血管性认知功能障碍病人血清微RNA-335-5p、血清应答因子水平及其临床意义

目的 探究血管性认知功能障碍（VCI）病人血清微RNA(miR)-335-5p、血清应答因子（SRF）水平及临床意义。方法以石家庄市人民医院2019年1月至2020年12月因脑卒中治疗后6个月出现VCI的110例病人为研究对象（VCI组）,其中非痴呆型血管性认知功能障碍（VCIND）者48例（VCIND组）、血管性痴呆（VD）者62例（VD组）。同时间段该院脑卒中未合并认知障碍者110例为对照组。分析各组病人发病时（入院次日）、发病后6个月、发病后1年血清miR-335-5p、SRF水平。logistic回归模型分析脑卒中病人发生VCI的影响因素。Pearson法分析血清miR-335-5p与SRF水平的相关性。受试者操作特征曲线（ROC曲线）分析血清miR-335-5p、SRF水平对VCI的预测价值。结果 VCI组发病时miR-335-5p水平0.76±0.15低于对照组1.06±0.07,而SRF水平1.52±0.24高于对照组1.01±0.09,差异有统计学意义（P<0.05）。发病时,对照组、VCIND组、VD组的miR-335-5p水平逐次降低（1.06±0.07比0....     

冠心病病人外周血微RNA-133b表达与预后的关系分析

目的 探究冠心病病人外周血微RNA-133b(miR-133b)表达水平,并分析其表达与病人预后的关系。方法 选取2019年7月至2021年1月于华北石油管理局总医院就诊的冠心病病人95例,其中稳定性冠心病（SACD）病人54例为SACD组,急性冠状动脉综合征（ACS）41例为ACS组,另选同期该院进行体检的健康人群60例作为对照组。采用实时荧光定量PCR法检测血清miR-133b水平;随访6个月,根据是否出现主要心脏不良事件,分为预后不良组（出现主要心脏不良事件,33例）和预后良好组（未出现主要心脏不良事件,62例）。采用Spearman相关性分析检验血清miR-133b水平与Gensini评分的关系;采用多因素logistic回归分析影响冠心病病人预后的危险因素;采用受试者操作特征曲线（ROC曲线）分析血清miR-133b水平对冠心病病人预后不良的预测价值。结果 SACD组、ACS组身体质量指数、高血压、吸烟史及血脂异常者比例高于对照组（P<0.05）,ACS组Gensini评分、病变支数≥3支占比高于SACD组（P<0.05）。ACS组、SACD组血清miR-133b...     

miR-27a-3p靶向调节突触膜胞吐2调控宫颈癌细胞增殖凋亡的机制研究

目的 观察微小RNA-27a-3p(miR-27a-3p)、调节突触膜胞吐2(RIMS2)对宫颈癌细胞增殖、凋亡的影响,并探究其作用机制.方法 选取2014年1月至2016年6月绵阳市中心医院收治的145例行手术切除的宫颈癌患者的癌组织及癌旁组织作为研究对象.运用实时荧光定量聚合酶链反应(RT-qPCR)法检测宫颈癌组...     

胃泌素释放肽前体片段31-98检测对小细胞肺癌的临床意义

目的 与神经元特异性烯醇化酶（ＮＳＥ）对照,探讨胃泌素释放肽前体片段３１－９８（ＰｒｏＧＲＰ３１－９８）检测对小细胞肺癌（ＳＣＬＣ）的临床意义。方法 采用ＥＬＩＳＡ检测３０例ＳＣＬＣ、３０例非小细胞肺癌、１５例肺良性疾病、１５例正常健康者和１０例治疗后ＳＣＬＣ患者血液ＰｒｏＧＲＰ３１－９８和ＮＳＥ值．采用ＲＯＣ曲线确定阈值,比较诊断准确性。结果 ＳＣＬＣ组血清ＰｒｏＧＲＰ３１－９８值显著高于对照组     

Huangqi Decoction,a compound Chinese herbal medicine,inhibits the proliferation and activation of hepatic stellate cells by regulating the long noncoding RNA-C18orf26-1/microRNA-663a/transforming growth factor-β axis

Objective:Huangqi Decoction (HQD),a classical traditional Chinese medicine formula,has been used as a valid treatment for alleviating liverfibrosis;however,the underlying molecular mechanism is still unknown.Although our previous studies showed that microRNA-663a (miR-663a) suppresses the proliferation and activation of hepatic stellate cells (HSCs) and the transforming growth factor-β/small mothers against decapentaplegic (TGF-β/Smad) pathway,whether long noncoding RNAs (lncRNAs) are involved i...     

血清miRNA-10b和miRNA-34a在子宫内膜异位症患者中的表达及与术后复发关系研究

目的探讨血清微小RNA（miRNA）-10b和miRNA-34a在子宫内膜异位症（EMT）患者中的表达及与术后复发关系。 方法选择就诊于承德医学院附属医院妇科2017年1月~2019年12月子宫内膜异位症患者126例作为观察组；另选择同期健康育龄期女性89例作为对照组。所有EMT患者均随访1年，采用门诊、电话或微信等方式，观察患者术后复发情况。采用实时荧光聚合酶链反应（RT-PCR）法测定血清miRNA-10b和miRNA-34a表达。比较EMT组与对照组血清miRNA-10b和miRNA-34a相对表达量；复发组与未复发组血清miRNA-10b和miRNA-34a相对表达量；采用ROC曲线分析miRNA-10b和miRNA-34a对EMT术后复发预测价值；采用多因素Logistic回归分析EMT术后复发危险因素；采用Pearson分析miRNA-10b和miRNA-34a与术后复发相关性。 结果EMT组血清miRNA-10b和miRNA-34a相对表达量高于对照组（P＜0.05）。随访1年，均完成随访，复发29例，未复发97例。复发组血清miRNA-10b和miRNA-34a相对表达量高于未复发组（P＜0.05）。经ROC曲线分析显示，miRNA-10b预测EMT术后复发中，敏感度为68.75%，特异度为69.23%；miRNA-34a预测EMT术后复发中，敏感度为66.67%，特异度为57.14%。经多因素Logistic回归分析显示，miRNA-10b和miRNA-34a为影响EMT术后复发危险因素。经Pearson分析，miRNA-10b和miRNA-34a与术后复发呈正相关。 结论血清miRNA-10b和miRNA-34a在EMT患者中表达升高，与术后复发呈正相关，且为影响EMT术后复发危险因素，及对EMT术后复发预测敏感度和特异度良好。     

