Abstract:Aim To investigate the effects of aging on the molecular expression of α- and β₁-subunit of large-conductance Ca²⁺-activated K⁺ （BK_Ca） channels in rat mesenteric arterial smooth muscle cells. Methods Young （4～5 months）, middle-aged （15～16 months）, and old （22～24 months） male Wistar rats were used. In vivo blood pressure and in vitro endothelium-removed mesenteric arterial tension were measured. Immunohistochemistry and Western Blot assay were also conducted. Results The systolic blood pressure and pulse pressure were significantly increased with aging. The vascular tone caused by norepinephrine （NE） strongly increased in a concentration dependent manner in each group, and aging reduced the sensitivity to NE in mesenteric arteries （MA）. Selective BK_Ca channel blocker （Iberiotoxin） induced a marked increase of vascular tension in MA in all three age groups. However, these effects were greatly decreased in old animals. Western Blot showed that the protein expression of BK_Ca α- and β₁-subunit was significantly reduced with aging, and the suppression of β₁ subunits was larger than that of α subunits. Conclusions These data suggest that aging induces decrease of molecular expression of α- and β₁-subunit of BK_Ca channels in MA myocytes, in which the suppression of β₁-subunit is more pronounced than α-subunit. This unparallel downregulation of two subunits may be the mechanism underlying the aging-associated decrease of BK_Ca channel contribution in regulating MA basal tone.

Abstract:Aim To explore the effect of urotensin Ⅱ （UⅡ） on expression of interleukin-6 （IL-6） in rat aortic adventitial fibroblast （AF） and its intracellular mechanisms. Methods Growth-arrested AF was incubated in serum-free medium with UⅡ （10^－10～10^－7 mol/L）. In order to explore the mechanism of UⅡ effects, the cells were pretreated with some inhibitors of signal transduction pathways for 30 min, and then incubated with UⅡ （10^－8 mol/L） for 3 h to 24 h. The IL-6 mRNA expression in the cells and secretion from the cells induced by UⅡ were evaluated by reverse transcription polymerase chain reaction （RT-PCR） and enzyme-linked immunosorbent assay （ELISA）, respectively. Results （1）UⅡ significantly increased IL-6 mRNA expression and protein secretion in rat AF, in a concentration-dependent （10^－10～10^－7 mol/L） and a time-dependent manner, with maximal effect at 10^－8 mol/L at 3 h for mRNA expression, or at 24 h for protein secretion （both P<0.01）. （2）The effect of UⅡ was inhibited by SB710411 （10^－6 mol/L）, nicardipine （10^－5 mol/L）, PD98059 （10^－5 mol/L）, H7 （10^－5 mol/L）, Y-27632 （10^－5 mol/L） and cyclosporine A （CsA） （10^－5 mol/L）, the inhibitors of UⅡ receptor, Ca^2＋ channel, mitogen activated protein kinase, protein kinase C, Rho kinase, and calcineurin, respectively. Conclusion UⅡ significantly induces IL-6 expression in rat AF, via activation of its receptor, Ca^2＋ channel, mitogen activated protein kinase, protein kinase C, Rho kinase and calcineurin signal transduction pathways, indicating that UⅡ induced-IL-6 expression is one of the important mechanisms responsible for accelerated atherosclerosis.

Abstract:Aim To investigate whether platelet factor 4 （PF4） modulates the matrix metalloproteinase-9（MMP-9） expression of macrophages. Methods THP-1 monocytes were differentiated into monocyte-derived macrophages by phorbol 12-myristate 13-acetate （PMA）. After incubation with PF4 （0～200 μg/L）, the MMP-9 expression of macrophages was determined by reverse-transcription polymerase chain reaction （RT-PCR） and Western blot. To determine the role of toll-like receptor 4 （TLR4） in the regulation of MMP-9 expression, macrophages were pretreated with TLR4 blocker for 30 min, then incubated with PF4. Results Macrophages that were untreated showed a relatively low MMP-9 and TLR4 mRNA or protein levels treatment of macrophages with PF4 increased MMP-9 and TLR4 expression. However, the high levels of MMP-9 and TLR4 expression induced by PF4 were significantly attenuated in the presence of TLR4 blocker.Conclusions PF4 may up-regulate MMP-9 expression in macrophages via TLR4.

