suggests that cMyBP-C can be used as an early indicator for evaluating the effect of PCI.

Abstract:The occurrence of major adverse cardiovascular events is the result of advanced atherosclerosis and plaque rupture. The research on the formation mechanism and treatment of vulnerable plaque has been on focus. The basic research and even the hot spot of studying vulnerable plaque is how to produce a progressive plaque like human beings’. At present, many different vulnerable plaque models have been produced in a variety of animals. In this review, the animal models of vulnerable plaque will be summarized and discussed. And this review may provide new ideas for the production of the vulnerable plaque model.

Abstract:Atherosclerosis (As) is an important cause of high morbidity and mortality of cardiovascular disease. It has serious harm to people's health and safety of life. Recent studies show that hydrogen sulfide (H₂S) as a gaseous signal molecule has important physiological functions in As lesions, and its deficiency may lead to the early development of As lesions. This review describes the protective effects of H₂S in the development of As, from biological lipid metabolism disorders, relationship between H₂S and anti-coagulation, inhibition of endothelial cell proliferation or migration, and that H₂S can change the characteristics of As metabolism. This article also puts forward some ideas and prospects for the further works.

Abstract:Cystatin C, as a cysteine protease inhibitor, is an indicator of renal damage. At present, many studies suggest that the cystatin C may be a risk factor for atherosclerosis formation, and play an important role in vascular damage of ischemic stroke. There is a certain correlation between cystatin C and carotid atherosclerosis occurrence, development and disease prognosis in patients with ischemic stroke. This article reviews the research on the correlation between cystatin C and carotid atherosclerosis in patients with ischemic stroke in recent years.