目的 评价急性心肌梗塞患者转往有条件医院行PCI治疗前应用替罗非班(血小板Ⅱb/Ⅲa受体拮抗剂)的临床疗效与安全性。方法 选取从2013年1月—2014年9月诊断为急性心肌梗塞行PCI治疗的患者共66例。随机分为观察组(确定转院行PCI治疗前在我院应用替罗非班) 34例、对照组(转运到花都区人民医院心内科行PCI治疗后应用替罗非班) 32例。观察比较两组患者首次造影的冠脉血流情况与术后的冠脉血流情况、PCI时心电图抬高的ST回落情况与心肌标志物峰值前移情况、住院期间与随访30天期间不良心血管事件(MAGC)的发生情况(支架内血栓与二次血运重建发生率、再梗塞率、心绞痛、死亡率)以及两组的不良反应。结果 观察组首次造影的冠脉血流优于对照组;术后的冠脉血流观察组优于对照组(P<0.05);PCI时心电图ST回落≥1/2的情况与TNI、CK-MB峰值前移情况优于对照组(P<0.05);不良心血管事件发生率较对照组少(P<0.05);不良反应发生率差异无统计学意义(P>0.05)。结论 急性心梗转院PCI患者,转院前应用替罗非班比转院后应用获益更大,安全性尚可。这类病人,在确定转院之时即时应用替罗非班是合理时机。

目的 探讨血糖控制情况对胰岛素抵抗型糖尿病合并肺结核的临床治疗转归的影响。方法 选取我站收治的胰岛素抵抗型糖尿病合并肺结核的患者180例,随机分成对照组和观察组两组,每组各90例,对照组给予常规监测晨起空腹血糖和餐后2 h血糖,观察组给予监测血糖谱(包括三餐前、三餐后2 h、凌晨3点和晨起空腹血糖);观察组与对照组中患者均利用2HRSZ(E)／10HR(E)方案来进行治疗;记录两组患者治疗前后空腹血糖、餐后2 h血糖、痰菌阴转情况、X线胸片病灶情况和空洞变化情况,对比分析两组的临床治疗效果。结果 观察组的痰菌阴转、X线胸片病灶、空洞变化等均比对照组的效果好,且两组差异有统计学意义(P＜0.05);观察组的总体有效率87.8%(79/90)高于对照组的71.1%(64/90),两组差异有统计学意义(χ²=7.655,P=0.006)。结论 控制血糖能有效提高胰岛素抵抗型糖尿病合并肺结核的临床治疗效果,在临床上值得推广应用。

目的 通过测试获取脑瘫外翻足患儿的足底压力参数特征,为设定步态康复训练方案提供参考。方法 根据纳入和排除标准,选择脑瘫患儿和健康儿童各15人,通过足底压力测试仪测得足底各部位压力分布、区域压力峰值及步态时相百分比,将两组结果进行统计学比较。结果 比较发现在足底接触面积、足底压力值,以及步态时相所占时间长短三方面均有指标存在差异,均有统计学意义(P<0.05)。结论 足底压力测试技术可使临床步态分析更加量化、精确化,为设定更有针对性的康复训练提供依据。

Objective Through the assessment to get the plantar pressure features of cerebral palsy children with talipes valgus, in order to design suitable treatment plan. Methods According to the inclusion criteria and exclusion criteria, we chose 15 cerebral palsy children with talipes valgus in experimental group, and 15 healthy children in control group. Through the test to get the plantar contact area, pressure parameters and the percent of gait phase. the two groups were compared with statistics method. Results There were significant differences between two groups on the plantar contact area, pressure parameters and the percent of gait phase. Conclusion Plantar pressure measurement makes clinic gait analysis more quantized and accurate, it will provide the evidence to plan the suitable treatment plan.

KOA是临床上最常见,发病起源于关节软骨的慢性退行性关节疾病。近年来,应用黄芪治疗KOA的报道不断增多,并且开展了大量的机制研究。本文综述了黄芪在KOA治疗中的应用现状及研究进展,同时指出从PPAR-γ信号通路探索黄芪干预KOA的具体分子机制具有积极的理论和实践意义。

神经元特异性烯醇化酶(neuron-specific enolase, NSE)是糖酵解途径中一种重要的同工酶;特异性位于神经元和神经内分泌细胞中。小细胞肺癌(small cell lung cancer,SCLC)细胞浆内含有神经内分泌颗粒,具有神经内分泌分化的特征,为恶性程度高的神经内分泌系统肿瘤。因此,NSE是SCLC诊断中最敏感的肿瘤标志物,在SCLC的临床诊断、治疗、预后均有重要应用价值,科学合理联合检测肿瘤标记物,将能为临床诊疗工作提供有力的帮助。

