Atherosclerosis (AS) is a common disease that seriously threatens human health. So far, the pathogenesis of AS has not been fully understood. This project investigates the effects of circARHGAP12 on AS and its regulatory mechanism. ApoE-/- knockout mice (ApoE) were adopted and reared with a high-fat diet to construct an AS model. Lentivirus was established to knock down the expression of circARHGAP12 in mice. After 12 weeks, the aorta was removed and the expression of circARHGAP12 was detected. Vascular oil red O staining was used to detect the degree of AS. The expression of inflammatory factors was detected by ELISA. Aortic smooth muscle cells (MASMCs) were cultured to evaluate the effects of circARHGAP12 on the phenotype of MASMCs. RNA pull-down and luciferase assay were used to verify the downstream target genes of circARHGAP12. In addition, the effects of circARHGAP12 on MASMCs proliferation and migration were detected by MTT and transwell assay. Compared with the normal group, the expression of circARHGAP12 in the MASMCs under ox-LDL treatment was elevated, and circARHGAP12 silencing could inhibit AS in vitro and in vivo. The results of the mechanism study showed that circARHGAP12 can directly bind with miR-630. In addition, miR-630 can also target EZH2 to modulate the transcription of TIMP2 and to influence the migration of MASMCs. circARHGAP12 is upregulated in AS. CircARHGAP12 knockdown can inhibit the progression of AS. This study expands on the role of circRNA in AS and provides potential targets for the treatment of AS.

以上海市中环线外圈沪太路上匝道为切入点,针对存在的拥堵节点及成因,设计了以ALINEA算法为基础的快速路入口匝道控制系统.方案中分析了交通拥堵的特征及影响因素,阐述了上匝道自动控制方法实现的基本逻辑,匝道控制的阈值确定以及与地面交通诱导的结合.该系统的离线模拟结果表明,ALINEA算法比较适用于快速路入口匝道的实时控制,可以明显缓解上匝道周边的交通拥挤,提高快速路主线的使用效率.

AIM:This study is undertaken to investigate the role and molecular mechanisms of miR-18a-5p in regulating pulmonary arterial hypertension (PAH) pathogenesis.METHODS:Gene expression and protein levels were determined by qRT-PCR and western blot, respectively; Cell counting kti-8 and Transwell migration assays were used to determine the biological functions of miR-18a-5p in pulmonary arterial smooth muscle cells (PASMCs); bioinformatics analysis, luciferase reporter assays were used to elucidate the mechanisms of miR-18a-5p.RESULTS:MiR-18a-5p was up-regulated in the clinical samples from PAH patients. PASMCs treated with hypoxia exhibited enhanced proliferative ability and upregulated miR-18a-5p expression. Knockdown of miR-18a-5p attenuated hypoxia-induced hyper-proliferation and enhanced migratory potential of PASMCs; while miR-18a-5p overexpression promoted PASMC proliferation and migration. Further mechanistic studies showed that Notch2 was a direct target of miR-18a-5p and was repressed by miR-18a-5p overexpression. The rescue studies indicated that Notch2 overexpression counteracted the enhanced proliferation and migration induced by miR-18a-5p mimics in PASMCs. Similarly, Notch2 overexpression also block the effects caused by hypoxia in PASMCs. Moreover, Notch2 expression was down-regulated in the PAH patients and was negatively correlated with miR-18a-5p expression. In vivo animal studies further revealed the up-regulation of miR-18a-5p and the down-regulation of Notch2 in the PAH rats.CONCLUSIONS:Collectively, this study identified the up-regulated miR-18a-5p in the PAH patients; our data suggest that miR-18a-5p contributes to the enhanced proliferation and migration of PASMCs via repressing Notch2 expression.

