Abstract:Aim To investigate the effect of OX40-OX40L interaction on the expression of nuclear factor of activated T cells c1 (NFATc1) and formation of the atherosclerotic plaques. Methods Atherosclerotic plaque model was randomly divided into the following groups:control group (n=11),OX40 activated group (n=11) and OX40 activated+PLKO.1-shNFATc1 group (n=11). Atherosclerotic plaque model was produced by perivascular carotid collar placement in ApoE－/－ mice. Masson staining was used to detect the composition of the plaque. Immunohistochemistry was used to observe the distribution of NFATc1 and CD68 in plaques. Mouse brain endothelial cells were divided into three groups:control group, OX40 activated group and OX40 inhibited group. The mRNA and protein level of NFATc1 was detected by real-time quantitative PCR (qRT-PCR) and Western blot respectively. Results In vitro, the expression level of NFATc1 was significantly increased in OX40 activated group, and were decreased in OX40 inhibited group(P<0.05). In vivo, the expression level of NFATc1 was significantly increased in OX40 activated group, and were decreased after the gene of NFATc1 being silenced(P<0.05). Masson staining revealed that the area of the plaque and fibrin proliferation was higher than the control group, while were decreased in OX40 activated+PLKO.1-shNFATc1 group. In vivo,compared with the control group, the distribution of NFATc1 and CD68 in the plaque were increased after the addition of agonist-OX40, which can be inhibited by silencing NFATc1. Conclusion OX40-OX40L interaction may regulate the expression of NFATc1 and promote the formation of the atherosclerotic plaque.

Abstract:Aim To explore the effect and significance of mammalian sterile 20-like kinase 1 (MST1) and its DNA methylation in the kidney damage of apolipoprotein E gene knocked-out (ApoE－/－) mice. Methods The experimental animals were divided into 2 groups:(1)ApoE－/－ group (n＝10):male ApoE－/－ mice were fed with high methionine diet; (2)Control group (n＝10):male C57BL/6J mice were fed with high methionine diet. After 14 weeks of feeding, serum creatinine and urea nitrogen levels in mice were determined by full automatic biochemical analyzer. PAS staining and transmission electron microscope were used to observe the renal tissue damage in mice. Real-time quantitative PCR and Western blot were used to detect the expression levels of MST1 mRNA and protein in mice kidney. MST1 DNA methylation level in mice kidney was detected by nested methylation specific PCR (nMS-PCR). Results Compared with the control group, serum levels of creatinine and urea nitrogen were increased by 1.1 times and 1.6 times in ApoE－/－ group (P＜0.01). PAS staining and transmission electron microscopy showed that the kidney was obviously damaged in ApoE－/－ group compared with control group. In ApoE－/－ mouse kidney, MST1 expression was positively correlated with serum creatinine and urea nitrogen levels (R²＝0.7571, P＝0.0012; R²＝0.7342, P＝0.0015). The result of nMS-PCR showed that renal MST1 DNA methylation level in ApoE－/－ group was significantly lower than that in control group (P＜0.01). Conclusions The upregulation of MST1 expression may play an important role in kidney damage of ApoE－/－ mice. DNA low methylation in MST1 promoter region may be an important mechanism of MST1 expression upregulation.

Abstract:Aim To explore the effect and mechanism of acid environment on media vascular calcification of chronic renal failure rats. Methods In vivo experiment:healthy male SD rats were randomly divided into control group, renal failure group, vascular calcification group and acid intervention group, calcification was measured by Alizarin red staining and enzyme linked immunosorbent assay. In vitro experiment:vascular smooth muscle cells (VSMC) were primarily cultured in vitro and randomly divided into control group, high phosphorus group, acid intervention group and inhibitor group, calcium deposition and ALP activity were measured by Alizarin red staining, quantification of calcium and enzyme linked immunosorbent assay, the expression of BMP-2, Smad1 and Runx2 was detected by RT-PCR and Western blot. Results In vivo experiment:the vascular calcification model of rats with chronic renal failure was successfully prepared. Compared with vascular calcification group, calcium deposition in acid intervention group decreased (P＜0.05).In vitro experiment:compared with control group, calcium deposition, alkaline phosphatase (ALP) activity and the expression of Runx2 in high phosphorus group increased (P＜0.05). Compared with high phosphorus group, calcium deposition, ALP activity and the expression of Runx-2, BMP-2 and Smad1 in acid intervention group decreased (P＜0.05). Compared with high phosphorus group, calcium deposition and the expression of Runx2 in inhibitor group also decreased (P＜0.05). Conclusions Acid environment can inhibit the occurrence of vascular calcification in chronic renal failure rats, the mechanism was presumably that vascular smooth muscle cells osteogenesis/chondrogenesis-like phenotypic transformation was inhibited by BMP-2 signaling pathway.

