Objective To investigate the serum levels of miR-141 and miR-181a in neonatal sepsis and their impact on the severity of the condition. Methods Fifty children with sepsis diagnosed and treated in the Neonatal Department of Hainan Modern Women’s and Children’s Hospital from June 2021 to August 2022 were selected as the research subjects. According to the sequential organ failure score（SOFA） of the children, they were divided into a mild group of 27 cases and a severe group of 23 cases. The levels of serum miR-141, miR-181a, C-reactive protein（CRP）, Calcitonin（PCT） and acute physiology and chronic health score（APACHE-Ⅱ） were compared between the two groups. Pearson’s method was used to analyze the correlation between serum miR-141, miR-181a and APACHE-Ⅱ, CRP, PCT. Multifactor logistic regression was used to analyze the factors affecting the severity of sepsis in children; ROC curve was used to analyze the value of miR-181a in predicting disease severity. Results The serum levels of miR-141 and miR-181a in the severe group were lower than those in the mild group, while CRP, PCT levels, and APACHE-Ⅱ scores were higher than those in the mild group（t=8.977, 5.972, 9.605, 7.981, 7.054, all P＜0.001）; Serum miR-141 and miR-181a were negatively correlated with APACHE-Ⅱ, CRP, and PCT（miR-141:r=-0.570,-0.741,-0.582, miR-181a:-0.569,-0.513,-0.576,P＜0.001）. High serum miR-141 and miR-181a levels are protective factors for exacerbation of sepsis in children [OR（95%CI）=0.33（0.18-0.52）, 0.27（0.14-0.46）], while high APACHE II scores, CRP levels, and PCT levels are risk factors for exacerbation[OR（95%CI）=1.56（1.14-1.83）, 2.18（1.52-2.71）, 1.67（1.27-1.93）].The AUC of serum miR-141, miR-181a, and their combination in predicting the severity of neonatal sepsis were 0.936, 0.856, and 0.959, respectively. The combination of the two was superior to their respective independent predictive efficacy（Z=5.318, 9.652,P＜0.001）. Conclusion The low expression of serum miR-141 and miR-181a in neonatal sepsis is negatively correlated with APACHE-Ⅱ score, CRP, and PCT. The elevated levels of miR-141 and miR-181a are protective factors for the worsening of sepsis in children, and have good predictive value for the changes in neonatal sepsis.

目的 探讨血清微小RNA-16-5p(miR-16-5p)和微小RNA-96-5p(miR-96-5p)水平与新生儿脓毒血症(NS)疾病严重程度和机体炎性反应的相关性.方法 选择 2020 年 3 月—2022 年 3 月海南现代妇女儿童医院收治的 52 例 NS 患儿作为脓毒血症组,同时选择同期住院的 52 例非脓毒血症患儿作为对照组.定量检测两组血清miR-16-5p、miR-96-5p、降钙素原(PCT)、C反应蛋白(CRP)和白介素 6(IL-6)含量,收集两组基线资料与入院 24h内临床检查结果.采用双变量Pearson相关性检验分析血清miR-16-5p、miR-96-5p水平与疾病严重程度和炎性反应指标的相关性.结果 脓毒血症组格拉斯哥昏迷评分(GCS)、急性生理学和慢性健康状况评分Ⅱ(APACHEⅡ)、序贯器官衰竭估计评分(SOFA)、白细胞计数(WBC)、血肌酐、PCT、CRP和IL-6 水平显著高于对照组,而血清白蛋白水平显著低于对照组(均P<0.05).脓毒血症组血清miR-16-5p表达水平显著高于对照组,而miR-96-5p表达水平显著低于对照组(均P<0.05).miR-16-5p 高表达者的 GCS 评分、APACHE Ⅱ评分、SOFA 评分、WBC、PCT、CRP 和 IL-6 水平均显著高于miR-16-5p低表达者(均P<0.05).miR-96-5p高表达者的APACHEⅡ评分、SOFA评分、WBC、PCT、CRP和IL-6 水平均显著低于miR-96-5p低表达者(均P<0.05).脓毒血症组血清miR-16-5p水平与GCS评分、APACHEⅡ评分、SOFA评分、WBC、PCT、CRP和IL-6 水平呈正相关(均P<0.05),而血清miR-96-5p水平与APACHE Ⅱ评分、SOFA评分、WBC、PCT、CRP和IL-6 水平呈负相关(均P<0.05).结论 NS患儿血清miR-16-5p水平升高,miR-96-5p水平降低,与疾病严重程度和机体炎性反应相关,提示miR-16-5p和miR-96-5p可作为NS早期诊断和病情评估的标志物.