目的 探讨光棒引导与传统喉镜气管插管在不稳定型颈椎骨折患者中的应用效果。方法 不稳定型颈椎骨折患者80例,按照随机数字表法随机分成光棒引导组和传统喉镜组各40例,记录两组患者的插管时间、插管总成功率,入室安静后(T0)、诱导后插管前(T1)、气管插管后即刻(T2)、气管插管后3 min(T3)时的收缩压(SBP)、舒张压(DBP)、心率(HR)、血浆去甲肾上腺素(NE)、肾上腺素(E) 和血管紧张素Ⅱ(ATⅡ)的变化和插管时气道并发症。结果 两组间插管时间(光棒组29.63±11.04s vs.喉镜组62.41±19.49 s)有统计学意义(P<0.001)。两组插管总成功率无统计学意义(P=0.305)。光棒组T2、T3时刻SBP、DBP、HR 、NE、E和ATⅡ均低于喉镜组(P<0.001)。光棒组气道并发症低于喉镜组无统计学意义(P>0.05)。结论 光棒引导气管插管较传统喉镜气管内插管插管时间短,对血流动力学和应激激素水平影响较轻。

目的 通过建立大鼠泛耐药铜绿假单胞菌肺炎模型,对其进行联合用药,观察疗效,以便为治疗泛耐株引起的感染提供理论基础。方法 选择体外药敏实验中各药物组合同时有效的一株铜绿假单胞菌建立小鼠肺炎模型,于感染后6小时给药,对照组腹腔注射0.5 mL生理盐水,治疗组分别用头孢他啶+阿米卡星+环丙沙星以及头孢他啶+阿米卡星+环丙沙星+氨氯地平两组用药方案连续治疗三天后,根据肺组织匀浆细菌计数及病理结果评价疗效。结果 体内药敏试验显示用药组不管有无氨氯地平干预,对细菌的清除作用与对照组比较差异有统计学意义(P﹤0.05),而两用药组之间比较,差异无统计学意义。结论 对泛耐药铜绿假单胞菌感染后肺炎模型,联合应用体外单药药敏试验耐药的抗菌药后对细菌仍有一定的清除作用,但加入氨氯地平干预未显示有明显的治疗效应。

目的 构建抑癌基因SEMA3B真核表达载体pcDNA3.1-SEMA3B,并检测其对肺癌A549细胞恶性生物学行为的影响。方法 应用PCR扩增SEMA3B全长cDNA片段,构建真核表达载体pcDNA3.1-SEMA3B。克隆PCR、双酶切法、基因测序验证过表达载体构建成功。将pcDNA3.1-SEMA3B真核表达载体和空载体pcDNA3.1分别转染入A549细胞中,应用qRT-PCR、Western blot检测SEMA3B mRNA、蛋白表达水平的变化;MTS法检测细胞增殖;流式细胞仪检测细胞凋亡、细胞周期;克隆形成实验检测细胞集落形成能力。结果 SEMA3B基因扩增片段与预测片段一致,克隆成功,且测序鉴定证实真核表达载体构建成功。转染pcDNA3.1-SEMA3B真核表达载体可上调SEMA3B mRNA、蛋白表达水平,且可抑制A549细胞的增殖,诱导凋细胞亡,细胞被阻滞在G1期,抑制细胞集落形成能力。结论 成功构建了SEMA3B基因真核表达载体,抑癌基因SEMA3B在肺癌恶性生物学进程中可能发挥重要作用。

Objective To construct the eukaryotic expression vector of the cancer suppressor gene, SEMA3B, and research the effects on malignant biological behavior of lung cancer A549 cells. Methods By reverse transcriptase-polymerase chain reaction (RT-PCR), the full length SEMA3B gene was amplified and then was inserted into pcDNA3.1. The recombinant plasmid pcDNA3.1-SEMA3B was confirmed correctly through double enzyme digestion and PCR identification, which was transfected into lung cancer A549 cells by lipid media transfection. The untransfected A549 and A549 transfected with pcDNA3.1 were used as controls. SMEA3B gene was detected by qRT-PCR and western blot. MTS assay, flow cytometry, and colony formation test were performed to evaluate the effect of overexpression of SEMA3B gene on A549 cell proliferation, apoptosis, cell cycle, and colony forming ability. Results The amplied fragment of SEMA3B gene by PCR was consistent with the anticipated result, the SEMA3B gene was cloned successfully. And the recombinant plasmid pcDNA3.1-SMEA3B was constructed successfully through gene sequence identification. After transfection of pcDNA3.1-SEMA3B, SEMA3B mRNA and protein expression levels were raised, and overexpression of SEMA3B gene in A549 cells significantly inhibited the proliferation of A549 cells, induced apoptotic cell death, blocked cell cycle in the G1 phase, and suppressed cell colony-forming ability. Conclusion The recombinant pcDNA3.1-SEMA3B is constructed successfully. SEMA3B gene can significantly inhibit the malignant biological behavior of lung cancer A549 cells.