Abstract:Aim To demonstrate the mechanisms of proteasome inhibition on norepinephrine （NE）-induced hypertrophic growth of neonatal rat cardiomyocytes（NRC） via studying the alteration of calcineurin（CaN） signaling pathway.Methods Proteasome inhibitor MG262 was cotreated with NE in NRC. Cell size was observed by phalloidin-stained technique. The expression of fetal genes and CaN was detected by using RNA dot blot analysis and Western blot analysis respectively. The fixed cells were immunofluorescence labeled with nuclear factor of activated T cell c4 （NFATc4） and visualized by fluorescence microscopy. Results Fetal genes of atrial natriuretic factor （ANF）, brain natriuretic peptide （BNP） and β-myosin heavy chain （β-MHC） mRNA as well as expression of CaN were upregulated and NFATc4 was predominantly expressed in nucleus on NE induced NRC. However, more than 2.1 fold NE-induced increase in cardiomyoctyes was markedly supressed by cotreatment with MG262（P<0.05）. NE-induced upregulation of CaN and fetal gene expression was significantly relieved by MG262（P<0.05）. NFATc4 was relocated from nucleus to cytoplasm. Conclusion MG262 attenuates agonist induced cardiomyocyte hypertrophy, at least in part, via inhibiting CaN signaling pathway.

Abstract:Aim To investigate the role of apolipoprotein E （ApoE） on the migration, proliferation, and differentiation of CD11b⁺Gr-1⁺ immature myeloid cells with ApoE genetic deficiency mice. Methods CD11b⁺Gr-1⁺ myeloid cells, CD11b⁺Gr-1^- monocytes, and CD11b^-Gr-1⁺ granulocytes in the peripheral blood, spleen, and bone marrow of ApoE^－/－ mice and control C57/B6 mice were analyzed by flow cytometry. Expression of ApoE in CD11b⁺ myeloid cells were examined by quantitative RT-PCR and immune-fluorescence co-staining with anti-CD11b and anti-ApoE. Cell cycle analysis was performed by flow cytometry. Results （1） Genetic deficiency of ApoE markedly promoted the migration of multiple myeloid subsets, in particular CD11b⁺Gr-1⁺ myeloid cells and CD11b⁺Gr-1^- monocytes. （2） Genetic deficiency of ApoE significantly increased the percentage of CD11b⁺Gr-1⁺ immature myeloid cells in the spleen and bone marrow of ApoE^－/－ mice compared with wild type mice. （3） ApoE was highly expressed in CD11b⁺ myeloid cells located in the spleen and bone marrow. （4） ApoE deficiency increased the percentage of CD11b⁺Gr-1⁺ myeloid cells in S cell cycle. Conclusions ApoE deficiency significantly promotes the proliferation, differentiation, and migration of CD11b⁺Gr-1⁺ immature myeloid cells in the spleen and bone marrow of ApoE^－/－ mice. Repressing the proliferation of CD11b⁺Gr-1⁺ immature myeloid cells and macrophage differentiation through an ApoE dependent signal pathway may provide a novel sight on the treatment of atherosclerosis.