Abstract:Aim To investigate whether exogenous hydrogen sulfide (H₂S) protects against high glucose (HG)-induced H9c2 cardiomyocyte injury and inflammation response by inhibiting reactive oxygen species (ROS)-Toll-like receptor 4 (TLR4) pathway. Methods Cell counter kit-8 (CCK-8) assay was used to measure the cell viability, the activity of lactate dehydrogenase (LDH) in the culture medium was measured with commercial kits, the levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) were detected by ELISA, the number of apoptotic cells was observed by Hoechst 33258 nuclear staining followed by photofluorography, the expression levels of TLR4 and Cleaved Caspase 3 were determined by Western blot, the intracellular level of ROS was detected by 2’,7’-dichlorfluorescein-diacetate (DCFH-DA) staining followed by photofluorography, mitochondrial membrane potential (MMP) was examined by Rhodamine 123 staining followed by photofluorography. Results After H9c2 cardiac cells were exposed to 35 mmol/L glucose (HG) for 24 h, the expression level of TLR4 was significantly increased. Pre-treatment of the cells with 1000 μmol/L N-acetyl-L-cysteine (NAC) for 60 min or with 400 μmol/L sodium hydrogen sulfide (NaHS) for 30 min before HG exposure considerably attenuated the up-regulation of TLR4 expression level induced by HG. HG induced considerable injuries and inflammatory response, leading to a decrease in cell viability, increases in the activity of LDH, the number of apoptotic cells, the expression of Cleaved Caspase 3, ROS generation, MMP loss as well as the secretion levels of IL-1β and TNF-α. Pre-treatment of the cells with 400 μmol/L NaHS for 30 min before HG exposure or co-treatment of the cells with 30 μmol/L TAK-242 (an inhibitor of TLR4) and HG for 24 h obviously reduced the above injuries and inflammatory response induced by HG. Conclusion Exogenous H₂S protects against the HG-induced H9c2 cardiomyocyte injury and inflammation response by inhibiting ROS-TLR4 pathway.

Abstract:Aim Through the establishment of atherosclerosis model in ApoE－/－ mice to investigate the effects of Ningxin Decoction, Xuesaitong and rosuvastatin on serum lipid, inflammatory factors and plaque structure. Methods Feed 80 ApoE－/－ mice aged 8 weeks with high-fat diet for 4 weeks at first. Eighty rats were randomly divided into four groups:Control group (n=20), NingxinJiedu Soup group (n=20), Xuesaitong group (n=20), Rosuvastatin group(n=20). Measure the body weight, tail artery blood pressure, detect total cholesterol (TC), triglyceride (TG) and low density lipoprotein cholesterol (LDLC) level after eight weeks. Detect the plaque. Analyze the expression level of IL-6, IL-1β, and TNF-α in the serum of rats. Results The ApoE－/－rats in Control group showed apparent differences from other three groups in blood total cholesterol, triglyceride, low density lipoprotein cholesterol. Among them, the ApoE－/－rat in Rosuvastatin group showed apparent differences from NingxinJiedu Soup group and Xuesaitong group. The ApoE－/－rat in Control group had no significant differences from other three groups in body weight, blood pressure. The concentration of IL-6, IL-1βand TNF-α in serum in Control group were higher than that in other three groups, while there were no obvious differences between the other three groups. Conclusions The animal model of atherosclerosis can be ideally established by ApoE－/－ rats and high lipid diet. Rosuvastatin has better effect in the control of plaque development, because of its lipid regulating effect. NingxinJiedu soup, Xuesaitong, rosuvastatin can reduce the expression of inflammatory factors. In addition, they also have the positive effect on fat adjustment and retarding atherosclerosis.

