Abstract:Aim To study the function of TRPC1 and Orai1 in store and receptor-operated Ca²⁺ entry and nitric oxide generation by SOC and ROC in human umbilical vein endothelial cell. Methods HUVEC were collected and cultured to the second-third passage. We silenced the expression of their genes in HUVEC by transfection constructed TRPC1 or Orai1 RNA interference plasmids. The interference efficiency of their proteins and mRNA levels were determined by Western blot and real-time PCR, respectively. The cell were incubated with CaR agonist spermine, CaR negative allosteric modulator Calhex231 and ROC analogue TPA, protein kinase C (PKC) inhibitor Ro31-8220, PKCs and PKCμ inhibitor Go6967. Intracellular Ca²⁺ concentration ( [Ca²⁺]i) was detected using the fluorescence Ca²⁺ indicator Fura-2/AM, the production of NO was determined by DAF-FM of every group in HUVEC. Results Compared with control group, shRNA targeted to the TRPC1 or Orai1 genes decreased their mRNA and protein levels, respectively (P<0.05)； The results of their mRNA levels by 84.50% and 76.10% and proteins levels were decreased by 83.98% and 71.73%； In four different treatment under the action of factors, the [Ca²⁺]_i and the net NO fluorescence intensity ratio values of transfection of TRPC1shRNA and Orai1shRNA group were significantly reduced (P<0.05). Conclusion TRPC1 and Orai1 participated in CaR-mediated Ca²⁺ influx and NO production activation mediated by SOC and ROC in HUVEC.

Abstract:Aim To obtain the differential microRNA expression profiles of exosomes derived from hypertrophic cardiomyocytes and normal cardiomyocytes. Further, target genes and signaling pathways were analyzed to explore the possible molecular mechanism of the differentially expressed microRNA involved in cardiac hypertrophy. Methods Primary culture of cardiac myocytes was prepared from three-day-old Wistar rats. The cells were then divided into two groups:model group and control group. In the model group, cardiomyocyte hypertrophy was induced by AngⅡ (1 μmol/L), whereas the cells in the control group were not given any treatment or only added culture medium. Additionally, the exosomes were isolated, and the differentially expressed microRNA of exosomes were obtained by microRNA sequencing technique. Furthermore, target genes of differentially expressed microRNA were identified by miRanda algorithm, and KEGG pathway analysis were carried out to identify significant biological processes and key gene/protein. Results Compared with the control group, 14 differentially expressed microRNA of exosomes in the model group were identified. Among 14 differentially expressed microRNA, 13 were up-regulated (including mmu-miR-2137, mmu-miR-5126, mmu-miR-690 and 10 were newly discovered microRNAs), and 1 were down-regulated (P<0.05). In addition, 54 target genes of differentially expressed microRNAs were obtained, and then local network diagrams were constructed using the target genes of the first 20 and their related microRNA. KEGG pathway analysis indicated that the differentially expressed microRNAs was involved in the regulation of several signaling pathways, including MAPK, PI3K-Akt, and Wnt pathways. Conclusion The microRNA expression profiles of exosomes derived from hypertrophic cardiomyocytes changed significantly. They regulated several signaling pathways through target genes, and further affected the pathophysiological process of cardiac hypertrophy.