Abstract:Aim To investigate the effect of angiotension Ⅱ （AngⅡ） on the expression of monocyte chemoattractant protein-1 （MCP-1） in rat glomerular endothelial cells （GEC） and the related mechanism. Methods Primary GEC were isolated from Sprague-Dawley （SD） rats. The synthesis of MCP-1 in rat GEC was determined by Western blot method. RT-PCR method was used to detect the expression of angiotensin Ⅱ type 1 receptor （AT1R）mRNA. Results AngⅡ stimulation increased the synthesis of MCP-1 and promoted the expression of AT1R mRNA in rat GEC. Telmisartan （TEL）, an AT1R blocker, blocked the effect of AngⅡ on rat GEC and decreased the expression of MCP-1.Conclusion AngⅡ induces MCP-1 production in rat GEC mediated by the AT1R.

Abstract:Aim To explore the relationship of plasma chemerin level and the expression of chemerin and chemerin receptor mRNA with inflammation in rats with atherosclerosis. Methods 82 male Wistar rats were randomly divided into 3 groups: control group, high-fat group and simvastatin treatment group. The rats were fed for fourteen weeks. Cardiac blood samples and aorta samples were taken from the rats. The thoracic aorta and abdominal aorta were prepared for HE staining and RT-PCR. The plasma levels of chemerin,hs-CRP,IL-6 and TNF-β were measured by ELISA. Chemerin and chemerin receptor mRNA expression levels were determined by RT-PCR. Results There were significant differences among three rat groups on the plasma levels of chemerin,hs-CRP,IL-6 and TNF-β, which showed high-fat group > simvastatin treatment group > control group（P<0.05）； Plasma chemerin levels of control group, high-fat group and simvastatin treatment group were positively correlated with hs-CRP（r0.664，0.804 and 0.709，P<0.05）. There were significant difference among three rat groups on chemerin and chemerin receptor mRNA expression levels, which showed high-fat group>simvastatin treatment group>control group（P<0.05）. Chemerin and chemerin receptor mRNA expression levels of high-fat group and simvastatin treatment group were positively correlated with hs-CRP，IL-6 and TNF-β（P<0.05）. Conclusion The plasma chemerin level and expression of the chemerin and chemerin receptor mRNA in rats with atherosclerosis were significantly correlated with inflammation. It implies that the pathway of chemerin-chemerin receptor may play pivotal roles in the pathogenesis and development of atherosclerosis through systemic inflammation.

Abstract:Aim To study the effects of visfatin on the maturity of DC2.4 cells and the mechanism of visfatin in the pathogenesis of atherosclerosis. Methods The DC2.4 cells were divided into four groups: normal control group, LPS group （LPS, 1 mg/L）, low-dose visfatin group （100 μg/L） and high-dose visfatin dose group （200 μg/L）. MHC-II, CD86 and CD80 expression were detected by flow cytometry. Tumor necrosis factor-α （TNF-α） and interleukin-12 （IL-12） levels in cell culture supernatant were measured by enzyme-linked immunosorbent assay. The ability of visfatin to stimulate allogeneic T lymphocytes was measured by mixed lymphocyte reaction assay. Results Compared with the control group, the synaptic of cells enlarged and cell volume increased in low-dose visfatin group, high dose visfatin group and LPS group. The levels of MHC-Ⅱ, CD80 and CD86 molecule expression increased, the supernatant TNF-α, IL-12 levels were significantly increased （P<0.05）. Compared with the control group, when stimulating cell∶effector cell ratio was 1∶10 and 1∶25, visfatin low dose group and high dose group and visfatin stimulation index LPS group was significantly higher （P<0.05）. Conclusion The results suggested that visfatin could participate in the development of atherosclerosis by activating T lymphocytes and initiating the immune inflammation response.

