：Thyroid hormones have been widely accepted to have complex effects on myocardium by regulation of ion channel, autonomic nervous system, non-specific inflammatory infiltration, therefore predisposing to reversible myocardium damage and multiple arrhythmias . However, atrial fibrillation (AF), advanced to irreversible complete heart block, QT (QTc) prolongation, torsade de pointes (TdP), ventricular flutter and fibrillation (VF) have never been reported at the same time in a patient with hyperthyroidism before.

目的 观察心肌梗死(MI)后大鼠予奥美沙坦酯(OLM)灌胃后血管紧张素Ⅱ(AngⅡ)1型(AT1)受体表达的变化,以及尼克酰胺腺嘌呤二核苷酸磷酸氧化酶(NOX)活性及其亚单位gp91phox表达的变化.方法 选择体质量270～380 g的雄性SD大鼠,随机分为对照组、奥美沙坦酯组、安慰剂组,对照组以5-0线穿绕但不结扎前降支(LAD);奥美沙坦酯组结扎LAD后予奥美沙坦酯灌胃(10 mg/kg)4周;安慰剂组LAD结扎后,经灌胃注入等容积蒸馏水4周.4周后称重并计算左室质量指数(LVMI),分离出左室中非梗死部位的心肌组织,检测AT1受体mRNA、gp91phox mRNA及其蛋白的表达程度、超氧阴离子自由基(O2-)水平、NOX活性.结果 安慰剂组LVMI、AT1受体mRNA的表达程度、gp91phox mRNA的表达程度、gp91phox蛋白同内参GAPHD的灰度比、O2-浓度、NOX活性均高于对照组及奥美沙坦酯组,差异均有统计学意义(P<0.05).gp91phox mRNA与AT 1受体mRNA表达程度呈正相关(r=0.729,P<0.05);O2-浓度与gp91phox mRNA表达程度及NOX活性呈正相关(r值分别为0.735,0.843,P<0.05).结论 心肌梗死后大鼠AT1受体被激活,NOX活性增加,O2-增多,氧化应激反应加剧,导致左室重构;奥美沙坦酯阻断AT1受体后,NOX活性及其亚单位gp91phox表达降低,O2-减少,从而减缓氧化应激反应,防止心肌梗死后左室重构.

Heart failure (HF) is often the inevitable manifestation of myocardial ischemia. Hypoxia can induce cardiomyocytes to express many microRNAs (miRNAs), which are highly expressed in exosomes. In addition, miR-22-3p is a marker in heart failure. Therefore, miR-22-3p was taken as the research object to explore its role and mechanism in HF. HF differentially expressed miRNAs were screened by bioinformatic analysis. The HF rats model was constructed and identified by detecting serum brain natriuretic peptide (BNP) and ultrasound analysis [left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS)]. The extracted exosomes were identified by transmission electron microscopy, and Western blot was used to detect the expressions of Tsg101 and CD63. Quantitative real-time polymerase chain reaction detected miR-22-3p expression in serum, exosomes, and serum without exosomes, while the cardiomyocytes cytotoxicity was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and PKH26 staining. After overexpressing/silencing miR-22-3p in cells, cell viability, apoptosis, and apoptosis-associated markers were detected. Bioinformatic analysis screened the target gene of miR-22-3p, which was verified by dual-luciferase assay. Regulation of miR-22-3p on FURIN was measured by rescue tests. In vivo experiments were verified the above results. MiR-22-3p was identified as the research object. BNP was increased in the model group, while LVEF and LVFS were decreased. MiR-22-3p was overexpressed in HF-treated serum and exosomes. Normal exosomes did not affect cardiomyocyte function, while high concentrations of HF-treated exosomes were cytotoxic. By regulating apoptosis-related genes, overexpressed miR-22-3p inhibited cell activity and promoted cell apoptosis. Silenced miR-22-3p with opposite effects counteracted effects of HF-treated exosomes. FURIN, target gene of miR-22-3p, was negatively regulated by miR-22-3p, while overexpressed FURIN promoted cell activity and inhibited apoptosis. In vivo research was consistent with the results of cell experiments. By regulating FURIN, miR-22-3p in exosomes increases the risk of HF damage.