BACKGROUD:Neonatal pericardial effusion (PCE) is one of the most severe complications of central catheters in neonates with its rapid progression and high mortality. We aim to estimate the overall incidence and mortality of catheter-related neonatal PCE, more importantly, to identify possible predictors for clinical reference. METHODS:We searched MEDLINE, Embase, Cochrane Library, Web of Science, china national knowledge infrastructure, Wanfang Data, and Sinomed databases for subject words "central catheter," "neonate," "pericardial effusion" and their random words till June 8, 2020. This meta-analysis is based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Possible predictors of occurrences and deaths were extracted and assessed cooperatively. The pooled incidence rate of catheter-related neonatal PCE was calculated using a random effects model. RESULTS:Twenty-one cohort studies and 99 cases were eligible. Pooled incidence is 3·8‰[2.2‰, 6.7‰]. Polyurethane catheters generate significantly more neonatal PCE than silicone counterparts (P < .01). 27% of the patients die. The mortality of patients with bradycardia is higher than others (P < .05). Catheters with a guidewire result in more deaths than umbilical venous catheter (UVC) and peripherally inserted central catheters (PICC) (P < .05). Without pericardiocentesis, mortality increases (P < .01). The difference of deaths between reposition and removing the catheter is insignificant (P > .05). CONCLUSION:Central catheters in Seldinger Technique (with a guidewire) put neonates at greater risk of PCE and consequent death. Silicone catheters excel at avoiding deadly catheter-related PCE, which could be a better choice in neonatal intensive care units (NICU). When catheter-related PCE occurs, timely diagnosis and pericardiocentesis save lives.

目的:探讨lncRNA LINC01419对小儿类风湿关节炎滑膜成纤维细胞增殖、迁移和侵袭的影响及分子机制.方法:取2017年1月至2019年12月本院21例小儿类风湿关节炎患者的滑膜组织及21例因骨折式创伤截肢者的膝关节正常滑膜组织;分离培养小儿类风湿关节炎滑膜成纤维细胞(RASFs),将其分为si-NC组、si-LINC01419组、pcDNA组、pcDNA-LINC01419组、miR-NC组、miR-320a组、si-LINC01419+anti-miR-NC组、si-LINC01419+anti-miR-320a组.实时荧光定量PCR(RT-qPCR)检测LINC01419和miR-320a的表达水平;四甲基偶氮唑盐比色法(MTT)检测细胞活性;Transwell检测细胞迁移和侵袭;Western blot法检测细胞周期蛋白D1(CyclinD1)、细胞周期蛋白依赖性激酶抑制剂1A(p21)、基质金属蛋白酶2(MMP-2)、基质金属蛋白酶9(MMP-9)蛋白表达;荧光素酶报告实验检测LINC01419和miR-320a的靶向关系.结果:与正常滑膜组织相比,小儿类风湿关节炎患者滑膜组织中LINC01419表达水平升高,miR-320a表达水平降低(P<0.05).抑制LINC01419表达或过表达miR-320a,细胞活性降低,迁移和侵袭细胞数降低,CyclinD1、MMP-2、MMP-9表达水平降低,p21表达水平升高(P<0.05).LINC01419靶向调控miR-320a的表达,干扰miR-320a表达逆转了抑制LINC01419表达对小儿类风湿关节炎滑膜成纤维细胞增殖、迁移和侵袭的抑制作用.结论:抑制LINC01419表达可能通过靶向上调miR-320a抑制小儿类风湿关节炎滑膜成纤维细胞增殖、迁移和侵袭.

目的 探究个性化预测新生儿坏死性小肠结肠炎(NEC)发病风险的列线图模型构建,为新生儿NEC的防治提供科学依据.方法 回顾性分析2017年10月 2019年12月海南现代妇女儿童医院与外院联合收集的1173例新生儿临床资料,根据是否发生NEC分为NEC组(n=46)与非NEC组(n=1127),采用Logistic回归模型分析影响NEC发生的独立危险因素,基于筛选出的独立危险因素利用R软件构建NEC发生风险的列线图模型,应用ROC曲线下面积检验模型预测效果并进行拟合优度验证.结果 新生儿NEC发生率为3.92％(46/1173);多因素Logistic回归分析显示,胎龄＜32周(OR=3.186)、出生体重＜1.5 kg(OR=2.520)、合并感染性休克(OR=2.517)、合并败血症(OR=2.566)、合并妊娠期糖尿病(OR=1.973)、人工喂养(OR=2.267)为影响新生儿NEC发生的独立危险因素(P＜0.05),产前使用地塞米松为保护性因素(OR=0.475,P＜0.05);该预测模型ROC曲线下面积为0.741;Hosmer-Lemeshow拟合优度检验x2=7.859,P=0.447;绘制列线图的校准曲线为斜率接近1的直线.结论 个性化预测新生儿NEC发病风险的列线图模型具有良好的区分度与准确度,可有效评估新生儿NEC的发生概率,能够为新生儿NEC的防治提供一定指导价值.