Abstract:Aim To observe the affection of angiotensin Ⅱ（AngⅡ） on hypoxia-inducible factor-1（HIF-1α）, vascular endothelial growth factor （VEGF）, prolyl hydroxylases-2 （PHD2）, factor inhibiting hypoxia-inducible factor-1（FIH-1）, and p-ERK expression in human umbilical artery smooth muscle cells （HUASMC）, and clarify the mechanism of PHD2, FIH-1, and p-ERK on HIF-1α expression on the condition of AngⅡ. Method HUASMC were divided into: （1） Control group: normal culture medium for 6 hours （2） AngⅡ group: 10^－6 mol/L AngⅡ culture medium for 6 hours （3） AngⅡ+PD98059 group: 10^－5 mol/L PD98059 added 1 hour before 10^－6 mol/L AngⅡ, and then for 6 hours.Gene expression of HIF-1α, VEGF, PHD2 and FIH-1 were checked by real-time PCR, and the corresponding proteins of above factors, and the p-ERK activation were checked with Western blot. Results （1） Compared with control group, AngⅡ promoted both gene and protein expression of HIF-1α and VEGF （P＜0.05）, and activated p-ERK （P＜0.05）, with the decreased FIH-1 gene and protein expression （P＜0.05）, but has no effect on PHD2 gene and protein expression in HUASMC. （2） Compared with AngⅡ group, both gene and protein expression of HIF-1α, VEGF and the p-ERK activation were significantly reduced （P＜0.05）, with the increased gene and protein expression of FIH-1（P＜0.05） in HUASMC. Conclusions （1） AngⅡ promoted both gene and protein expression of HIF-1α and VEGF in HUASMC.Its mechanism is that activated ERK pathway inhibited FIH-1, leading post-translational reduction of degradation of HIF-1α. （2） ERK inhibitor weakened the promoted affection of AngⅡ on HIF-1α and VEGF.

Abstract:Aim To investigate the distribution characteristics of brachial-ankle pulse wave velocity （BaPWV） and its correlation with the clinical indicators in crowd undergoing physical examination. Methods The subjects from the Health Medical Center of Chinese PLA General Hospital from May 2009 to February 2012 were enrolled as the object of study. The gender, age, hypertension history, smoking and alcohol status were recorded. The blood pressure was measured and the pulse pressure （PP） was calculated The weight and height were measured on a human body composition analyzer and the body mass index （BMI） was obtained The fasting blood glucose （FBG）, triglyceride （TG）, total cholesterol （TC）, high density lipoprotein cholesterol （HDLC）, low density lipoprotein cholesterol （LDLC）, blood uric acid （BUA）, high sensitivity C-reactive protein （hs-CRP）, homocysteine （Hcy）, serum creatinine （SCr）, hemoglobin （Hb） concentration were tested by drawing blood The BaPWV was measured on an arteriosclerosis detector. The total 20748 subjects undergoing all the inspection items related to this investigation were the object of study. The distribution characteristics of BaPWV of the subjects and its relationship with the above indices were analyzed. Results （1）The value of BaPWV≥1400 cm/s is taken as the critical point of arteriosclerosis. It was found that abnormal BaPWV data were observed for varying age groups with both the average BaPWV and abnormal detection rate rising with age. （2）The values of BaPWV of the male are slightly higher than those of the female The average value of BaPWV for smokers is higher than that of non-smokers The average value of BaPWV for subjects with hypertension history is markedly higher than that of subjects with normal blood pressure For subjects with varying alcohol drinking habits there exists significant differences in BaPWV and occasional alcohol drinkers showed, however, relatively low BaPWV. （3） Logistic regression analysis indicates that the age, hypertension history, smoking status, BMI, PP, FBG, TG, TC, LDLC, hs-CRP, Hcy, SCr, BUA, Hb and alcohol drinking etc.are all significant factors related to abnormal BaPWV. Conclusions The distribution characteristics of BaPWV is coincident with that of arteriosclerosis in adult population and its influencing factors is basically in accord with traditional factors related to arteriosclerosis. As one of non-invasive physical examination indicators, BaPWV can objectively reflect the degree of arteriosclerosis, thus providing the dependence for health intervention.