患者男性,28岁,因"胸闷、心慌2月余"入院.入院心电图示心房扑动;超声心动图提示左室增大、左室收缩舒张功能减退;心腔内电生理检查诊断三尖瓣峡部依赖型心房扑动.应用腔内超声(ICE)构建三尖瓣峡部模型,发现一憩室深度5.4 mm、宽度8.1 mm;沿三尖瓣峡部行线性射频消融,心房扑动终止并转为窦性心律,但峡部双向传导阻滞不完全;随后导管采用倒U造型,在ICE指导下贴靠憩室底部和后壁,予以补充消融后,峡部形成完全性双向传导阻滞;反复心房刺激未诱发心动过速.术后心电图示窦性心律,动态心电图示偶发房性早搏.

目的 探讨急性ST段抬高型心肌梗死患者(ST-segment elevation myocardial infarction,STEMI)首次住院期间发生室壁瘤的危险因素.方法 收集2018年1月—2020年10月住院的STEMI患者共757例,根据是否发生室壁瘤分为两组,其中,室壁瘤组共90例,无室壁瘤组共667例;回顾性收集两组患者的临床资料,并对可能导致室壁瘤发生的危险因素进行单因素分析,选择有意义的指标进行多因素Logistic回归分析,并对有价值的指标绘制ROC曲线.结果(1)本研究中STEMI后发生室壁瘤的机率为11.89％.(2)单因素分析发现,室壁瘤组患者的年龄、心率、左房内径、左室收缩末期内径、N末端脑钠肽前体、D二聚体、纤维蛋白原、纤维蛋白降解产物、中性粒细胞百分比、高密度脂蛋白、总胆红素和血肌酐显著高于无室壁瘤组;女性、胸痛时间≥12 h、前壁心肌梗死、高血压病史、糖尿病病史、Killip分级>1、罪犯血管为前降支比例显著低于无室壁瘤组,而在吸烟史、罪犯血管为右冠及回旋支比例、左室射血分数(left ventricular ejection fraction,LVEF)、淋巴细胞计数、甘油三酯、前白蛋白、白蛋白和肾小球滤过率显著低于无室壁瘤组.(3)将单因素分析中有统计学意义的指标纳入多因素Logistic回归分析后示,年龄[OR=1.036(1.013～1.060)]、前壁心肌梗死[OR=10.068(2.348～43.166)]和LVEF[OR=0.902(0.862～0.943)]为室壁瘤的影响因素(P<0.05).(4)将多因素Logistic回归分析中的连续变量LVEF、年龄及LVEF联合年龄进行ROC曲线绘制,得到三者的曲线下面积分别为0.797、0.671和0.811.结论 高龄、LVEF降低和前壁心肌梗死为STEMI患者发生室壁瘤的危险因素,LVEF联合年龄对室壁瘤发生的预测价值更高.

目的 研究CARTO3三维标测系统的VisiTag模块指导下心房颤动(简称房颤)患者射频消融术后中期疗效和安全性.方法 采用单中心回顾性研究方法,选择2016年11月至2018年6月在苏州大学附属第一医院行射频消融术的房颤患者为研究对象.所有患者均在CARTO3三维标测系统VisiTag指导下行肺静脉隔离及心房线性消融,设置导管稳定性参数为最大移动范围2.5 mm、最小时间5 s;FOT:40％、最小压力5 g;采用逐点式量化消融术式.术后每3个月随访1次,若患者出现症状及时行常规心电图和24 h动态心电图检查.应用Kaplan-Meier生存曲线分析房颤患者消融术后中期成功率.房颤复发定义为3个月空白期后无抗心律失常药物的情况下出现持续时间大于30 s的房性心动过速、心房扑动或房颤.结果 共入选121例房颤患者,年龄(62.2±9.3)岁,其中男性61例(50.4％),阵发性房颤79例(65.3％).随访时间中位数为23(20.4,28.0)个月,总体消融成功率为77.7％,其中阵发性房颤成功率为79.7％,持续性房颤成功率为73.8％,两者间差异无统计学意义(log-rank,P=0.372).围手术期心包压塞发生率为0.8％,无脑栓塞、症状性肺静脉狭窄、心房食管瘘等严重并发症.结论 Visi-T ag模块指导下房颤射频消融可以提高术后中期成功率且安全性较高.