目的 利用可视化软件CiteSpace分析近20年儿童注意缺陷多动障碍（ADHD）及其共患病的相关文献,得出该领域的研究现状和发展趋势,为儿童注意缺陷多动障碍及其共患病的研究和诊疗提供参考。方法 检索2004—2024年发表在中国知网、维普、万方数据库关于儿童注意缺陷多动障碍及其共患病的相关文献,运用CiteSpace软件对纳入文献进行可视化分析,对来源、机构、发文量、作者、关键词绘制科学知识图谱。结果 共纳入383个机构、500个作者、235种期刊、577篇有效文献。自2012年发文量总体上呈波动上升趋势;在发文来源中,《中国儿童保健杂志》以47篇居首;研究机构以北京大学精神卫生研究所为代表;王玉凤作者发文21篇为最多;ADHD患儿的主要共患病为抽动障碍、癫痫、对立违抗障碍、学习障碍;主要治疗药物为托莫西汀;主要影响患儿的执行功能。ADHD患儿共患病研究分为3个阶段,第一阶段为2004—2009年,研究对象主要为品行障碍、对立违抗障碍、学习障碍、焦虑障碍,主要研究内容为患儿的脑损伤与基因;第二阶段为2009—2017年,重视研究患儿的心理问题,如焦虑、抑郁,也重视患儿的生活及家庭环境;第三阶段为2017—2024年,重点研究托莫西汀、阿立哌唑等药物,并重视ADHD共患癫痫的研究。结论 目前对ADHD共患病的研究仍较为局限,主要集中研究共患抽动障碍、对立违抗障碍、癫痫,未来应重视研究其他共患病,进一步探索更好的诊治方法。

Objective To analyze the literature on attention deficit hyperactivity disorder（ADHD）and its comorbidities in children in the past 20 years by using the visualization software CiteSpace, and to obtain the research status and development trend of this field, so as to provide reference for the research, diagnosis and treatment of ADHD and its comorbidities in children. Methods The relevant literature on ADHD and its comorbidities in children published in CNKI, VIP and Wanfang data bases from 2004 to 2024 was searched, and the included literature was visually analyzed by CiteSpace 6. 2R6 software, and the scientific knowledge graph was drawn by the source, institution, number of publications, authors and keywords. Results A total of 383 institutions, 500 authors, 235 journals, and 577 valid articles were included. Since 2012, the number of published documents has fluctuated and increased. Among the sources of publication, the Chinese Journal of Child Health ranked first with 47 articles. The research institutions were represented by the Institute of Mental Health of Peking University. Wang Yufeng was the most prolific author with 21 articles. The main comorbidities of ADHD children were tic disorder, epilepsy, oppositional defiant disorder and learning disorder. The main treatment drug was tomoxetine. It mainly affects the executive function of the children. The study on comorbidity in children with ADHD was divided into three stages. The first stage was from 2004 to 2009. The research objects mainly included conduct disorder, oppositional defiant disorder, learning disorder and anxiety disorder, and the main research content was brain injury and genes in children. The second stage, from 2009 to 2017, focused on the psychological problems of children, such as anxiety and depression, and also paid attention to the life and family environment of children. The third stage was 2017-2024, focusing on tomoxetine, aripiprazole and other drugs, and paying attention to the study of ADHD co-induced epilepsy. Conclusions The current research on ADHD and its comorbidities is still limited, and its pathogenesis should be explored in the future, so as to quickly and accurately identify comorbidities and further study better treatments.