目的 探讨呼吸道合胞病毒(RSV)下呼吸道感染肺炎病儿外周血血浆中微小RNA-145(mir-145)表达与外周血单个核细胞(PBMC)中T淋巴细胞亚群的关系.方法 选取2017年1月至2018年12月海南现代妇女儿童医院收治的RSV下呼吸道感染肺炎病儿126例作为RSV肺炎组,同期在本院进行体检的健康儿童130例作为健康对照组.RSV肺炎组根据病情严重程度分为轻度组(n=54)、重度组(n=72),并依据重度组是否给予机械通气分为非机械通气组(n=38)、机械通气组(n=34).利用实时荧光定量PCR(qRT-PCR)检测外周血血浆中mir-145表达水平,使用流式细胞仪及配套试剂盒检测PBMC中T淋巴细胞亚群CD3+、CD4+、CD8+水平,并用MRFlow流式细胞分析软件自动行CD3+、CD4+、CD8+绝对计数,同时计算CD4+/CD8+值.结果 RSV肺炎组病儿血浆mir-145表达[(1.74±0.48)比(0.99±0.26)]及PBMC中CD8+水平[(30.75±8.39)％比(21.64±5.92)％]均显著高于健康对照组(P<0.05),PBMC中CD3+[(59.04±16.12)％比(68.77±18.35)％]、CD4+水平[(31.27±8.01)％比(46.90±12.84)％]及CD4+/CD8+值[(1.02±0.28)比(2.17±0.63)]均明显低于健康对照组(P<0.05).重度组病儿血浆mir-145表达[(1.87±0.55)比(1.52±0.40)]及PBMC中CD8+水平[(33.96±9.10)％比(25.34±7.02)％]均明显高于轻度组病儿(P<0.05),PBMC中CD3+[(57.05±15.83)％比(63.28±17.21)％]、CD4+水平[(23.78±6.62)％比(38.09±10.14)％]及CD4+/CD8+值[(0.70±0.21)比(1.50±0.39)]均显著低于轻度组病儿(P<0.05).重度RSV肺炎机械通气组病儿血浆mir-145表达[(1.95±0.58)比(1.68±0.45)]及PBMC中CD8+水平[(34.92±9.18)％比(28.17±7.49)％]均显著高于非机械通气组病儿(P<0.05),PBMC中CD3+[(54.72±13.53)％比(61.83±16.04)％]、CD4+水平[(20.45±5.79)％比(34.03±8.85)％]及CD4+/CD8+值[(0.59±0.17)比(1.21±0.36)]均明显低于非机械通气组病儿(P<0.05).RSV肺炎病儿血浆mir-145表达与PBMC中CD3+水平呈负相关(P<0.05),与PBMC中CD4+水平呈负相关(P<0.05),与PBMC中CD8+水平呈正相关(P<0.05),与CD4+/CD8+值呈负相关(P<0.05).结论RSV下呼吸道感染肺炎病儿外周血血浆中mir-145表达水平升高,其高表达可能与T淋巴细胞亚群异常有关.

目的 观察芍药苷对缺氧缺血性脑损伤(HIBD)新生大鼠认知功能的影响.方法 用颈外动脉插入线栓法建立HIBD新生大鼠模型,将HIBD新生大鼠随机分为模型组(n=25)及实验组(n=25);假手术组(n=25)仅分离左侧颈总动脉、颈外动脉,但不结扎.实验组腹腔注射20 mg·kg-1芍药苷,假手术组与模型组腹腔注射等量生理盐水,每日1次,连续腹腔注射21 d.用Morris水迷宫测定新生大鼠的空间学习记忆能力;用蛋白免疫印迹法检测新生大鼠脑组织沉默信号调节因子1(SIRT1)、磷酸化NF-κB(p-NF-κB)蛋白的表达水平.结果 假手术组、模型组及实验组新生大鼠第5 d的逃避潜伏期分别为(7.12±1.59),(20.38±5.81),(11.23±2.36)s;穿台次数分别为(6.45±1.67),(1.69±0.58),(4.16±0.93)次;脑组织SIRT1蛋白相对表达量分别为0.94±0.06,0.16±0.05,0.57±0.11;p-NF-κB蛋白相对表达量分别为0.19±0.07,0.86±0.12,0.69±0.13.上述指标,模型组分别与假手术组和实验组比较,差异均有统计学意义(均P<0.05).结论 芍药苷可改善认知功能障碍,其作用机制可能与激活SIRT1/NF-κB信号通路的转导相关.