Enhanced apoptosis of cardiomyocytes in suffering overloaded saturated fatty acids (SFAs) can result in myocardial infarction and cardiac dysfunction. The function of vascular endothelial growth factor (VEGF) in cardiomyocyte protection was not clearly described. To investigate the preservative effects of VEGF sensitization on ceramide-mediated programmed cell death of cardiomyocytes, palmitate-induced injury in H9c2 cells was established as an in vitro model. Results revealed that 0.5 mM palmitate application effectively led to debased viability and activated apoptotic factors. A significant time-dependent relation between PAL and cardiomyocyte injury was observed. The apoptosis rate was increased greatly after 16 h of treatment with 0.5 mM PAL. In addition, cell viability was restored by VEGF overexpression during treatment with 0.5 mM PAL. Reduced apoptosis rate and expression of caspase 3, Bax, and NF-κB p65 were observed in this process, while boosted Bcl-2, p-JNK/JNK expression and activity of caspase 3 were checked. However, p-ERK/ERK levels did not exhibit a significant change. These findings indicated the protective effects of VEGF in confronting the ceramide-induced cardiomyocyte apoptosis, and would devote therapeutic targets for cardiovascular safeguard in dealing with fatty acid stress.

Background: An effective diagnostic and prognostic marker based on the gene expression profile of classic Hodgkin lymphoma (cHL) has not yet been developed. The aim of the present study was to investigate potential markers for the diagnosis and prediction of cHL prognosis. Methods: The gene expression profiles with all available clinical features were downloaded from the Gene Expression Omnibus (GEO) database. Then, multiple machine learning algorithms were applied to develop and validate a diagnostic signature by comparing cHL with normal control. In addition, we identified prognostic genes and built a prognostic model with them to predict the prognosis for 130 patients with cHL which were treated with first-line treatment (ABVD chemotherapy or an ABVD-like regimen). Results: A diagnostic prediction signature was constructed and showed high specificity and sensitivity (training cohort: AUC=0.981,95% CI 0.933-0.998, P<0.001, validation cohort: AUC=0.955,95% CI 0.895-0.986, P<0.001). Additionally, nine prognostic genes (LAMP1, STAT1, MMP9, C1QB, ICAM1, CD274, CCL19, HCK and LILRB2) were screened and a prognostic prediction model was constructed with them, which had been confirmed effectively predicting prognosis (P<0.001). Furthermore, the results of the immune infiltration assessment indicated that the high scale of the fraction of CD8 + T cells, Ml macrophages, resting mast cells associated with an adverse outcome in cHL, and naive B cells related to prolonged survival. In addition, a nomogram that combined the prognostic prediction model and clinical characteristics is also suggested to have a good predictive value for the prognosis of patients. Conclusion: The new markers found in this study may be helpful for the diagnosis and prediction of the prognosis of cHL.