目的 探讨抗增殖蛋白2（PHB2）脓毒症心肌损伤线粒体功能的调控机制。方法 体外培养大鼠心肌细胞株（H9C2）,分为对照组、脂多糖（LPS）组、LPS+PHB2 siRNA（si-PHB2）组。检测氧化应激指标细胞内丙二醛（MDA）水平、荧光探针检测细胞内活性氧（ROS）水平;线粒体指标：三磷酸腺苷（ATP）水平、线粒体膜电位、线粒体电镜、线粒体半定量评分;免疫印迹法检测PHB2、PTEN诱导激酶1（PTNKI）、帕金蛋白（Parkin）、线粒体转录因子（TFAM）的表达。结果 LPS刺激后MDA水平和ROS水平升高、ATP水平低,LPS+si-PHB2组MDA（6.21±0.39 vs 3.59±0.33, P<0.05）、细胞内的ROS（15 131.37±88.72 vs 8 628.67±71.95, P<0.05）的水平较LPS组升高,ATP（3.46±0.34 vs 4.52±0.25, P<0.05）和线粒体膜电位水平（0.33±0.04 vs 0.55±0.09, P<0.05）进一步降低;电镜观察显示与正常组相比,LPS组、LPS+si-PHB2组出现不同程度线粒体损伤,线粒体损伤半定量评分显示LPS+si-PHB2组的损伤较LPS组更为明显（1.42±0.10 vs 0.81±0.04, P<0.05）; 免疫印迹法结果显示LPS处理后PHB2、PINK1、Parkin 表达上调,TFAM表达下调,LPS+si-PHB2组的线粒体自噬相关蛋白PINK1（1.33±0.06 vs 1.79±0.21, P<0.05）、Parkin（1.43±0.08 vs 1.86±0.09, P<0.05）和线粒体生物发生关键蛋白TFAM（0.29±0.01 vs 0.74±0.06, P<0.05）表达均较LPS组降低。结论 LPS可促进大鼠心肌细胞PHB2表达,si-PHB2干扰后线粒体自噬蛋白和生物发生蛋白表达抑制,心肌细胞氧化应激损害和线粒体功能障碍加重,提示PHB2表达上调可能恢复线粒体稳态改善脓毒症心肌损伤的线粒体功能。

Objective To explore the regulatory mechanism of septic myocardial injury by prohibitin 2（PHB2）. Methods Rat myocardial cell lines（H9C2）were cultured in vitro and divided into control group,LPS group,LPS + PHB2 siRNA（si-PHB2） group. The indicators for detecting oxidative stress include the levels of intracellular malondialdehyde（MDA）and reactive oxygen species（ROS）. The indicators for mitochondrial detection include adenosine triphosphate（ATP）levels,mitochondrial membrane potential,mitochondrial electron microscopy,and semi-quantitative mitochondrial scoring. Western blotting was used to detect the expression of PHB2,PTEN induced putative kinase（PINK1）,Parkin,mitochondrial transcription factor A（TFAM）. Results After LPS stimulation,MDA level and intracellular ROS level increased,ATP level decreased. Compared with LPS group,MDA（6. 21±0. 39 vs 3. 59±0. 33, P<0. 05）level and intracellular ROS level（15 131. 37±88. 72 vs 8 628. 67±71. 95, P<0. 05）in LPS + si-PHB2 group increased significantly,while ATP（3. 46±0. 34 vs 4. 52±0. 25, P<0. 05）and MMP（0. 33±0. 04 vs 0. 55±0. 09, P<0. 05）level further decreased. Compared with the normal group,the structure of mitochondria in LPS group and LPS + si-PHB2 group was damaged in different degree. The semi-quantitative score of mitochondrial damage showed that the damage in LPS + si-PHB2 group was more obvious than that in LPS group（1. 42±0. 10 vs 0. 81±0. 04, P<0. 05）. Western blotting showed that the expression of PHB2,PINK1 and Parkin were up-regulated and the expression of TFAM was down-regulated after LPS treatment,mitohagy-related proteins PINK1（1. 33±0. 06 vs 1. 79±0. 21, P<0. 05）,Parkin（1. 43±0. 08 vs 1. 86±0. 09, P<0. 05）and mitochondrial biogenetic protein TFAM（0. 29±0. 01 vs 0. 74±0. 06, P<0. 05）in LPS+si-PHB2 group were lower than those in LPS group. Conclusions LPS can promote the expression of PHB2 in rat cardiomyocytes. After interfering with PHB2 expression,we found that mitochondrial autophagy and biogenesis are inhibited,and mitochondrial dysfunction,oxidative stress exacerbated,suggesting that the up-regulation of PHB2 expression may restore mitochondrial homeostasis and improve mitochondrial function in septic myocardial injury.