Objective To investigate the feasibility, accuracy and senaitivety of echo tracking (ET) technology on carotid elasticity in rabbits. Methods Thirty-nine healthy New Zealand rabbits were divided into 4 groups,which group 1,2,3 were experimental groups and group 4 was control group. Experimental groups were fed with high cholesterol diet,control group were fed with basic diet. The parameters of elasticity of carotid were measured with ET technology, including pressure-strain elasticity modulus(Ep), stiffness parameter(β), arterial complianee(AC), pulse wave velocity( PWV), augmentation index (AI) at the interval of 0,4,8,12 weeks of the experiment respectively. Blood-fat level of all rabbits were checked and the common carotid artery was examined pathologically,which were compared and analyzed then. Results With the prolong of the experiment time,the Ep and β raised, but the AC reduced. There were significant difference between experimental group 1 (4 weeks) and basement,which were same between experimental group 2 (8 weeks) and experimental group 1, between experimental group 3(12 weeks) and experimental group 2( P<0.05). PWV increased comparing with basement in the end of 8 weeks,which increased obviously in the end of 12 weeks,meanwhile was higher than in the end of 8 weeks,which there were significant differences ( P<0.01 ). AI had no change all the time. Conclusions ET technology is accurate and reliable in detecting early atherosclerosis. Probe maintenance tool can keep the steady of checking progress, sensitive of result and repeatability.

Humans ; Malocclusion, Angle Class I ; therapy ; Orthodontic Appliance Design

Cytophagocytosis ; Humans ; Plaque, Atherosclerotic ; physiopathology

Objective To evaluated the effect of the regional cooperative rescue model implemented on the length of time from first medical contact (FMC) to balloon dilation (B),economic expense and prognosis in patients with acute coronary syndrome (ACS).Methods Patients with ACS (including ST-segment elevation and non-ST-segment elevation) selected from other hospitals within 24 hours after onset were treated with emergency percutaneous coronary intervention.Patients were divided into two groups, regional cooperative rescue group and control group without the regional cooperative rescue model approved.The lengths of FMC-to-B time and Door-to-B time (from arrival at emergency department or OPD to balloon dilation),time required for patients referred to our hospital,cardiac function,averaged hospital costs,average hospital stay,percentage of medication used and a major adverse cardiac event (MACE) were analyzed.Results Mean FMC-to-B time,Door-to-B time,referral time and time consumed to obtain informed consent were significantly shorter [(106±33) min,(31 ±8) min,(62 ±18,8 ±3) min] vs.[(231 ±35) min,(109 ±26) min,(98 ±31) min,(28 ±11) min,respectively] by implementing the regional cooperative rescue compared with control group,and LVEF was increased,and LVED was deceased inregional cooperative rescue group.The mean costs [(44 123.0 ±3 427.0) yuan vs.(51 587.0 ±5 621.0)] yuan,days of hospital stay [(8.7 ±4.1) vs.(13.2 ±6.4)] and percentage of medication used were significantly decreased in the regional cooperative rescue group.The incidence of MACE inregional cooperative rescue group was 6.2％,whereas the incidence in control group was 16.8％.Conclusions The regional cooperative rescue model can improve the prognosis and decrease the FMC-to-B time,the rate of MACE and financial burden in patients with ACS.

Aim To investigate whether necroptosis mediates chemical hypoxia-induced HT22 mouse hippocampal cell injury and inflammation.Methods HT22 hippocampal cells were exposed to cobalt chloride (CoCl2) to establish a model of the chemical hypoxia-induced injury and inflammation.The expression level of RIP3 (an index of necroptosis) was determined by Western blot.Cell counter kit-8 (CCK-8) assay was used to test the cell viability.Lactate dehydrogenase (LDH) activity in the culture medium was measured with commercial kits.Mitochondrial membrane potential (MMP) was examined by rhodamine123 staining followed by photofluorography.The intracellular level of reactive oxygen species (ROS) was detected by 2', 7'-dichlorfluorescein-diacetate (DCFH-DA) staining followed by photofluorography.The secretion levels of interleukin-1β (IL-1β) and tumor necrosis factor-a (TNF-α) were measured by ELISA.Results Treatment of HT22 hippocampal cells with 600 μmol·L-1 CoCl2 for 36 h markedly induced cytotoxicity, leading to a decrease in cell viability to (52.0±2.65) % , indicating that chemical hypoxia-induced cellular injury model was successfully set up.Besides, CoCl2 induced considerable injuries and inflammation, evidenced by increases in LDH activity, ROS production, MMP loss, as well as the secretion levels of IL-1β and TNF-α.Co-treatment of the cells with 40~100 μmol·L-1 Nec-1 (a specific inhibitor of necroptosis) and CoCl2 markedly attenuated the decrease in viability induced by CoCl2, reaching the best anti-cytotoxicity inhibitory effect at 80 μmol·L-1.Meanwhile, the co-treatment with 80 μmol·L-1 Nec-1 blocked the above injuries and inflammatory response induced by CoCl2.In addition, treatment of HT22 hippocampal cells for 6~48 h up-regulated the expression of RIP3, and Nec-1 alleviated the up-regulation of RIP3 expression level induced by CoCl2.Conclusion Necroptosis mediates chemical hypoxia-induced HT22 hippocampal cell injury and inflammation.