目的 探讨平均血小板体积(MPV)与行PCI术的急性ST段抬高型心肌梗死(STEMI)患者住院期间主要心脏不良事件的关系.方法 选择2018年1月—2019年6月本院行PCI术且资料完整的STEMI患者共253例,根据有无MACE事件分为非MACE组196例和MACE组57例.比较两组患者的一般资料和实验室指标,采用多因素logistic回归分析MACE的预测因素,绘制受试者工作特征曲线(ROC曲线)评价MPV对住院期间MACE的预测价值.根据ROC曲线的截断点将患者分为高MPV组176例及低MPV组77例,比较两组间MACE的发生率.结果(1)两组间性别、高血压、糖尿病、血肌酐、总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、血小板计数、血红蛋白和白细胞计数差异无统计学意义(P>0.05);NT-proBNP、高敏肌钙蛋白、MPV、红细胞分布宽度和左室射血分数(LVEF)比较差异均有统计学意义(P<0.05).(2)多因素logistic回归分析显示LVEF[OR=0.001,95％CI(0.000-0.114)]和MPV[OR=1.403,95％CI(1.053-1.869)]是住院期间不良事件的独立预测因素.(3)ROC曲线显示,MPV预测住院期间MACE事件的曲线下面积为0.642[95％CI(0.562-0.722)],最佳截断值为10.25,灵敏度为86.0％,特异度为36.2％.(4)高MPV组住院期间MACE发生率明显高于低MPV组(P<0.05).结论 MPV是行PCI术的急性STEMI患者住院期间不良事件的独立预测因素.

目的 探讨特发性室性早搏(室早)的发生与自主神经机制之间的关系.方法 采用单中心回顾性研究方法,选择24 h动态心电图记录到频发室早(≥10000次/d或室早负荷≥10％)的156例特发性室早患者(室早组)和同期健康体检者84例(对照组)为研究对象.根据24 h动态心电图检查结果,计算心率变异性指标rMSSD、pNN50、高频功率(HF)、标准化的高频功率(HFnorm)、低频功率(LF)与HF的比值(LF/HF).比较两组自主神经张力间的差异,并分析室早负荷与自主神经张力变化的关系.结果 与对照组相比,室早组患者rMSSD、pNN50、HF和HFnorm均明显增加(P<0.01),LF/HF显著降低(P<0.01).室早组患者24 h室早负荷与rMSSD、pNN50和HF呈正相关(相关系数分别为0.492、0.425、0.372,P<0.01),而与LF/HF呈负相关(相关系数为-0.206,P<0.05);其中28.8％(45/156)的患者每小时室早负荷与每小时HFnorm呈正相关,16.0％(25/156)的患者与每小时LF/HF呈正相关,53.8％(84/156)的患者与每小时HFnorm和每小时LF/HF均无相关性.结论 部分特发性室早的发生与交感和(或)迷走神经张力变化相关.

Vascular endothelial dysfunction is a vital pathological change in hypertension, which is mainly caused by apoptosis and oxidative stress injury of vascular endothelial cells. Peptidomics is a method for the direct analysis of small bioactive peptides in various biological samples using liquid chromatography-mass spectrometry (MS)/MS. Given the advantages of the low molecular weight, optimum targeting and easy access to cells, peptides have attracted extensive attention in the field of drug research. However, to the best of our knowledge, little is currently known regarding the role of peptides in vascular endothelial injury. In order to investigate the peptides involved in vascular endothelial protection, MS was used to analyze the peptide profiles in the supernatant of human umbilical vein endothelial cells (HUVECs) stimulated by Ang II. The results revealed that 211 peptides were identified, of which six were upregulated and 13 were downregulated when compared with the control group. Subsequently, the present study analyzed the physical and chemical properties and biological functions of identified peptides by bioinformatics, and successfully screened a peptide (LLQDSVDFSLADAINTEFK) named VMP-19 that could alleviate the apoptosis and oxidative stress injury of HUVECs induced by Ang II. In conclusion, to the best of our knowledge, the present study was the first to use peptidomics to analyze the peptide profiles of supernatant secreted by HUVECs, and revealed that the novel peptide VMP-19 could protect HUVECs from apoptosis and oxidative stress injury. The results of the present study could provide novel insights into treatment strategies for hypertension.