Abstract:Aim To summarize the clinical manifestation and the characteristic of coronary angiography of patients with the gel-like coronary thrombotic lesions, and to explore the experiences and technique of percutaneous coronary intervention （PCI） for the peculiar coronary lesions. Methods The data was retrospectively analyzed from 6 patients with the gel-like coronary thrombotic lesions. Results Six patients were diagnosed as acute ST-segment elevation myocardial infarction （STEMI）, and the infarction related arteries （IRA） were all right coronary artery. They received selectively PCI one to three weeks after heart attack. Coronary angiography revealed that total occlusion and thrombus occurred in IRA, accompanied with antegrade blood flow of grade TIMI 0. But, the antegrade blood flow in IRA remained the level of grade TIMI 0～1 after guide wires pass through the occlusion. Predilation failed to improve markedly the level of antegrade blood flow, and so did not thrombus aspiration and tirofiban. However, the IRA got antegrade blood flow of grade TIMI 3 after the stent implantation. Conclusion The gel-like coronary thrombotic lesions in IRA results from undissolved and partly fibrotic thrombus after myocardial infarction, and commonly occurs in right coronary artery.

Abstract:Aim The roles of monocyte/macrophage subsets （Mon1, Mon2, Mon3） are different on atherosclerotic inflammation. The aim of this article is to identify the distribution of monocyte Mon2 in patients with different clinical types of coronary artery disease, and to reveal correlation between monocyte Mon2 and atherosclerosis. Methods Totally 90 patients with coronary artery disease （stable angina pectoris, SAP, 28 unstable angina pectoris, UAP, 30 and acute myocardial infarction, AMI, 32） and 5 controls were enrolled. Mon2 were evaluated with CD14⁺CD163⁺using flow cytometry. Correlation between Mon2 and coronary score was evaluated using unitary linear recursive analysis. Results Monocyte Mon2 proportions were significantly different between patients with coronary artery disease and controls （P0.001）, furthermore among patients with coronary artery disease, Mon2 proportions had significant difference in SAP （24.3 %, 19.1%～29.5%）, UAP （ 11.1 %, 6.1%～16.9%） and AMI group（ 8.2 %, 3.3%～13.1%） , respectively. Value of CD163 MFI had significant difference in SAP （1.58, 1.38～1.78）, UAP （1.21, 1.04～1.39） and AMI group （1.10, 0.94～1.27）, respectively. However, no correlation was found between coronary score and Mon2 proportion and CD163 MFI. Conclusions The distribution of monocyte Mon2 varies was correlated with type of coronary artery disease.

Abstract:Aim To investigate the relationship among scavenger receptor class B type Ⅰ （SR-BⅠ） single gene polymorphisms （exon 1 and intron 5）, the risk of coronary heart disease （CHD） and blood lipid concentration in Tianjin Han Chinese population. Methods SR-BⅠ exon 1 and intron 5 polymorphisms were genotyped in 370 CHD patients and 143 healthy adults undergoing coronary angiography by polymerase chain reaction-restriction fragment length polymorphism （PCR-RFLP）. The concentrations of blood lipid were examined in all subjects. Results Intron 5 genotype was similar between two groups. SR-BⅠ exon 1 allelic frequencies of G and A were 0.988, 0.012 and 0.997, 0.003 in CHD and control groups respectively. There was no significant difference between the distribution of AluI polymorphism and the allele frequency in CHD and control groups （P>0.05）. Serum levels of high density lipoprotein cholesterol （HDLC） and apolipoprotein AⅠ （ApoAⅠ） in the GA＋AA genotype subgroup was significantly higher than in GG genotype subgroup among CHD group male subjects （P<0.05）. Conclusion The exon 1 polymorphism of SR-BⅠ gene may not be associated with susceptibility to CHD and severity degrees of coronary lesions in Tianjin Han Chinese population, but A allele of SR-BⅠ exon 1 can lead to the elevated HDLC and ApoAⅠ concentration in male CHD patients.