Human immunodeficiency virus-associated pulmonary arterial hypertension (HIV-PAH) is a long-term cardiovascular complication of AIDS patients, with an incidence of about 0.5%. The onset of HIV-PAH is insidious and lack of specific symptoms with poor prognosis. The pathogenesis is complicated while the bystander effect of HIV or the complication of HIV is possible mechanism. Echocardiography is an important diagnostic method and facilitates early screening of patients. At present, there is no specific drug targeted HIV-PAH, and the treatment strategy is to follow the treatment recommendations for idiopathic pulmonary arterial hypertension on the basis of highly active antiretroviral therapy, while the interaction between two types of drugs should be considered. This paper will mainly focus on the pathogenesis and treatment of HIV-PAH.

Objective To study whether Nεcarboxymethyl lysine(CML)can form a good molecular docking with the scavenger receptor CD36and induce a stable interaction.Methods The interaction between CML and CD36was studied by co-immunoprecipitation.The binding mode and affinity of CD36to CML were tested using AutoDock 4.2,iBabel and XQuartz-2.7.7software respectively. Results Co-immunoprecipitation showed that anti-CD36antibody magnetic bead could precipitate CD36from the total protein in RAW264.7cells and anti-CML could detect CD36 binding CML.CD36had a good molecular docking with CML,CD36and CML interacted stably with each other.The affinity of CML to 4Q4Bprotein structure of CD4extracellular domain was -29.62kJ/mol.ARG82,ASN71and THR70were the products of amino acid receptor interaction. Further docking analysis showed that CML could form 3interacting hydrogen bonds with 4Q4B,and the docking prediction inhibition constant was 6.92with a root mean square deviation of 2.54.Conclusion A good molecular docking between CML and 4Q4Bprotein structure of CD36extracellular domain can induce a stable interaction between CML and CD36.Hydrogen bonding is the main interaction mode.

Objective To study the effect of tissue plasminogen activator (t-PA) on p57NTR ,inflammatory reaction ,immune regulation and oxidative stress and its effect on intimal hyperplasia .Methods The vascular injury treatment was performed in the diabetic rabbit model with carotid arterial adventitia stripping ,meanwhile t-PA controlled release microspheres were given ,the nerve distribution in the local blood vessels was observed by immunohistochemical staining .The change of nerve remodeling in the control group and treatment group was observed ,meanwhile the effect of giving t-PA controlled release microspheres on the release of ace-tylcholine and norepinephrine was detected .RT-PCR was used to detect local vascular tissue inflammation ,immune effects and oxi-dative stress .The sympathetic neurons and smooth muscle cell co-culture was adopted ,then giving glyoxal treatment as the athero-sclerosis cell model .With the t-PA treatment group as the intervention group ,the effect of t-PA on the number of cholinergic neu-ron ,and synaptic connections between the smooth muscle cells and acetylcholine secretion was observed .The change of t-PA-MMP-p75NTR and NF-kappa B signaling pathway were detected by RT-PCR .Results The vascular injury treatment was performed in the diabetic rabbit model with carotid arterial adventitia stripping ,meanwhile t-PA controlled release microspheres were given ,the nerve distribution in the local blood vessels was observed by immunohistochemical staining .The change of nerve remodeling in the control group and treatment group was observed ,meanwhile the effect of giving t-PA controlled release microspheres on the release of acetylcholine and norepinephrine was detected .RT-PCR was used to detect local vascular tissue inflammation ,immune effects and oxidative stress .The sympathetic neurons and smooth muscle cell co-culture was adopted ,then giving glyoxal treatment as the ath-erosclerosis cell model .With the t-PA treatment group as the intervention group ,the effect of t-PA on the number of cholinergic neuron ,and synaptic connections between the smooth muscle cells and acetylcholine secretion was observed .The change of t-PA-MMP-p75NTR and NF-kappa B signaling pathway were detected by RT-PCR .Conclusion t-PA activates MMPs and feedback in-hibits p75NTR-NF-kappa B signaling pathway to increase vascular adventitia autonomic nerve reconstruction and delay the occur-rence and development of atherosclerosis disease .