目的 探讨阵发性房颤(paroxysmal atrial fibrillation,PAF)患者经量化消融术后心脏结构和功能的变化.方法 回顾性分析经量化消融的188例PAF患者的临床资料和术后随访资料,其中64例在Carto3系统Visitag模块指导下进行逐点式射频消融,124例在消融指数指导下进行逐点式射频消融.根据术后复发与否分成两组:复发组(n=31)和未复发组(n=157).房颤复发定义为3个月空白期后出现持续时间≥30 s的房性心动过速、心房扑动、房颤等快速型房性心律失常.利用心脏超声检查测量术前和术后3个月的心房和心室内径、左室收缩和舒张功能等指标.结果 ① 平均随访时间为(14.4±8.3)个月,房颤量化消融总体成功率为83.5％(157/188),PAF伴左心房内径(LAD)<40 mm和LAD≥40 mm者量化消融成功率分别为89.1％(57/64)和80.6％(100/124);②未复发组术后LAD和右心房内径(RAD)明显缩小、二尖瓣E峰流速显著降低(P均<0.05);而复发组术后RAD明显缩小(P<0.05),左室射血分数(left ventricular ejection fraction,LVEF)显著增加(P<0.05),两组其他指标间的差异无统计学意义;③ 消融术前,与PAF伴LAD<40 mm者比较,PAF伴LAD≥40 mm者的LAD、RAD、左心室舒张末期内径(LVEDD)、左心室收缩末期内径(LVESD)、二尖瓣E峰和三尖瓣反流压明显增大,LVEF值显著降低(P均<0.05);PAF伴LAD<40 mm患者术后RAD明显缩小、二尖瓣A峰明显降低(P均<0.05);PAF伴LAD≥40 mm患者术后LAD、RAD显著减小,二尖瓣E峰明显降低,LVEF明显增加(P均<0.05).结论 量化消融治疗PAF患者的中远期成功率较高,并且可部分逆转左右心房重构以及心室功能.

BackgroundCachexia is defined as an involuntary decrease in body weight, which can increase the risk of death in cancer patients and reduce the quality of life. Cachexia-inducing factors (CIFs) have been reported in colorectal cancer and pancreatic adenocarcinoma, but their value in diffuse large B-cell lymphoma (DLBCL) requires further genetic research.MethodsWe used gene expression data from Gene Expression Omnibus to evaluate the expression landscape of 25 known CIFs in DLBCL patients and compared them with normal lymphoma tissues from two cohorts [GSE56315 (n = 88) and GSE12195 (n = 136)]. The mutational status of CIFs were also evaluated in The Cancer Genome Atlas database. Based on the expression profiles of 25 CIFs, a single exploratory dataset which was merged by the datasets of GSE10846 (n = 420) and GSE31312 (n = 498) were divided into two molecular subtypes by using the method of consensus clustering. Immune microenvironment between different subtypes were assessed via single-sample gene set enrichment analysis and the CIBERSORT algorithm. The treatment response of commonly used chemotherapeutic drugs was predicted and gene set variation analysis was utilized to reveal the divergence in activated pathways for distinct subtypes. A risk signature was derived by univariate Cox regression and LASSO regression in the merged dataset (n = 882), and two independent cohorts [GSE87371 (n = 221) and GSE32918 (n = 244)] were used for validation, respectively.ResultsClustering analysis with CIFs further divided the cases into two molecular subtypes (cluster A and cluster B) associated with distinct prognosis, immunological landscape, chemosensitivity, and biological process. A risk-prognostic signature based on CCL2, CSF2, IL15, IL17A, IL4, TGFA, and TNFSF10 for DLBCL was developed, and significant differences in overall survival analysis were found between the low- and high-risk groups in the training dataset and another two independent validation datasets. Multivariate regression showed that the risk signature was an independently prognostic factor in contrast to other clinical characteristics.ConclusionThis study demonstrated that CIFs further contribute to the observed heterogeneity of DLBCL, and molecular classification and a risk signature based on CIFs are both promising tools for prognostic stratification, which may provide important clues for precision medicine and tumor-targeted therapy.