Abstract:Aim To explore the effects of nuciferine on the expression of microRNA-33a-5p (miR-33a-5p) and ATP-binding cassette transporter A1/G1 (ABCA1/G1) in THP-1 derived macrophages. Methods Macrophages were derived from THP-1 monocytes by PMA. Macrophages were randomly divided into four groups:normal cells, cells incubated with oxidized low density lipoprotein (ox-LDL), cells treated with nuciferine, cells pretreated with nuciferine were incubated with ox-LDL. Macrophages were valued by red O staining. The expression of miR-33a-5p and ABCA1/G1 were determined by RT-PCR and Western blot. Results Compared with the normal cells, lipid droplets were increased while the expression of miR-33a-5p were downregulated and ABCA1/G1 were upregulated in the cells incubated with ox-LDL. Compared with the normal cells, lipid droplets had no change while the expression of miR-33a-5p were downregulated and ABCA1/G1 were upregulated significantly in the cells treated with nuciferine. Compared with the cells incubated with ox-LDL, lipid droplets were dramaticlly decreased while the expression of miR-33a-5p were downregulated and ABCA1/G1 were upregulated significantly in the cells treated with nuciferine and ox-LDL. Conclusions Nuciferine downregulates miR-33a-5p expression and upregulates ABCA1/G1 expression in THP-1 derived macrophages and decreases the degree of foam formation.

Abstract:Aim To analyze the effect of Toll like receptor 3 (TLR3) agonist PolyI∶C on the proliferation and apoptosis of human umbilical cord blood-derived endothelial progenitor cells (EPC) and its mechanism. Methods Endothelial progenitor cells were treated with different concentrations of PolyI∶C sequentially, and then the phase of cell cycle and cell apoptosis were tested by flow cytometry. CCK-8 assay was used to detect the effect of TNF-α and IL-1β on the apoptosis of endothelial progenitor cells, and the effect of Caspase 8 inhibitior, Caspase 9 inhibitior and IL-1 receptor 1 neutralizing antibody (anti-IL-1R1) on PolyI∶C-induced apoptosis. Results Compared with the control group, PolyI∶C at high concentrations of 1 and 10 g/L significantly decreased the proportion of cells in S phase and G2/M phase.Moreover, PolyI∶C down-regulated the gene expression of cyclin A, B1, D1 and E, inducing cell cycle arrest in G0/G1 phase. Additionally, PolyI∶C induced the apoptosis of endothelial progenitor cells in a dose-dependent manner. Caspase 8 and Caspase 9 inhibitors did not reduce PolyI∶C-induced apoptosis of endothelial progenitor cells. TNF-α had no effect on apoptosis of endothelial progenitor cells. IL-1β induced cell apoptosis in a dose-dependent manner. Moreover, when endothelial progenitor cells pre-treated with anti-IL-1R1, then re-stimulated with PolyI∶C, the cell apoptosis induced by PolyI∶C was decreased. Conclusions PolyI∶C at high concentrations inhibited endothelial progenitor cells proliferation by inducing cell cycle arrest in G0/G1 phase and inducing cell apoptosis of endothelial progenitor cells. PolyI∶C induced the apoptosis of endothelial progenitor cells through up-regulating the expression of IL-1β via activating TLR3. Endogenous and exogenous apoptosis pathway and TNF-α did not contribute to PolyI∶C-induced cell apoptosis.

Abstract:Aim To investigate the protective effect of moderate exercise training on isoproterenol-induced cardiac hypertrophy and the potential mechanism. Methods Thirty-two SD rats were randomly assigned to following groups:control group, isoproterenol group, isoproterenol plus exercise training group and exercise training group. Isoproterenol was injected intraperitoneally for two weeks to create the cardiac hypertrophy model. Rats were forced to swim for 1 hour with nothing attached to the tail,6 days per week for 4 weeks. Heart mass index (HMI) and left ventricular mass index (LVMI) of rats were calculated using weighing method. Surface area of cardiomyocyte was detected by HE staining.The mRNA expression levels of atrial natriuretic peptide (ANP), brain natriuretic peptide(BNP), transforming growth factor-β1(TGF-β1), tumor necrosis factor-α(TNF-α) and interleukine-1 beta (IL-1β) were measured by Real-time PCR and the proteins expression of p65 and IκB were measured by Western blot. Results Compared with the control group, isoproterenol group showed the significantly increases of HMI, LVMI, surface area of cardiomyocyte,mRNA levels of ANP, BNP, TGF-β1, TNF-α, IL-1β and the protein expression of p65 in nuclei. Whereas the expression of IκB was decreased. Compared with isoproterenol group, isoproterenol plus exercise training group decreased HMI, LVMI and surface area of cardiomyocyte. In addition, isoproterenol plus exercise training group significantly down-regulated mRNA expression of ANP, BNP, TGF-β1, TNF-α and IL-1β and p65 protein expression in nuclei while increased the protein expression of IκB. Conclusion Moderate exercise training attenuates cardiac hypertrophy induced by isoproterenol via NF-κB signaling in rats.