Abstract:Aim By comparing characteristics in patients with recurrent cerebral infarction and first cerebral infarction with computed tomography angiography （CTA）， to explore possible factors in patients with recurrent cerebral infarction. Methods We retrospectively analysed the test results of 140 cases of recurrent cerebral infarction patients and 235 cases of patients with head and neck CTA, and compared the characteristics of the two groups of patients with head and neck vascular lesions. Results Head and neck artery stenosis rate in patients with recurrent cerebral infarction was higher than that in patients with first cerebral infarction （90.0% vs. 64.7% P＜0.01）. Head and neck artery moderate stenosis and severe stenosis proportions in patients with recurrent cerebral infarction were higher than those in patients with first cerebral infarction （34.9% and 45.2% vs. 19.7% and 15.8% P＜0.01）. The incidence of head and neck artery plaque in patients with recurrent cerebral infarction was higher than that in patients with first cerebral infarction （91.4% vs. 66.4%, P＜0.01）. The proportion of soft plaque and ulcer plaque in patients with recurrent cerebral infarction were significantly higher than those in patients with first cerebral infarction （36.3% and 48.0% vs. 22.7% and 37.3% P＜0.05）. Conclusions Recurrent cerebral infarction is related to head and neck artery stenosis, the degree of stenosis and unstable plaque, the degree of stenosis and plaque may be one cause of recurrent cerebral infarction.

Abstract:Aim To investigate the association between Fractalkine receptor CX3CR1 gene 249V/I polymorphism and early-onset coronary artery disease （CAD） and lipid ratios in patients with no classic risk fators. Methods By polymerase chain reaction and restriction fragment length polymorphism （PCR-RFLP）, we examined the frequencies of V249I among early-onset CAD patients （n149 ＜50 years）, late-onset CAD patients （n150 ＞65 years） and healthy controls （n149, 47～93 years） without known CAD risk factors. We compared plasma total cholesterol （TC）/high density lipoprotein cholesterol （HDLC） ratio and apolipoprotein B （ApoB）/apolipoprotein A1 （ApoA1） ratio among the groups and mutation carriers and non-carriers. Results There were significant differences in 249V/I allele frequencies among the three groups （P<0.0001）. TC/HDLC and ApoB/ApoA1 ratios were significantly higher in early-onset CAD patients compared with late-onset CAD patients and healthy controls （P<0.0001） and independent on either mutation. Conclusions The I249 allele of the Fractalkine receptor CX3CR1 gene may be associated with the age of patients with CAD. We also found an independent association between high lipid ratios and the age of patients with CAD.

Abstract:Aim To investigate serum levels of homocysteine（Hcy） and nonesterified fatty acid （NEFA）in patients with coronary heart disease （CHD） and relationship between homocysteine, nonesterified fatty acid levels and cardiac severity. Methods A case-control study was conducted in 451 CHD patients diagnosed by clinics. They were divided into three groups: stable angina pectoris（SAP） group（n267）,unstable angina pectoris（UAP） group（n55）and acute myocardial infarction（AMI） group（n129）. All patients and 103 healthy controls were measured the serum Hcy and NEFA concentrations by automatic biochemical analyzer. Furthermore,their changes were analysed based on CHD severity （NYHA Ⅰ-Ⅳ function classification）. The two-sample u-test or t-test was used for statistical test,The P value less than 0.05 was considered statistically significant. Results The serum levels of Hcy were 16.7±10.4，16.8±5.8 and 19.8±11.1 μmol/L in SAP，UAP and AMI groups, which were all significantly higher than healthy controls（13.6±9.2 μmol/L）（P<0.05）,the serum levels of Hcy in AMI group was also significantly higher than both SAP group and UAP group（P<0.05）. The concentrations of NEFA were 513.5±232.6 mEq/L and 774.7±415.3 mEq/L in UAP group and AMI group,which were also significantly higher than healthy controls（353.5±142.1mEq/L）（ P<0.05）,while its serum levels of NEFA in SAP group was 332.7±137.9 mEq/L,which was not significantly higher than that in healthy controls（P>0.05）. Furthermore, statistical test showed that the concentrations of Hcy was increased along with increment of CHD severity （NYHA cardiac functional classification）（P<0.05）,while the levels of NEFA didn’t change compared with it,which occurred only on NYHA Ⅳclassification （P<0.05）. Conclusion There are sulfurated amino acid and fat metabolic disorders in CHD patients. Sulfurated amino acid and fat metabolic disorders may play a certain role in the occurrence and development of CHD