Abstract:Aim To investigate the role of scavenger receptor CD36 in carboxy methyl lysine (CML) inhibition of foam cell migration. Methods (1)The effect of CML on lipid accumulation and cell migration of RAW264.7 macrophages was observed, followed by observing the interaction of CML with CD36. The experiment was divided into:control group, oxidized low density lipoprotein (ox-LDL) group (40 mg/L ox-LDL), CML group (40 mg/L ox-LDL+10 μmol/L CML); (2)To observe the role of CD36 in CML inhibition of foam cell migration, the experiment was divided into two parts. Firstly, the effects of CD36 inhibitor SSO on the migration of RAW264.7 foam cells was investigated:control group (40 mg/L ox-LDL+10 μmol/L CML) and SSO group (40 mg/L ox-LDL+10 μmol/L CML+25 μmol/L SSO); And then the effect of different receptor blockade on CML inhibition of foam cell migration was observed:control group (40 mg/L ox-LDL+10 μmol/L CML), anti-CD36 group (40 mg/L ox-LDL+10 μmol/L CML+2 μmol/L anti-CD36), anti-RAGE group (40 mg/L ox-LDL+10 μmol/L CML+2 μmol/L anti-RAGE), malBSA group (40 mg/L ox-LDL+10 μmol/L CML+400 nmol/L malBSA). Some related detections were performed after 24 h of 1%BSA medium intervention (oil red O staining, Transwell cell migration experiments, immunoprecipitation experiments, CD36 immunofluorescence staining, etc). Results Cholesterol oxidase method quantification and oil red O staining qualitative showed that CML can effectively promote the accumulation of lipid droplets in RAW264.7 macrophages and form key components of atherosclerotic plaques--foam cells. Transwell cell migration experiments and quantitative analysis showed that:compared with the control group, the number of migrating foam cells in the ox-LDL group decreased by 43.5%(P<0.05); Compared with ox-LDL group, CML reduced the number of foam cell migration by 49.2%(0.287±0.031 vs 0.565±0.061,P<0.05),the result indicated that CML inhibited RAW264.7-derived foam cell migration. Immunoprecipitation experiments and immunofluorescence staining showed that there was a significant interaction between CML and CD36 in foam cells. Further more, after using SSO or neutralizing antibody anti-CD36 to block CD36 and scavenger receptor inhibitor malBSA block all scavenger receptors, the number of migrated cells was significantly higher than that of the control group(P<0.05). Statistical analysis showed that, the cell migration index of anti-CD36 group was 81.3% in malBSA group(2.35±0.39 vs 2.89±0.41, P<0.05). Conclusion Scavenger receptor CD36 may be a key node for CML inhibition of RAW264.7 foam cell migration.

Abstract:Aim To observe the changes of blood pressure level and large-conductance calcium-activated potassium channels (BKCa) current in aortic vascular smooth muscle cell (VSMC) in rats after high-salt diet. Methods 3 weeks old male Wister rats were randomly divided into two groups:control group and model group, 24 rats in each group. The control group was given with normal diet (containing 0.5% NaCl), and the model group was treated with high-salt diet (containing 4% NaCl). The blood pressure in rats was measured by tail artery manometry. Whole-cell patch clamp technique was used for recording BKCa currents in rat aortic VSMC membrane. Results In the model group, the blood pressure increased significantly from the eighth week, and the blood pressure gradually increased with the prolongation of the high-salt diet time. At the tenth, twelfth, fourteenth and sixteenth week, the blood pressure in the model group was significantly higher than that in the control group (P＜0.01). The BKCa current and current density of aortic VSMC membrane in the model group increased significantly with the prolongation of the high-salt diet time. At the eighth, twelfth and sixteenth week, the peak current density of BKCa in the model group was significantly higher than that in the control group, and the difference was statistically significant (P＜0.05). Conclusion High-salt diet can lead to elevated blood pressure in rats. The BKCa current density in rats increases gradually with the increase of blood pressure due to high-salt diet.

Abstract:Aim To investigate the effects of licochalcone A(Lico A)on the expression of inflammatory cytokines in macrophages of human acute monocytic leukemia cell line (THP-1) induced by lipopolysaccharide (LPS) in vitro. Methods 100 μg /L phorbol ester (PMA) was used to induce THP-1 cells for 48 hours, after the differentiation of THP-1 cells, which became macrophage, and cells were divided into control group, LPS group and LPS combined with concentration (20, 0,5 mg/L) of Lico A. The levels of interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) were detected by ELISA. The levels of Toll like receptor-4(TLR-4) and nuclear factor kappa B (NF-κB) mRNAs were tested by real-time PCR. The levels of TLR-4, NF-κB,Iü kappa B kinase alpha (IKKα), phosphorylated IKB-alpha (p-IKB-α), cyclooxygenase-2 (COX-2) and isoform of nitric oxide synthase (iNOS) proteins were examined by Western blot. Results The expression levels of TNF-α, IL-1 and IL-6 were up-regulated in the v macrophages after stimulated by LPS, Lico A could reduce the elevated expression levels of TNF-α, IL-1 and IL-6 induced by LPS. The expression of TLR-4 significantly increased after stimulated by LPS and NF-κB was activated. Lico A could reverse the above changes and prevent the activation of NF-κB. Conclusion Lico A could inhibit LPS-induced inflammatory response in THP-1 macrophages via TLR-4 /NF-κB pathway.