MicroRNAs (miRNAs) have already been proposed to be implicated in the development of ischaemic stroke. We aim to investigate the role of miR‐130a in the neurological deficit and angiogenesis in rats with ischaemic stroke by regulating X‐linked inhibitor of apoptosis protein (XIAP). Middle cerebral artery occlusion (MCAO) models were established by suture‐occluded method, and MCAO rats were then treated with miR‐130a mimics/inhibitors or/and altered XIAP for detection of changes of rats’ neurological function, nerve damage and angiogenesis in MCAO rats. The oxygen‐glucose deprivation (OGD) cellular models were established and respectively treated to determine the roles of miR‐130a and XIAP in neuronal viability and apoptosis. The expression levels of miR‐130a and XIAP in brain tissues of MCAO rats and OGD‐treated neurons were detected. The binding site between miR‐130a and XIAP was verified by luciferase activity assay. MiR‐130a was overexpressed while XIAP was down‐regulated in MCAO rats and OGD‐treated neurons. In animal models, suppressed miR‐130a improved neurological function, alleviated nerve damage and increased new vessels in brain tissues of rats with MCAO. In cellular models, miR‐130a inhibition promoted neuronal viability and suppressed apoptosis. Inhibited XIAP reversed the effect of inhibited miR‐130a in both MCAO rats and OGD‐treated neurons. XIAP was identified as a target of miR‐130a. Our study reveals that miR‐130a regulates neurological deficit and angiogenesis in rats with MCAO by targeting XIAP.

Objective To observe the effect of lncRNA DIGIT on vascular endothelial cell tube formation.Methods Human microvascular endothelial cells (HMEC-1) were cultured in vitro.The changes of tubes/nucleus ratio were observed by microscope.The expression of mRNA and protein was detected by real-time fluorescent quantitative polymerase chain reaction (FQ-PCR) and Western blotting.The DIGIT expression in human microvascular endothelial HMEC-1 cells was silenced by DIGIT transfection with shRNAs targeting.The effects of DIGIT silencing on cell vitality (Typan Blue Staining Cell Viability Assay Kit),migration ability (Trans-Well method),apoptosis [Annexin V-fluoresceine isothiocyanate (FITC) apoptosis detection method] and tube formation ability (microscope mapping method) were observed.The effects of DIGIT silencing on cell viability,migration,apoptosis and tube formation were then assessed.Results HMEC-1 cells were cultured for 24 h.The ratio of tubes/nucleus was increased with the time prolonged.The mRNA levels of vascular endothelial growth factor (VEGF),vascular endothelial growth factor receptor 2 (VEGFR2),CD144,and endothelial nitric oxide synthase (eNOS) were all significantly up-regulated (F =11.813,10.336,13.201,10.125,P ＜ 0.01),and all these four angiogenesis-associated proteins accumulated with the prolonged time.Cell viability (80.29 ± 4.68) ％ vs.(62.50 ± 4.78) ％,migration capacity (99.65 ± 3.07) ％ vs.(37.53 ± 2.78) ％,and tubes/nucleus ratio (0.691 ± 0.060) vs.(0.192 ± 0.020) were all significantly reduced in sh-DIGIT group when compared with sh-NC group (F =20.386,33.573,13.471,P ＜ 0.01).DIGIT silencing down-regulated the levels of B cell lymphoma/leukemia-2 (bcl-2),VEGF,VEGFR2,CD144 and eNOS,up-regulated bcl-2 associated X protein (bax),and activated cysteinyl aspartate-specific protease (Caspase)-3 and Caspase-9 expression.Conclusion LncRNA DIGIT plays an important role in promoting growth,migration and tubule formation in endothelial cells,and DIGIT may be effective molecular targets for the treatment of atherosclerosis.

Objective To analyze the clinical characteristics and significance of congenital inferior vena cava malformation (IVCM).Methods The clinical data of IVCM from 2013 to 2018 were studied.The clinical manifestations,diagnostic methods and characteristics were analyzed.Results There were 2 cases of double inferior vena cava (DIVC),3 cases of LIVC,1 case of LIVC + DIVC,1 case of IVCA,1 case of LIVC + IVCA near cardiac segment,1 case of reentrant inferior vena cava (RIVC) and 1 case of linear inferior vena cava (IVC).Among them,6 cases were complicated with DVT,3 cases were misdiagnosed as budd-chiari syndrome (BCS),and 1 case was complicated with severe deep venous insufficient (DVI).Conclusion IVCM is rare and often ignored because of nonspecific manifestations,but it is an important risk factor for many diseases.It has important clinical significance in abdominal,pelvic and retroperitoneal surgery and vascular interventional therapy.Neglecting may lead to serious consequences.