Abstract:Aim To study the relationgship and the clinical significance between plasma fibrinogen and fractional flow reserve (FFR) in coronary intermediate lesions. Methods The patients were from Department of Cardiovascular of Affiliated Hospital of Xuzhou Medical College. Their coronary artery lesions were assessed by CAG from February 2013 to November 2015, the degree of coronary artery stenosis ranged from 50% to 70%. According to the FFR, the patients were divided into two groups:the FFR≥0.8 group (n＝23) and the FFR＜0.8 group (n＝14). Plasma fibrinogen, total cholesterol, triglyceride, uric acid and blood glucose were detected. After controlling the influencing factors of fibrinogen and coronary artery lesions, the correlation between firinogen and FFR was analyzed by correlation analysis and ROC curve.Results Partial correlation analysis showed that fibrinogen was negatively correlated with FFR (r＝－0.477, P＜0.01). The levels of fibrinogen in the FFR＜0.8 group were higher than those in the FFR≥0.8 group (3.50±0.72 g/L vs. 2.68±0.63 g/L, P＜0.05). ROC analysis showed that the best cutoff vlaue was 2.692 g/L with the biggest sum of sensitivity and specificity (0.929 and 0.652, respectively), when FFR＝0.8 as a boundary. Conclusions Plasma fibrinogen can be used to detect myocardial ischemia in coronary intermediate lesions, it is associated with the degree of myocardial ischemia in coronary intermediate disease and can be used as a predictor of myocardial ischemia and stent implantation in coronary intermediate disease.

Abstract:Aim To sreen differential genes associated with coronary heart disease in Uygur, Kazakh, and Han population of Xinjiang using gene microarray expression profiles. Methods A case-control study including 9 cases (3 cases in Uygurs, 3 cases in Kazakhs, and 3 cases in Hans) with coronary heart disease confirmed by coronary angiography and 9 gender-, age-, and ethnic-matched normal controls was designed for the present study. Human whole genome expression microarray was used to screen differential genes associated with coronary heart disease. Results 33 genes associated with coronary heart disease were differentially expressed, 26 genes associated with coronary heart disease in Han population were differentially expressed, 2 genes associated with coronary heart disease in Uygur population were differentially expressed, while the differentially expressed genes were not screened in Kazakh population. Through GO and Pathway analysis, the differentially expressed genes were related to immune response. Conclusion The results of gene microarray screening showed that the differentially expressed genes were mainly related to immune response.

Abstract:Aim To investigate the relationship between connective tissue growth factor (CTGF) rs9399005 gene polymorphism and serum CTGF level, coronary heart disease (CHD). Methods The serum CTGF levels were detected by enzyme linked immunosorbent assay in 214 cases of CHD and 64 cases of normal control group. CTGF gene rs9399005 single nucleotide polymorphism (SNP) was analyzed by Sanger method. Baseline clinical data, serum CTGF and genotype distribution frequencies were compared between the two groups. CTGF rs9399005 SNP and genetic susceptibility to CHD were analyzed by non conditional Logistic regression, and CTGF levels of different genotypes were compared.The relationships between CTGF level and coronary artery lesions, CHD severity were analyzed. Results The age, smoking, hypertension, body mass index, high density lipoprotein cholesterol, apolipoprotein A1, CTGF difference were statistically significant between the two groups (P＜0.05). The distribution of rs9399005 genotype CC, CT, TT, and allele C,Tü was statistically significant in the two groups (χ² was 12.5,7.148 respectively, all P＜0.01). The CHD risk of carrying CT was 1.134 times of CC, TT was 1.406 times of CC,Tü allele was 1.327 times of C allele. There was significant difference in serum CTGF level between different genotypes (F＝3.284, P＝0.034). There was significant difference in the main branche lesions of CHD among all genotypes (χ²＝13.872, P＝0.022). Conclusions CTGF rs9399005 SNP is related to genetic susceptibility of CHD. T alleles is associated with the severity of CHD, coronary artery lesions and serum CTGF level.