Possible Transmitral Pressure Gradient Elevation in MitraClip XTR

A 74-year-old man presented with dyspnea due to severe mitral regurgitation (MR) caused by rupture of the chordae tendineae. Percutaneous edge-to-edge mitral valve repair was performed using the MitraClip system (Abbott Vascular, Santa Clara, CA). After leaflet grasping via an XTR clip, transesophageal echocardiography (TEE) revealed marked reduction of MR, but elevation of the transmitral gradient was detected no matter how the position of grasping was changed. Finally, we replaced the XTR to the NTR system. After leaflet grasping via an NTR clip, TEE revealed marked reduction of MR from severe to mild and an adequate transmitral gradient.     

Alisol A 24-acetate protects oxygen–glucose deprivation-induced brain microvascular endothelial cells against apoptosis through miR-92a-3p inhibition by targeting the B-cell lymphoma-2 gene

ContextAlisol A 24-acetate has been used to treat vascular diseases. However, the underlying mechanisms still remain unclear.ObjectiveThe present study evaluated the antiapoptotic effect of alisol A 24-acetate on brain microvascular endothelial cells (BMECs) and explored the underlying mechanisms.Materials and methodsBMECs were injured through oxygen -glucose deprivation (OGD) after alisol A 24-acetate treatment. Cell viability and half-maximal inhibitory concentration (IC₅₀) were measured using CCK-8, whereas inflammatory factors and oxidative stress indicators were measured using enzyme linked immunosorbent assay. Cell invasion and wound healing assays were detected. Cell apoptosis was assessed using flow cytometry. B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X (Bax) expression were analyzed using Western blotting. Dual-luciferase assay was applied to detect target genes of miR-92a-3p.ResultAlisol A 24-acetate had an IC₅₀ of 98.53 mg/L and inhibited cell viability at concentrations over 50mg/L. OGD induced apoptosis and promoted miR-92a-3p overexpression in BMECs. However, alisol A 24-acetate treatment suppressed inflammation, improved migration and invasion abilities, increased Bcl-2 expression, inhibited Bax expression, and repressed apoptosis and miR92a-3p overexpression in OGD-induced BMECs. MiR-92a-3p overexpression promoted cell apoptosis and suppressed Bcl-2 expression, whereas its inhibitor reversed the tendency. Alisol A 24-acetate treatment relieved the effects of miR-92a-3p overexpression. Dual-luciferase assay confirmed that miR-92a-3p negatively regulated the Bcl-2 expression.ConclusionsThese findings suggest that alisol A 24-acetate exerts antiapoptotic effects on OGD-induced BMECs through miR-92a-3p inhibition by targeting the Bcl-2 gene, indicating its potential for BMECs protection and as a novel therapeutic agent for the treatment of cerebrovascular disease.     

幽门螺杆菌感染诱导微小RNA?181c对胃癌细胞增殖和侵袭的影响

目的探讨幽门螺杆菌(Hp)感染诱导微小RNA-181c(miR-181c)对胃癌细胞增殖、侵袭和迁移的影响。方法采用实时定量PCR(QPCR)检测Hp感染人正常胃黏膜GES-1细胞和胃癌细胞(BGC-823、SGC-7901、AGS)的miR-181c水平。采用脂质体向SGC-7901细胞转染miR-181c抑制物(Inhibitor组)或阴性对照序列(NC组),另取未转染的细胞为对照组;转染48 h后采用QPCR检测miR-181c水平,活细胞计数(CCK-8)法、划痕实验和Transwell小室实验检测细胞增殖活力、划痕愈合率和穿膜细胞数以评估细胞增殖、迁移和侵袭能力,QPCR和Western blotting检测Bcl-2、基质金属蛋白酶(MMP)-9和神经型钙黏蛋白(N-cad)水平。结果QPCR检测结果显示Hp感染后各细胞的miR-181水平较感染前均升高(P<0.05),GES-1、BGC-823、SGC-7901和AGS细胞Hp感染后的miR-181c水平分别为感染前的4.37、1.63、3.25和2.09倍。与对照组和NC组相比,Inhibitor组SGC-7901细胞的miR-181c水平和转染48、72 h后的增殖活力降低(P<0.05);Inhibitor组SGC-7901细胞的划痕愈合率和穿膜细胞数量分别为(21.679±3.762)%和(128.056±21.463)个,低于对照组的(65.004±2.309)%和(325.07±34.082)个及NC组的(65.675±2.914)%和(328.035±31.391)个,差异有统计学意义(P<0.05);与对照组和NC组相比,Inhibitor组的Bcl-2、MMP-9和N-cad水平均降低(P<0.05)。对照组和NC组上述指标的差异无统计学意义(P>0.05)。结论Hp感染可升高胃癌细胞的miR-181c水平,下调该miR-181c水平对增殖、侵袭和迁移具有明显抑制作用,为Hp感染的胃癌治疗提供了新的靶点。