Abstract:Aim To investigate the relationship of central arterial pressure （CAP） and carotid intima-media thickness,cardiac hypertrophy. Methods 314 cases of patients with hypertension from January 2009 to October 2011 were chosen in the First Affiliated Hospital of Xinjiang Medical University. Those patients were checked for ankle-brachial pulse wave velocity, central aortic pressure, carotid intima-media thickness, and wall thickness. The subjects were divided into carotid intima-media thickness＜0.9 mm group, and carotid intima-media thickness ≥0.9mm group. Subjects were divided into group with left ventricular hyperthrophy and group without left ventricular hypertrophy. To explore the correlation, BaPWV （pulse wave velocity）, CSP （systolic blood pressure of central aortic pressure）, CDP （diastolic blood pressure of central aortic pressure）, CPP （pulse pressure of central aortic pressure）, AP（augmentation pressure） were contrasted between the two groups. Results The BaPWV （pulse wave velocity）, CSP （systolic blood pressure of central aortic pressure）, AP（augmentation pressure）, AIx （augmentation index）, CPP（pulse pressure or central aortic pressure） were associated with carotid intima-media thickness, left ventricular hypertrophy, and the statistical comparison was significant （P<0.05）. Conclusions The BaPWV （pulse wave velocity）, CSP （central aortic systolic pressure）, AP （increase pressure）, AIx （augmentation index）, CPP （central aortic pressure pulse pressure） may be associated with carotid intimal thickening and related cardiac hypertrophy.

Abstract:Aim To observe the level of plasma N-terminal pro-brain natriuretic peptide （NT-proBNP） and heart function in children with ventricular septal defect （VSD） after interventional therapy combined alprostadil injection. Methods A total of 120 patients with VSD for cardiac catheter occlusion were enrolled in this study. All the patients were randomized to alprostadil group （n60） and control group （n60）. Levels of plasma NT-proBNP were measured before and the third day and sixth month after cardiac catheterization, respectively. Before and the seventh day and sixth month after cardiac catheterization, the parameters of left ventricular end diastolic diameter （LVEDD）, left ventricular end systolic diameter （LVESD）, left ventricular end systolic volume （LVESV）, left ventricular end diastolic volume （LVEDV） and left ventricular ejection fraction （LVEF） were measured by echocardiography. Results The parameters of LVEDD, LVESD, LVESV and LVEDV in the sixth month after catheterization were decreased significantly as compared to those before catheterization in the two groups （P<0.05, respectively）, while those in the alprostadil group were more decreased as compared with the control group （P<0.05）.There was no difference in plasma NT-proBNP level between control group and alprostadil group before catheterization （P>0.05）. In the sixth month after catheterization, plasma NT-proBNP level decreased significantly as compared to that before catheterization in the two groups （P<0.01, respectively）, while that in the alprostadil group were more decreased as compared with the control group （P<0.01）. Conclusions Alprostadil injection combined interventional therapy can further reduce the level of plasma NT-proBNP and improve heart function in the children with VSD.