Abstract:Aim To study the effects of 7-difluoromethyl-5,4′-dimethoxygenistein (dFMGEN) on the apoptosis to H₂O₂-induced vascular endothelial cells and its molecular mechanism. Methods The oxidative stress injury model was established by human umbilical vein endothelial cells induced by 1 mmol/L H₂O₂. The experiment was divided into blank control group, H₂O₂ group, vehicle group, 100 μmol/L genistein group and different concentrations (0.1,0.3,1, 3,0 μmol/L) dFMGEN groups. The reactive oxygen species (ROS) generation was examined by DCFH-DA activated fluorescence flow cytometry (FCM). Apoptotic morphology was observed by acridine orange staining under fluorescence microscopy. The apoptotic rate was detected by PI staining FCM. The expression of Caspase-3 was determined by Western blot. Results When vascular endothelial cells were treated with 1 mmol/L H₂O₂ for 24 h, the generation of ROS was highly added, obvious morphological changes of apoptosis was found by acridine orange staining under fluorescence microscopy, the apoptotic rate was increased and the expression of Caspase-3 was up-regulated. After pretreating with dFMGEN, results showed that dFMGEN could reduce the release of ROS, decrease the apoptotic rate and down-regulate the expression of Caspase-3. Conclusion dFMGEN can effectually inhibit the apoptosis of vascular endothelial cells induced by H₂O₂, which is probably due to the decrease of ROS generation and downregulation of Caspase-3, thereby inhibiting apoptosis of vascular endothelial cells induced by H₂O₂.

Abstract:Aim To investigate the effect and possible mechanisms of the different concentrations of magnesium ions on aortic rings calcification induced by high phosphorus in rats. Methods Aortic rings were isolated from rat thoracic aorta and cultured in vitro, and randomly divided into control group, high phosphorus group and magnesium intervention group(final concentrations of magnesium ions were 1,2 and 3 mmol/L). Aortic rings were cultured with 10% fetal bovine serum in control group. After 14 days of intervention, the expressions of L-type calcium channel (LTCC)α_1c β₃ subunit, Runt-related transcription factor 2 ( Runx2 ) and smooth muscle 22α ( SM22α ) were detected by Immunohistochemistry. Calcium concentration of aortic rings was measured by Von Kossa staining and quantification of calcium. Results Compared with control group, calcified nodules in high phosphorus group was increased, and calcified nodules gradually reduced with the increased magnesium ion concentration in the intervention group. The expression of LTCCα_1c、β₃ subunits in high phosphorus group increased (P<0.05). With the increase of magnesium ion concentration, the expression of Runx2、LTCC α_1c、β₃ decreased (P<0.05) and the expression of SM22α increased (P<0.05) in high magnesium group. There results of Pearson correlation analysis showed that SM22α was negatively corelated with Runx2(r=-0.671,P=0.001),and LTCCα_1c subunit was positively corelated with Runx2(r=0.712, P<0.001), LTCCβ₃ subunit was positively corelated with Runx2(r=0. 0.692, P<0.001). Conclusion Magnesium can promote high phosphorus induced rat aortic rings calcification, and its mechanism is possibly achieved by downregulatiing LTCC α_1c β₃ protein expression, and reducing the transformation of VSMCs into osteogenic/osteogenic phenotype.