Background: TANK (TRAF family member associated NF-κB activator) acts as a member of scaffold proteins participated in the development of multiple diseases. However, its function in process of cardiac hypertrophy is still unknown. Methods and Results: In this study, we observed an increased expression of TANK in murine hypertrophic hearts after aortic banding, suggesting that TANK may be involved in the pathogenesis of cardiac hypertrophy. We generated cardiac-specific TANK knockout mice, and subsequently subjected to aortic banding for 4–8 weeks. TANK knockout mice showed attenuated cardiac hypertrophy and dysfunction compared to the control group. In contrast, cardiac-specific TANK transgenic mice showed opposite signs. Consistently, in vitro experiments revealed that TANK knockdown decreased the cell size and expression of hypertrophic markers. Mechanistically, AKT signaling was inhibited in TANK knockout mice, but activated in TANK transgenic mice after aortic banding. Blocking AKT signaling with a pharmacological AKT inhibitor alleviated the cardiac hypertrophy and dysfunction in TANK transgenic mice. Conclusions: Collectively, we identified TANK accelerates the progression of pathological cardiac hypertrophy and is a potential therapeutic target.

Background: Although there are concerns regarding their clinical use, embryonic stem cells (ESCs) hold a great promise for cardiac repair. Exosomes deriving from ESCs constitute a promising alternative for heart restoration. However, their effects in hypertension-induced heart failure are still unknown. Objective and Methods: To investigate the effects of ESCs-derived exosomes on hypertension-induced heart failure and the underlying mechanisms, sustained transverse aortic constriction (TAC) was performed on 8-week-old C57BL/6 male mice. After 1 months, ESCs-derived exosomes were isolated and injected intravenously once a week for 6 weeks. Echocardiography, wheat germ agglutinin (WGA), Masson staining, immunohistochemistry, and tube formation assays were all involved in our study. Results: Proteomics analyses revealed that ESC-derived exosomes contain FGF2 protein. Tube formation induced by these exosomes could be inhibited by FGF2R siRNA interference. ESCs-derived exosomes evidently attenuated TAC-induced heart failure, improving cardiac function and promoting myocardial angiogenesis which can be attenuated by selective FGF2 inhibitor AZD4547. Conclusions: ESC-derived exosomes attenuate TAC-induced heart failure mostly by promoting myocardial angiogenesis. FGF2 signaling plays a vital role in the myocardial angiogenesis induced by ESC-derived exosomes.

目的 探讨消融指数(AI)指导心房颤动(简称房颤)导管消融的短期疗效及安全性.方法 选择2018年6月至2019年5月在苏州大学附属第一医院拟行射频消融术的房颤患者116例为研究对象,其中阵发性房颤患者75例 、持续性房颤患者41例.所有患者均在Carto3三维标测系统AI指导下应用压力监测导管行环肺静脉隔离及心房线性消融,相邻消融点间距离<6 mm,肺静脉前壁和嵴部AI≥400以及后壁 、顶部和下壁AI≥300为消融目标.术后每3个月随访1次,若患者出现症状及时行心电图和24 h动态心电图检查.消融成功标准:3个月空白期后无抗心律失常药物的情况下未发生持续时间>30 s的房性心律失常.结果 ①AI指导下房颤消融时间为(60.8±10.6)min,每消融点阻抗下降为(11.5±6.3)Ω,肺静脉单圈隔离成功率为91％;② 随访时间为(9.1±3.2)个月,失访3例,阵发性和持续性房颤患者消融成功率分别为90.4％ 及87.5％;③ 在围手术期及随访过程中,仅术中发生1例一过性脑缺血发作,术后心脏超声发现少量心包积液2例,无心包压塞 、脑栓塞 、肺静脉狭窄和心房食管瘘等严重并发症.结论 AI指导下行房颤导管消融术是安全可行的,可提高房颤消融效率 、肺静脉单圈隔离率及短期疗效.