This study aimed to investigate the role and underlying mechanism of exosomes secreted by oxidized low-density lipoprotein (oxLDL)-stimulated macrophages in the progression of atherosclerosis (AS). Exosomes from peripheral blood of AS patients or oxLDL-treated macrophages were co-cultured with human neutrophils. Neutrophil extracellular traps (NETs) were detected by immunofluorescence staining. The levels of inflammatory cytokines were quantified by enzyme-linked immunosorbent assay (ELISA). The expression levels of miR-146a and superoxide dismutase 2 (SOD2) were determined by quantitative real-time PCR (qRT-PCR) and western blot. The generation of intracellular reactive oxygen species (ROS) was observed by using dichlorofluorescin diacetate (DCFH-DA). ApoE-deficient mice were fed with high-fat diet (HFD) to induce AS. Atherosclerotic plaques were evaluated by Oil red O (ORO) and hematoxylin-eosin (HE) staining. Our results showed that miRNA-146a was enriched in serum-derived exosomes of AS patients and oxLDL-treated macrophage THP-1-derived exosomes. Importantly, exosomal miR-146a secreted by oxLDL-treated macrophages promoted ROS and NETs release via targeting SOD2. In addition, intravenous administration of oxLDL-treated THP-1 cells-derived exosomes into AS mice significantly deteriorated AS in vivo. Our findings indicate that exosomal miR-146a derived from oxLDL-treated macrophages promotes NETs formation via inducing oxidative stress, which might provide a novel scientific basis for the understanding of AS progression.

Atherosclerosis is one of the most prevalent and important cardiac diseases, involving the heart and brain. This study aimed to explore the impacts of lncRNA Divergent to GSC induced by TGF-b family signaling (DIGIT) on vascular endothelial cells tube-formation capacity so as to reveal the potentials of DIGIT in atherosclerosis therapy. DIGIT expression in human microvascular endothelial HMEC-1 cells was silenced by transfection with shRNAs-targeted DIGIT. The effects of DIGIT silence on cell viability, migration, apoptosis, and tube formation were then assessed. Additionally, the cross-regulation between DIGIT and miR-134, and between miR-134 and Bmi-1 was detected to further reveal through which mechanism (s) DIGIT mediated HMEC-1 cells. The results showed that DIGIT silence significantly reduced cell viability, migration, tube-like structures formation, and induced apoptosis in HMEC-1 cells. DIGIT worked as a sponge for miR-134, and the anti-growth, anti-migratory, and anti-tube-formation functions of DIGIT silence on HMEC-1 cells were abolished by miR-134 suppression. Bmi-1 was a target of miR-134, and Bmi-1 upregulation abolished miR-134 overexpression-diminished cell growth, migration, and tube formation of HMEC-1 cells. Furthermore, Bmi-1 upregulation activated PI3K/AKT and Notch signaling pathways. In conclusion, our study demonstrated that lncRNA DIGIT accelerated tube formation of vascular endothelial cells through sponging miR-134. Our findings suggest that DIGIT and miR-134 may be promising molecular targets for atherosclerosis therapy.

传统的道路信息系统运维均基于设备状态的方式来管理,往往不能满足实时性和最终数据应用的要求.本文主要以交通工程的参数组合理论为基础进行数据的甄别和修补,以提高采集的数据质量为目的来开展系统的维护工作,并开发相应的软件系统来提高效率.

Atherosclerosis is one of the most prevalent and important cardiac diseases, involving the heart and brain. This study aimed to explore the impacts of IncRNA Divergent to GSC induced by TGF-b family signaling (DIGIT) on vascular endothelial cells tube-formation capacity so as to reveal the potentials of DIGIT in atherosclerosis therapy. DIGIT expression in human microvascular endothelial HMEC-1 cells was silenced by transfection with shRNAs-targeted DIGIT. The effects of DIGIT silence on cell viability, migration, apoptosis, and tube formation were then assessed. Additionally, the cross-regulation between DIGIT and miR-134, and between miR-134 and Bmi-1 was detected to further reveal through which mechanism(s) DIGIT mediated HMEC1 cells. The results showed that DIGIT silence significantly reduced cell viability, migration, tube-like structures formation, and induced apoptosis in HMEC-1 cells. DIGIT worked as a sponge for miR-134, and the antigrowth, anti-migratory, and anti-tube-formation functions of DIGIT silence on HMEC-1 cells were abolished by miR-134 suppression. Bmi-1 was a target of miR-134, and Bmi-1 upregulation abolished miR-134 overexpression-diminished cell growth, migration, and tube formation of HMEC-1 cells. Furthermore, Bmi-1 upregulation activated PI3K/AKT and Notch signaling pathways. In conclusion, our study demonstrated that lneRNA DIGIT accelerated tube formation of vascular endothelial cells through sponging miR-134. Our findings suggest that DIGIT and miR-I 34 may be promising molecular targets for atherosclerosis therapy.