Abstract:Aim To investigate the association between high density lipoprotein (HDL) subclasses and IL-6 concentration in patients with metabolic syndrome (MS). Methods The MS subjects (n=135) and healthy controls (n=77) were selected. The levels of IL-6 were determined by enzyme-linked immunosorbent assay (ELISA) kits. According to the levels of plasma IL-6, the MS subjects were divided into three groups:low IL-6 group (IL-6≤66.76 ng/L), middle IL-6 group (66.76 ng/L3b, HDL_3c, plasma total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDLC), LDLC/HDLC and ApoB₁₀₀/ApoAI were significantly increased in MS subjects (P<0.05 or P<0.01), while HDL_2a, HDL_2b, preβ2-HDL, apolipoprotein AI (ApoAI) and high density lipoprotein cholesterol (HDLC) were significantly decreased in MS subjects (P<0.05 or P<0.01). Compared with the control group of the same sex, the relative content of HDL subclass of male or female in MS group was significantly different (P<0.05 or P<0.01). Compared with the same group of males, the level of lipids, apolipoproteins in control group and MS group were no statistical significance (P>0.05). The correlation analysis showed that IL-6 was positively correlated with the level of preβ1-HDL and HDL_3b and negatively correlated with the level of HDL_2b. Conclusion The plasma IL-6 levels were increased in MS patients, and the particle size of HDL showed a shift toward smaller size. The increasing of IL-6 may be related to HDL subclasses distribution abnormality and dyslipidemia.

Abstract:Aim To explore the predictive value of red blood cell distribution width (RDW) for in-stent restenosis (ISR) after coronary stenting with drug-eluting stent (DES) in patients of type 2 diabetes. Methods The study retrospectively searched data at Tianjin Nankai Hospital for 582 unstable angina pectoris patients with type 2 diabetes who underwent PCI from January 2012 to December 2016. Among these patients, 292 patients with coronary DES implantation were enrolled in this study. The ISR was analyzed by coronary angiography analysis at a mean follow-up of eight months. According to whether ISR was detected, type 2 diabetes patients were divided into two groups:the ISR group (n=45) and the non-ISR group (n=247). Patients' clinical and demographic characteristics were recorded including age, gender, smoking, anamnesis, RDW, C-reactive protein (CRP), cardiac ultrasound, coronary angiography, and so on. Results The body mass index (BMI) levels were higher in the ISR group than that in the non-ISR group (P<0.05). Patients with ISR had higher smoking rates (P<0.05). In addition, patients in the ISR group had significantly higher RDW levels compared with patients in the non-ISR group both at admission and at follow-up (P<0.01, respectively). Furthermore, the ISR group had significantly longer stent length and lower stent diameter compared with the non-ISR group (P<0.01, respectively). In an univariate model using RDW as a continuous variable, there was a significantly positive association between RDW levels and the incidence of ISR (P<0.01). Further multivariate logistic regression analysis revealed that BMI, smoking, RDW, CRP, stent length, and stent diameter were associated independently with ISR. Conclusion Elevated RDW has predictive value for ISR occurrence in type 2 diabetes patients with coronary DES implantation, which indicates that a chronic inflammatory response might be involved in the pathogenesis of ISR.

Abstract:Aim To investigate the effect of radiofrequency catheter ablation on glomerular filtration rate in patients with nonvalvular atrial fibrillation(AF). Methods A prospective study was conducted in 121 patients with atrial fibrillation who underwent radiofrequency ablation, including 105 patients with paroxysmal atrial fibrillation and 16 patients with persistent AF. Enzyme assay was applied to measure serum creatinine, eGFR was calculated by using CKD-EPI equation, all patients underwent radiofrequency ablation(circumferential pulmonary vein isolation+ablation), eGFR, hemoglobin, high sensitive C-reactive protein, N-terminal natriuretic peptide were assessed preoperatively, left atrial diameter, left atrial area and left ventricular ejection fraction were measured by echocardiography. All the data were followed 6 and 12 months after operation, and the effect of sinus rhythm after radiofrequency catheter ablation on eGFR in patients with atrial fibrillation was analyzed statistically. Results There was no statistical difference in age, sex, body mass index, hypertension, diabetes, dyslipidemia and salt (P＞0.05), while there was statistical difference in AF time (P＜0.05) between the two groups. Compared with preoperative baseline, left atrial diameter and left atrial area decreased, left ventricular ejection fraction increased, hemoglobin, hypersensitive C-reactive protein, N-terminal natriuretic peptide decreased, eGFR increased (P＜0.05) in two groups 6 and 12 months after radiofrequency catheter ablation. Compared with preoperative baseline, left atrial diameter and left atrial area decreased, left ventricular ejection fraction increased, hemoglobin, hypersensitive C-reactive protein, N-terminal natriuretic peptide decreased, eGFR increased (P＜0.05) in paroxysmal atrial fibrillation group 6 and 12 months after radiofrequency catheter ablation. Compared with preoperative baseline, left atrial diameter and left atrial area decreased, left ventricular ejection fraction increased, hemoglobin, hypersensitive C-reactive protein, N-terminal natriuretic peptide decreased, eGFR increased in persistent AF group 6 and 12 months after radiofrequency catheter ablation. The differences were statistically significant(P＜0.05). Conclusion Radiofrequency ablation of sinus rhythm can improve the glomerular filtration rate and the renal function in patients with atrial fibrillation.