Objective: To investigate the feasibility and efficacy of the establishment of regional cooperative acute ST-segment elevation myocardial infarction (STEMI) rescue network among the prefectural-level city hospitals in China. Methods: Based on real-time remote electrocardiogram transmission and "120" emergency systems, we established a regional collaborative STEMI treatment network with our hospital as the network unclears including 8 second-class affiliated hospitals of Jiangsu University in 2013. STEMI treatment time, therapeutic effects and economic indexes were compared before (from January 2010 to December 2012, 180 cases, pre-network) and after (From January 2013 to December 2015, 374 cases, post-network) the establishment of the regional collaborative STEMI treatment network. Results: Post establishment of the rescue network, mean first medical contact (FMC) to balloon (FMC-to-B) time, referral time and obtaining informed consent time were all significantly decreased from (191±41), (94±18), (25±9) minutes to (93±19), (53±18), (7±5) minutes, respectively, in comparison with the pre-network era(all P<0.05). There was a trend of prolonged FMC-to-B time in proportion to aging of STEMI patients(trend P<0.05). Three months post discharge, LVEF was higher (55.3%±10.7% vs. 48.8%±12.1%, P<0.05) and LVEDd was lower ((49.1±10.8)mm vs.(51.8±9.2)mm, P<0.05) in the post-network group compared to pre-network group.In-hospital mortality was also significantly reduced post the establishment of the rescue network (2.14%(8/374) vs. 3.89%(7/180), P<0.05). The results also showed that the total costs (42 017(25 069, 75 148)yuan vs.51 030(28 137, 105 861)yuan), days of hospitalization ((9.1±4.5) days vs. (15.3±4.8)days) and percentage of medicine and consumables were all significantly decreased in the post-network group compared to pre-network group(all P<0.05). Conclusion Establishment of the regional cooperative rescue network is feasible among the prefectural-level city hospitals in China. Establishment of such network can improve the prognosis and decrease the FMC-to-B time, the rate of in-hospital mortality and financial burden of patients with STEMI, and serves as an effective strategy to improve the rescue ability for STEMI patients.

Objective: To investigate whether CD137 induces primary vascular muscle cells (VSMCs) phenotype transformation through activating nuclear factor of activated T-cells 1(NFATc1) signaling. Methods: VSMCs were obtained from aorta of C57BL/6J mice (8 weeks, male) through tissue-piece inoculating. Cells were divided into control group, CD137 agonist group (treated with CD137L recombinant protein) and anti-CD137 group (treated with anti-CD137 antibody). In si-RNA transfection assay, cells were divided into si-control group and si-NFATc1 group which were transfected with control or si-NFATc1 sequence respectively. The levels of NFATc1 and other phenotype related protein such as α-smooth muscle actin (α-SMA), smooth muscle myosin heavy chain (SM-MHC), vimentin were detected by Q-PCR and Western blot. Nuclear protein expression and activity of NFATc1 were detected by immunofluorescence and Western blot. Transwell assay was performed to measure the migration of VSMCs. Results: According to Western blot, the expression of NFATc1 and vimentin was significantly upregulated (5.07±0.36 vs. 1.00±0.00, P<0.05; 3.23±0.27 vs. 1.00±0.00, P<0.05) while α-SMA and SM-MHC expressions was significantly downregulated (0.73±0.15 vs. 1.00±0.00, P<0.05; 0.45±0.05 vs. 1.00±0.00, P<0.05) in CD137 agonist group compare to control group. Compared with CD137 agonist group, the expression of NFATc1 and vimentin was significantly downregulated (1.56±0.27 vs. 5.07±0.36, P<0.05; 1.21±0.17 vs. 3.23±0.27, P<0.05), but the levels of α-SMA and SM-MHC were significantly upregulated (2.01±0.43 vs. 0.73±0.15, P<0.05; 2.85 ±0.32 vs. 0.45±0.05, P<0.05) in anti-CD137 group. Compared with si-con group, the expression of SM-MHC and α-SMA was significantly upregulated while the expression of vimentin was significantly downregulated in si-NFATc1 group. Transwell assay results demonstrated that migration cell numbers was significantly higher in CD137L group compared with control group(3.85±0.31 vs. 1.00±0.00, P<0.05), this effect was significantly attenuated by inhibiting NFATc1. Conclusion CD137 could induce VSMC phenotype transformation through activating NFATc1 signaling.