Abstract:Aim To explore the changes and clinical value of cystatin C （CysC） level in gravidas with pregnancy-induced hypertension syndrome（PIH）. Methods 92 cases gravidas with PIH were selected as the observation group, including 34 cases of mild PIH, 31 cases of moderate PIH and 27 cases of severe PIH. 60 cases of normal gravidas were used as control group. The CysC level and serum creatinine （SCr）, blood urea nitrogen （BUN）, uric acid （UA） leve of all gravidas were detected in late pregnancy and postpartum 7 days. Results The cystatin C level in severe PIH gravidas was inscreased significantly compared with the healthy gravidas and mild PIH gravidas and moderate PIH gravidas in late pregnancy （P<0.05）. And more severity of PIH more obvious differences. The SCr,UA and BUN level in severe PIH gravidas were significantly inscreased compared with the healthy gravidas and mild PIH gravidas in late pregnancy （P< 0.05）. The cystatin C level in all gravidas were decreased in postpartum 7 days compared with late pregnancy. The SCr,UA and BUN level were increased in the healthy gravidas and mild PIH gravidas, and the SCr, UA level were decreased in severe PIH gravidas in postpartum 7 days compared with late pregnancy. But the level of CysC and UA were significantly increased in severe PIH gravidas compared with the healthy gravidas and mild PIH gravidas in postpartum 7 days （P<0.01）. Correlation analysis showed the blood pressure related to CysC and UA closely（P<0.01）. Conclusion The CysC level in gravidas with PIH especially in gravidas with severe PIH have obvious change, which combined with other indicators of renal function can sensitively reflect the impairment of renal function and postpartum recovery in gravidas with PIH.

Abstract:Aim To investigate the effect of different fasting blood glucose （FBG） levels on ankle-brachial index （ABI） in the elderly population. Methods 101510 workers who had participated in Kailuan health examination in 2006～2007 were stratified randomly, and 5440 participants with sufficient information for questionnaires and blood biochemical tests were recruited. ABI was tested in 2010～2011 Kailuan health examination, and 5189 were included for the final analysis. According to the American Diabetes Association guidelines, the study population was divided into three groups by FBG in 2010～2011 examination: ideal blood group （FBG＜5.6 mmol/L）, impaired fasting glucose （IFG） group （5.6 mmol/L≤FBG＜7.0 mmol/L） and diabetes mellitus group （FBG≥7.0 mmol/L or diabetes mellitus patients）. Multivariate Logistic regression analysis were used to calculate the rate for ABI. Results ABI in different groups were 1.10±0.09, 1.09±0.11 and 1.08±0.13 （P＜0.05）, the detection rates of ABI≤0.9 in different groups were 2.97%, 4.74% and 8.81% （P＜0.05）. Multivariate Logistic regression analysis showed that diabetes mellitus was the risk factor for ABI≤0.9, OR value was 1.97 （95% CI was 1.32～2.96）. In the female population, IFG and diabetes mellitus were risk factors for ABI≤0.9, OR value was 2.26 （95% CI was 1.25～4.07） and 2.37 （95% CI was 1.06～5.26）. Conclusion FBG is an independent risk factor for ABI,more pronounced in women.

Abstract:Atherosclerosis is a chronic inflammatory disease. Platelets and lymphocytes are involved in the progress of atherosclerosis. Platelets can interact with lymphocytes via direct contact or release soluble mediators and regulate the function of lymphocyte, even form “platelet-lymphocyte” aggregates, and subsequently promote the recruitment of lymphocyte into the injured vessel wall. Platelet-lymphocyte interaction influences the development of atherosclerosis and may be a promising therapeutic target. This review will focus on the platelet-lymphocyte interaction and its relationship with atherosclerosis.

Abstract:Adipose tissue is an important metabolic organ involved in energy balance. Excess accumulation of white adipose tissue （also called energy storage fat） leads to obesity, atherosclerosis and other health problems. Thermogenic fat （including brown and beige adipose tissue） has the potential to anti-obesity by thermogenic effects which can consume calories. Documents demonstrate that brown/beige adipocytes are originated from multiple precursor cells. The present review is mainly focused on the regulatory molecular mechanisms for the formation of thermogenic fat including PRDM16, PPARγ, SIRT1 and other factors.