目的 探讨激光联合大隐静脉高位结扎术治疗老年下肢静脉曲张的疗效.方法 选择2011年1月至2014年12月来该院治疗的下肢静脉曲张患者150例,均为单侧患肢,随机分成对照组和观察组各75例.对照组患者采用大隐静脉高位结扎术联合分段抽剥术进行治疗.观察组患者采用大隐静脉高位结扎术联合激光共同治疗.结果 观察组患者术中出血量、手术时间少于对照组,切口数量＞1个的患者少于对照组,术后疼痛程度优于对照组,术后下床活动时间、住院时间短于对照组(均P＜0.01).结论 采用激光联合大隐静脉高位结扎术治疗老年患者下肢静脉曲张疗效显著,能有效缩短住院时间,减轻患者疼痛,减少患者术中出血量.

Surgical site infection (SSI) is an important component of infections acquired from hospital. The most significant feature of vascular surgery different from other surgeries is frequent application of artificial grafts. Once SSI occurs after vascular operations with grafts, it might results in a serious disaster. Staphylococcus aureus and coagulase-negative Staphylococcus are the most common pathogenic bacteria for SSI after vascular surgery. Although SSI in vascular surgery often lacks of typical clinical characters, some clinical symptoms, laboratory data and certain imaging procedures may help to diagnose. In most cases of SSI after vascular procedures, the artificial grafts must be removed and sensitive antibiotics should be administered. However, for different cases, personalized management plan should be made depending on the severity and location of SSI.

目的：探讨中西医结合治疗动脉硬化性闭塞症的疗效，为动脉硬化性闭塞症的临床治疗提供理论依据。方法本研究选取2012年4月～2013年4月我院门诊收治的动脉硬化性闭塞症患者70例作为研究对象，并随机分为对照组和观察组，各35例，对照组患者采用前列地尔及阿司匹林治疗，观察组患者在对照组治疗的基础上加用通心络胶囊治疗，对比两组患者的疗效。结果对照组患者的治疗情况为：无效6例，有效16例，显效9例，治愈4例，治疗总有效率为82.9%；观察组患者的治疗情况为：无效1例，有效19例，显效10例，治愈5例，治疗总有效率为97.1%，观察组患者的治疗总有效率较对照组明显提高（P＜0.05）。结论中西医结合治疗动脉硬化性闭塞症具有良好效果，值得推荐。

目的：分析外科手术治疗下肢动脉硬化闭塞症的临床效果，为该病的临床治疗提供参考。方法将我院2014年3月至2015年3月收治的73例下肢动脉硬化闭塞症患者随机分为对照组（30例）和治疗组（33例），分别给予常规药物治疗及外科手术治疗，对两组治疗效果进行分析。结果治疗组患者患肢皮肤温度为（36.4±1.6）℃，踝肱指数为（0.7±0.2），均显著高于对照组（P<0.005）。结论外科手术治疗下肢动脉硬化阻塞症可有效缓解患者的临床症状，可在极大程度上改善患者预后，值得临床推广。