Doxorubicin (DOX), a wide-spectrum chemotherapeutic agent, is recognized to have cardiotoxic side effects when it is applied in hematological diseases and solid tumor management. However, the mechanisms behind the DOX-induced anomaly of vascular homeostasis remain mostly elusive. qRT-PCR and immumohistochemical staining indicated cardiac increase of miR-526b-3p, and decrease of CD31 and CD34 in DOX-treated mice. The regulatory function of miR-526b-3p on cardiac function and cardiac microvessel density was detected via the transfection of miR-526b-3p mimics or inhibitor into Human Umbilical Vein Endothelial Cells (HUVECs) and the administration of rAAV in mice. HUVECs proliferation, apoptosis, tube formation, and migration were inspected by EdU, flow cytometry, tube formation and transwell assays. MiR-526b-3p was anti-proliferative but apoptosis-initiating in HUVECs, and aggravated cardiac abnormalities caused by DOX. Mechanically, the relationship between miR-526b-3p and VEGFA was disclosed by qRT-PCR. VEGFA and STAT3 interaction was confirmed by ChIP and luciferase reporter assay. MiR-526b-3p targeted STAT3 to reduce VEGFA transcription. We designed rescue assays and presented that the negative effects of miR-526b-3p on cardiac dysfunction and HUVECs were rescued by VEGFA reintroduction in DOX-affected mice. Overall, miR-526b-3p accelerated doxorubicin-induced cardiotoxicity through modulating STAT3/VEGFA, highlighting that targeting miR-526b-3p as a potential method to protect against DOX-induced cardiac dysfunction.

Background: lncUCA1 is abundantly expressed in the heart, indicating it may be important in maintaining normal myocardial function. However, the underlying mechanism of lncUCA1 in heart disease, particularly myocardial infarction (MI), is still in its infancy. Methods: LncUCA1 and miR-143 expression were measured in hearts of MI models. Overexpression and knockdown of lncUCA1 in neonatal rat cardiomyocytes were performed to confirm the effects of lncUCA1 in hypoxia-induced apoptosis. Results: The expression of lncUCA1 decreased but miR-143 increased inversely in MI heart. Overexpressing lncUCA1 protected cardiomyocytes from H/R induced apoptosis via inhibiting miR-143, which regulates apoptosis by targeting MDM2/p53 pathway. While silencing lncUCA1 caused miR-143 upregulation and H/R-induced apoptosis increase. Moreover, miR-143 was proved to be a competitive target of lncUCA1. Conclusions: lncUCA1 might protect cardiomyocyte against H/R induced apoptosis by suppressing miR-143 and modulated the following downstream MDM2/p53 signaling pathway, indicating the therapeutic potential of targeting lncUCA1 for MI.

OBJECTIVE To evaluate the presence of cardiovascular involvement and analyze potential risk factors independently associated with cardiovascular involvement in primary Sjögren's syndrome (PSS) patients. METHODS We recruited a cohort of 367 PSS patients and 367 age- and gender-matched controls from the First Affiliated Hospital of Wenzhou Medical University. Demographic, clinical and laboratory data, and overt cardiovascular involvement events were recorded. Potential risk factors associated with cardiovascular involvement were determined by multivariate analyses. RESULTS PSS patients had a significantly higher cardiovascular involvement rate than that of the controls (61.6% versus 29.7%; p<0.01). Compared with PSS patients without cardiovascular involvement, those with cardiovascular involvement were significantly older; had higher rates of hypertension, diabetes, hypoalbuminemia, and hyperlipemia; were more likely to have extraglandular organ involvement; and had a higher level of C-reactive protein (CRP) (all p<0.05). In the multivariate analysis, age, hypertension, and extraglandular organ involvement were found to be risk factors independently correlated with cardiovascular events in PSS patients. CONCLUSIONS PSS patients are more vulnerable to cardiovascular diseases (CVDs). In addition to traditional CVD risk factors such as age and hypertension, extraglandular organ involvement was found to be independently associated with cardiovascular involvement in PSS patients, which suggests the need for early detection and prevention measures to improve the prognosis in those patients.

To investigate the early diagnostic and prognostic value of microRNA-1 in patients with acute chest pain.