Abstract:Aim To investigate the correlation between rs3732378 single nucleotide polymorphism of chemokine CX3C receptor 1 (CX3CR1) gene and acute coronary syndrome (ACS). Methods 951 cases of Han population in northern China were collected continuously, of which 520 cases were male, 431 cases were female, and the age was 35-75 years old. According to the results of coronary angiography (CAG), the selected subjects were divided into two groups:(1)case group (n＝512):ACS patients; (2)control group (n＝439):non coronary heart disease patients. The case group was divided into three subgroups according to the number of vascular lesions that were examined by CAG. The genotypes of rs3732378 single nucleotide polymorphisms of CX3CR1 gene were determined by sequencing. Multiple factor Logistic regression was used to analyze the relationship between the CX3CR1 gene rs3732378 polymorphism and the risk of ACS. The expression of chemokine CX3C ligand 1 (CX3CL1) in plasma was detected by enzyme-linked immunosorbent assay. Results There was no significant difference in the distribution frequency of rs3732378 genotypes and alleles of CX3CR1 gene in the two groups (P＞0.05). The overall and stratified analysis of rs3732378 polymorphisms and ACS risk showed that three genotypes TT, TC and CC of CX3CR1 rs3732378 polymorphisms did not increase the risk of ACS (P＞0.05). Subgroup analysis showed that the genotype and allele of rs3732378 polymorphic loci were not related to the number of coronary artery lesion (χ²＝0.135, P＝0.998; χ²＝0.026, P＝0.987). There was no significant difference in the expression level of CX3CL1 among three rs3732378 genotypes in the case group and the control group (P＞0.05). Conclusion The rs3732378 polymorphism of CX3CR1 gene is not a susceptible gene of ACS, and rs3732378 polymorphism does not increase the risk of ACS in the Han population of northern China.

Abstract:Aim To investigate the relationship between intron 4a/b gene polymorphisms of endothelial nitric oxide synthase (eNOS) gene and coronary artery ectasia (CAE). Methods The research was performed by case-control study. The CAE group included 30 patients with coronary artery ectasia on coronary angiogram. The control group contained 41 patients with normal coronary artery. The study collected the data of patients'gender, age, smoking history, drinking history, ect. Polymorphism chain reaction (PCR) technique was used to identify the eNOS intron 4a/b gene polymorphisms. Results The lesion involved single coronary artery in most cases was 46.7%(14 cases), the lesions involved in two and three vessels were 26.7%(8 cases)and 26.7%(8 cases), respectively. The right coronary artery (RCA) was the most frequently involved vessel (44.4%), the left anterior descending artery (LAD) and the left circumflex artery (LCX) were 31.5% and 24.1%, respectively. The frequencies of eNOS gene phenotypes in CAE group and control group for “aa”, “ab”, “bb” were 13.3%, 33.3%, 53.3% and 4.9%, 17.1%, 78%(P＞0.05), respectively. The presence of “a” type allele of eNOS gene in CAE group and control group were 30% and 13.4%(P<0.05), respectively. Logistic regression analysis showed that “a” type allele of eNOS gene was an independent risk factor for CAE (P<0.05, OR =3.327, 95% CI=1.083 ~ 10.226). Conclusion The “a” type allele of eNOS gene may be an independent risk factor for the occurrence of CAE.