Background: Angiotensin-converting enzyme (ACE) I/D polymorphism has been indicated to be correlated with aortic aneurysm (AA) susceptibility, but study results are still debatable. Thus, a meta-analysis was conducted. Methods: Databases including PubMed, Embase, Web of Science, and Chinese National Knowledge Infrastructure (CNKI) were searched. Data were extracted and pooled odds ratios (OR) with 95% confidence intervals (CI) were calculated. Results: Ten studies with 3557 cases and 5231 controls were included in this meta-analysis. The association between ACE I/D genotype and AA risk was significant (OR=1.30; 95%CI, 1.07–1.57; p<0.01; I2=68%). When stratified by ethnicity, a significantly elevated risk was observed in Caucasians (OR=1.31; 95%CI, 1.07–1.61; p<0.01; I2=71%). In the abdominal AA subgroup, a significantly increased risk was observed (OR=1.29; 95%CI, 1.03–1.62; p=0.02; I2=73%). However, ACE I/D polymorphism was not associated with thoracic AA risk (OR=1.33; 95%CI, 0.85–2.07; p=0.21; I2=52%). Subgroup analysis on blood pressure status showed that an increased risk was found in hypertensive patients (OR=1.52; 95%CI, 1.02–2.26; p=0.04; I2=0%) but not in normotensive subjects (OR=1.46; 95%CI, 0.72–2.96; p=0.30; I2=25%). Conclusions: In conclusion, this meta-analysis suggested that ACE I/D polymorphism is a risk factor for AA.

To investigate pathogen distribution and drug resistance of incision infection caused by vascular operation to reduce postoperative incision infection, this paper retrospectively reviewed and analyzed 635 in-hospital patients taking vascular operation during Jan. 2008 and Dec. 2012. Analyzed data were statistically processed by SPSS 13.0 software, which resulted in 16 infected cases with 2.52% infection rate. A total of 27 pathogens wasisolated from specimens submitted for inspection, including 17 strains of Gram positive bacteria (62.96%) and 10 Gram negative bacteria (37.04%). Besides high sensitivity to imipenem, all bacteria were able to resist antibacterial drugs. Incision infection is proved in this research to be reduced effectively by some means, like complication correction before operation and reasonable application of antibacterial drugs after operation. While during an operation, it is necessary to operate strictly in a bacterium-free environment and wash incisions thoroughly.

Integrin (ITG) alpha 5 beta 1 is a dominant fibronectin receptor that is abundantly expressed on the surface of vascular smooth muscle cells (VSMCs). However, the association between integrin alpha 5 beta 1 and the proliferation and migration of VSMCs has yet to be elucidated. The aim of the present study was to characterize the roles of ITG alpha 5 and ITG beta 1 in the proliferation and migration of VSMCs, and to determine the effects of ITG alpha 5 beta 1 on integrin-linked kinase (ILK) and focal adhesion kinase (FAK) mRNA expression. Lentiviral expression vectors as well as RNA interference vectors of ITG alpha 5 and ITG beta 1 were successfully constructed and transfected into VSMCs to obtain ITG alpha 5- and ITG beta 1-overexpressing or -silenced cells, respectively. Cell cycle distribution, proliferation and migration were analyzed in the transfected VSMCs in order to clarify the roles of ITG beta 1 and ITGa5 in the proliferation and migration of VSMCs. ITG beta 1 was markedly associated with the proliferation and migration of VSMCs, and FAK was shown to be involved in the signaling pathways of ITG beta 1. ITG alpha 5 did not exert any effects on VSMCs. The results of the present study may provide a possible therapeutic target for the prevention and treatment of early vascular disease associated with VSMCs.

目的：分析下肢浅静脉曲张手术对下肢深静脉瓣膜功能不全的影响。方法：对我院2014年3月～2015年3月收治的60例下肢深静脉瓣膜功能不全且行下肢浅静脉曲张手术患者的临床资料进行回顾性分析，对患者手术前后瓣膜功能变化进行比较和分析。结果：经治疗，29例患者瓣膜反流消失，22例瓣膜功能有所好转，9例无法判断。术后 VCT 平均值及峰值流速均下降显著，差异具统计学意义（P ＜0.05）。结论：采用下肢浅静脉曲张手术对下肢深静脉瓣膜功能不全患者进行治疗，可有效改善患者下肢深静脉瓣膜功能，值得临床推广。

The commodity character of popular literature featuring ancient novels and drama was reflected in the advertising for literary works and selling them for profit.Advertising for popular literature mainly included public solicitation of articles and advertising in the form of comments,pictures,audio promotion,gifts,and discounts.Advertising permeated literary creation,publication and dissemination and was the historical representation of the commodity character of popular literature.