Abstract:Aim To observe the correlation of serum cystatin C, high-sensitive C-reactive protein (hs-CRP) level and virtual histology-intravascular ultrasound characteristics of culprit vessels in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS). Methods 114 patients were divided into two groups according to the clinical characteristics:NSTE-ACS group and SAP group, 70 patients with NSTE-ACS, 44 patients with SAP. All patients underwent coronary angiography and virtual histology-intravascular ultrasound. Serum levels of cystatin C and hs-CRP were measured respectively. Culprit vessels were identified by comprehensive assessment including ST-T changes of ECG, ventricular wall motion abnormality of ultrasound examination and the complex lesion diagnosed by coronary angiography. A quantitative estimation with virtual histology intravascular ultrasound of all 70 culprit lesions in NSTE-ACS group and all 44 culprit lesions in SAP group. Then their correlations were analyzed. Results ①The serum levels of cystatin C and hs-CRP were significantly higher in NSTE-ACS group than those of SAP group(all P<0.01). ②The plaque burden, plaque area and necrotic core percentage of culprit lesions in NSTE-ACS group was significantly higher than those of SAP group (P<0.05 or P<0.01). ③Correlation analysis showed that, the serum level of cystatin C was positively correlated with hs-CRP and necrotic core percentage (r=0.634 and 0.602, all P<0.01), and was negatively correlated with HDLC (r=－0.466, P<0.01). The serum level of hs-CRP was positively correlated with plaque burden and plaque area (r=0.454 and 0.427, P<0.01 or P<0.05). Conclusions The serum cystatin C level is significantly increased in patients with NSTE-ACS, and it was associated with unstable composition of necrotic core of culprit vessels. The serum cystatin C level can be used for evaluating the stability of coronary lesions in patients with NSTE-ACS.

Abstract:Aim To study the incidence rate and risk factors of postoperative delirium in patients with acute aortic dissection. Methods The perioperative clinical data of 173 patients with acute type A aortic dissection were retrospectively analyzed, including 151 males and 22 females, aged 45.4±10.3 years old. According to the appearance of postoperative delirium, patients were divided into delirium and non-delirium group, and the independent risk factors for postoperative delirium were analyzed. Results There were 72 cases with postoperative delirium in all of the patients, the incidence rate was 41.6%. Univariate and multivariate Logistic analysis showed that deep hypothermic circulatory arrest time (OR＝11.7,5%CI was 2.61～43.08), the lowest postoperative oxygenation index (OR＝2.6,5%CI was 1.43～5.72), duration of mechanical ventilation (OR＝4.2,5%CI was 1.36～15.59), hypernatremia (OR＝3.1,5%CI was 1.03～8.37), the amount of midazolam (OR＝1.8,5%CI was 1.07～2.04) were independent risk factors of postoperative delirium in patients with Stanford A aortic dissection. Conclusions The incident rate of postoperative delirium of Standford A aortic dissection patient is relatively high, deep hypothermic circulatory arrest time, the lowest postoperative oxygenation index, midazolam dosage, duration of mechanical ventilation and hypernatremia are independent risk factors of postoperative delirium in patients with aortic dissection.

Abstract:Aim To explore the effect of anti-Helicobacter pylori (Hp) on the oxidative stress related indicators and prognosis in patients with acute cerebral infarction (ACI). Methods In 125 cases of patients with ACI, routine 14C urea breath test was performed to detect Hp infection. 84 cases of Hp infection were randomly divided into treatment group of 42 cases and control group of 42 cases. Two groups were given conventional drug therapy, and treatment group was added with anti-Hp therapy. Serum oxidized low density lipoprotein (ox-LDL) and superoxide dismutase (SOD) levels in all patients were detected by enzyme-linked immunosorbent assay (ELISA). The changes of ox-LDL and SOD were observed before and after treatment in the two groups. The neural function recovery was observed, and the recurrence rate of cerebral infarction was observed in half year and 1 year. Results Hp infection rate was 67.2% in 125 patients with ACI. With the increase of Hp infection degree, serum ox-LDL level was increased (F＝16.143, P＜0.01) and SOD level was decreased (F＝55.686, P＜0.01). After treatment, serum ox-LDL level in treatment group was lower than that in control group (P＜0.01), and SOD level was higher than that in control group (P＜0.01). The total effective rate of neural function recovery in treatment group was higher than that in control group (P＜0.01). The recurrence rates of cerebral infarction in treatment group were lower than those in control group in half year and 1 year (P＜0.05). Conclusions Hp infection is an important risk factor for ACI. Active anti-Hp treatment can significantly reduce the oxidative stress reaction in patients with cerebral infarction, improve the efficiency of treatment, and reduce the recurrence rate of cerebral infarction in the short term.