Abstract:Aim The computational fluid dynamics (CFD) technique was used to simulate the changes of blood flow in different degrees of coronary artery stenosis, to explore the relationship between the change of coronary artery hemodynamics and different stenosis. Methods The right coronary arterial geometric model was reconstructed with CT images. The model of stenosis was defined as 0%(normal vascular), 30%(mildly stenosis), 60%( moderate stenosis) and 90%(severe stenosis), respectively. The model of vascular hemodynamics was established respectively. Numerical simulations were performed to compare the hemodynamics between the different vascular models. Results By comparing the hemodynamic numerical simulations of four kinds of stenosis, with the severe of the stenosis, the vortex flow becomes more obvious, the velocity of the flow showed faster in stenosis. In the proximal vascular region of stenosis, wall pressure (wall pressure, WP) was gradually increased; on the other hand, the WP showed lower in the region after the stenosis. The wall shear stress (WSS) distribution at the stenosis site always showed higher, and in the moderate and severe stenosis model, the high WSS region was found in the distal vascular region of stenosis, and the other distal vascular region of stenosis showed low WSS. Moreover, on the velocity and distribution of vascular blood flow, proximal and distal vascular region of the stenosis were also changed. Conclusion CFD based on CT images maybe reconstruct the coronary arterial hemodynamic model accurately, and the coronary arterial hemodynamic model with diverse stenosis may simulate coronary arterial stenosis. As hemodynamic risk factors, the vortex of stenosis posterior flow and the high WSS in the distal vascular region of stenosis which showed in moderate and sever stenosis model maybe aggravated atherosclerosis of coronary artery, and further aggravated the vascular stenosis.

Abstract:Aim To explore the relationship between serum monocyte chemoattractant protein-1 (MCP-1) level and MCP-1 2518G/A polymorphism in patients with acute myocardial infarction (AMI) in Chinese Han population in Lianshui County of Northern Jiangsu. Methods Serum MCP-1 level was measured by ELISA, and the MCP-1 2518 G/A polymorphism was genotyped by PCR-RFLP in 94 patients with AMI and 73 control subjects. Results Serum MCP-1 level(expressed in M/IQR) was significantly higher in AMI group (186.24/285.15 ng/L) than that in control group (100.71/134.02 ng/L, P＝0.001). Multiple linear regression analysis revealed that the serum MCP-1 level was negatively correlated with male, positively correlated with smoking, history of diabetes mellitus and hypertension, but unrelated with old age and dislipidemia in AMI group. After adjustment for hypertension, diabetes mellitus, age, gender, dislipidemia,and smoking, serum MCP-1 level of higher than 75% quantile was positively correlated with the risk of AMI (OR=2.4,5%CI was 1.061～7.204, P=0.037). There was no significant difference in genotype distribution and allele frequency of MCP-1 2518G/A between AMI group and control group (P＞0.05). There was no significant difference in serum MCP-1 level among the genotypes of the control group and the AMI group (P＞0.05). Conclusion Serum MCP-1 level was significantly higher in AMI group than that in control group in Chinese Han population in Lianshui County of Northern Jiangsu. Serum MCP-1 level was affected by sex, hypertension, diabetes, and smoking, but serum MCP-1level of higher than 75% quantile was an independent predictor of AMI. MCP-1 2518G/A polymorphism did not increase the susceptibility of AMI, nor affect the serum level of MCP-1.

Abstract:Aim To evaluate application value and analyze risk factors of cardio-ankle vascular index (CAVI) in arterial stiffness in peritoneal dialysis patients. Methods A total of 95 patients with end-stage kidney disease undergoing peritoneal dialysis were enrolled, baseline characteristics and laboratory measurements were collected, and CAVI was determined. According to CAVI, the patients were divided into high CAVI group (CAVI≥9) and normal CAVI group (CAVI＜9). Results The CAVI was significantly higher in high CAVI group (9.85±0.73) than that in normal CAVI group (7.67±0.81). The age (54.64±5.68 years), dialysis duration (48.32±30.43 months), pulse pressure (57.41±12.43 mmHg), serum correctional calcium (2.52±0.28 mmol/L), phosphorus (2.22±0.66 mmol/L), calcium-phosphorus product (5.59±1.70), fasting blood glucose (6.02±1.83 mmol/L) were significantly higher in high CAVI group than those in normal CAVI group, hemoglobin (83.96±20.53 g/L) and serum albumin (32.40±5.22 g/L) were significantly lower in high CAVI group than those in normal CAVI group.Spearman correlation analysis showed that CAVI was positively correlated with age, dialysis duration, pulse pressure, serum correctional calcium, phosphorus, the calcium-phosphorus product, fasting blood glucose, hs-CRP(r values were 0.0,0.0,0.4,0.7,0.1,0.8,0.5,0.298 respectively, each P＜0.05), and negatively with serum albumin, 25-hydroxyvitamin D (r values were －0.335, －0.222, each P＜0.05). Multiple linear regression analysis showed that age and serum albumin were independent risk factors of CAVI. Conclusion CAVI can be used as an index of noninvasive detection of atherosclerosis in patients with peritoneal dialysis, early detection of CAVI and improving nutrition can reduce the risk of atherosclerosis in peritoneal dialysis patients, the incidence of cardiovascular events, and improve the prognosis.

Abstract:sub>2-glycoprotein I (β₂-GPI), a main autoantigen in patients with antiphospholipid syndrome (APS), binds to the negative lipid components, such as oxidized low density lipoprotein (ox-LDL) and cardiolipin, thereby forming a stable β₂-GPI immune complex. β₂-GPI immune complexes and the immune response induced by anti-β₂-GPI immune complex antibodies significantly promote the formation of atherosclerotic plaques and vascular injury in patients with antiphospholipid syndrome. This review summarized the formation mechanism and the effects of β₂-glycoprotein I immune complex and the effect of β₂-glycoprotein I immune complex in the pathogenic process. The mechanism of β₂-GPI-DⅤ blocking the formation of β₂-GPI/ox-LDL complex was introduced, which provided possible drug targets and therapeutic ideas for cardiovascular diseases, especially atherosclerosis, caused by β₂-GPI/ox-LDL immune complex.

Abstract:Ischemic stroke is a common and frequently occurring disease, with high morbidity and mortality, which seriously threatens human health. At present, the common clinical treatment is mainly focused on various measures to improve cerebral circulation, such as thrombolysis, antithrombotic therapy, antiplatelet therapy, defibrinogen therapy, haemodilution and so on. The irreversible injury of neurons is the main reason for the difficulty of achieving satisfactory results. In recent years, the technology of isolation and cultivation of neural stem cells with potential for self-renewal and differentiation has gradually matured in vitro. More and more researches show that the transplantation of neural stem cells into ischemic stroke animal models can achieve effective treatment. In this paper, the biological characteristics of neural stem cells and the mechanism and progress of neural stem cell transplantation for ischemic stroke are reviewed.

Abstract:Atherosclerosis (As) is the main pathological basis of cardiovascular and cerebrovascular diseases, which seriously threatens human life and health. As occurs in abnormal shear stress sites, and microRNAs regulated by shear stress are called “shear stress sensitive microRNAs”. Shear stress-sensitive microRNAs are involved in many aspects of the pathogenesis of As. This review summarizes the recent advances in the mechanism of shear stress-sensitive microRNAs in the development and progression of As.

Abstract:The incidence of hypertension has increased year by year, high blood pressure and the resulting target organ damage has become one of the main killers of human health. Early diagnosis and treatment of hypertension and its target organ damage have important implications for improving the prognosis of the patients and reducing morbidity and mortality. With the increase in awareness of the pathophysiology of hypertension-arteriosclerosis-target organ damage, the degree of concern for atherosclerosis is also increasing. Studies have shown that arteriosclerosis test ambulatory arterial stiffness index (AASI) and arteriosclerosis target organ damage is closely related. This review summarizes the advances in the clinical application of AASI in hypertensive patients.