Abstract:Aim To study the distribution of blood lipid in hypertensive population and to explore the clinical applications of non-HDLC (non high density lipoprotein cholesterol) in evaluating the occurrence of stroke. MethodsA multistage, stratified clustering sampling scheme was conducted from 2004 to 2006 in the rural areas of Fuxin County, Liaoning Province to investigate the blood lipid level of interviewees who were supposed to be followed up in 2014. 4 915 interviewees were available eventually. The levels of non-HDLC were divided into 4 groups:<3.25 mmol/L, 3.25～ mmol/L, 3.78～ mmol/L, 4.33～ mmol/L to research the relationship between non-HDLC and stroke according to the quartile division of non-HDLC. Results With the increasing of the level of non-HDLC, the crude incidences of total stroke and ischemic stroke went up in accordance while the crude incidence of hemorrhagic stroke increased for a bit and then decreased apparently. Comparing with the group of <3.25 mmol/L, the risks of total stroke [RR=1.39(1.11～1.75),P=0.004] and ischemic stroke [RR=1.75(1.32～2.32),P<0.001] were high and meaningful statistically when non-HDLC≥4.33 mmol/L and meaningless statistically. Comparing with the group of <3.25 mmol/L, when non-HDLC <4.33 mmol/L, the relationship of relative risk between hemorrhagic stroke and the level of non-HDLC was not clear.Conclusions The increasing level of non-HDLC was related to total stroke and ischemic stroke and unrelated to hemorrhagic stroke in hypertensive population. The lipid level of rual hypertensive population should be monitored and controlled intensively to decrease the occurance of correlative cardiovascular diseases.

Abstract:mTOR is a serine/threonine kinase, mainly involved in two kinds of signal pathway in regulation. mTOR signaling pathway can regulate cell growth, proliferation and apoptosis. While the mTOR can regulate the process of atherosclerosic development about endothelial cells migration and proliferation, macrophage autophagy, smooth muscle cells proliferation and migration. By inhibiting or activating mTOR in different periods, the vulnerable plaque of atherosclerosis can be stabilized and the development of atherosclerosis can be prevented. mTOR signaling pathway plays a multifaceted effect in atherosclerosis progression. This paper mainly review the relationship of mTOR signaling pathway and atherosclerosis. It provides a new direction for the clinical treatment.

Abstract:Osteoporosis and atherosclerosis are very common diseases associated with elder patients, it has higher incidence rate and more complications, they are the major risk factor for increased mortality. With the increasing of the patient’s age, the clinical connections between them have become increasingly closer. In recent years, OPG/RANKL/RANK pathway is the research high lights and it is a milestone in the research history of osteoporosis. The researchers come to realize that this signal pathway also played an invaluable role in atherosclerosis, enabling researchers conduct extensive research potential between the system and atherosclerosis. This article is about OPG/RANKL/RANK pathway as a bridge connection between them, exploring their common pathogenesis and clinical relationships, for providing further integrated concept in clinical work with these molecules as targets for designing and generating new drugs.

Abstract:Vascular calcification is highly prevalent in patients with coronary artery disease and, when present, is associated with major adverse cardiovascular events, including an increased risk of cardiovascular mortality. The pathogenesis of vascular calcification is complex and is now recognized to recapitulate skeletal bone formation. Vascular smooth muscle cells (SMC) play an integral role in this process by undergoing transdifferentiation to osteoblast-like cells, disrupting calcium and phosphate homeostasis, diminishing the activity of osteoclast-like cells with mineral resorbing capacity. Recent advances have identified microRNA (miRNA) as key regulators of this process by directing the complex genetic reprogramming of SMC and the functional responses of other relevant cell types relevant for vascular calcification. This review will detail the regulatory role of miRNA in SMC-mediated vascular calcification.

Abstract:Sulfatide is a major component in the nervous system and is found in many systems generally, which is believed to play an important role in the pathophysiology of nervous system. However, Sulfatide palys a unique role in the physiologic mechanism not only in the nervous system but also in other systems with the development of the detection means and related research on sulfatide. Sulfatide has been found to be involved in the mechanism of human cardiovascular diseases such as atherosclerosis in recent research. And it also has the “dual function” on procoagulant and anticoagulation.The biological function of sulfatide comes to be valued, and the research progress in recent years on the role of sulfatide in pathophysiology of various systems is reviewed.

Abstract:Intracranial branch atheromatous disease (BAD) was first described in 1989 as a mechanism of small infarct due to an occlusion or stenosis at the origin of a deep penetrating artery of the brain. BAD remained a negelected concept for decades. In recent years, the wider diffusion of magnetic resonance imaging techniques brought new attention to the BAD. It is still lack of consistency both in the terminology and in the subsequent ischemic infarctions. We review the definition of BAD, as well as the associated clinical and imaging features.