目的 研究氯吡格雷联合低分子肝素对老年急性心肌梗死(acute myocardial infarction, AMI)患者血清中血脂及炎性因子的影响,为临床AMI的治疗提供参考依据。方法 选取新乡医学院第一附属医院于2016年10月—2019年11月期间收治的老年AMI患者112例,按照随机分配的原则分成两组,即对照组和观察组,每组病例各56例,治疗方式为对照组单给予口服氯吡格雷进行治疗,观察组给予口服氯吡格雷与皮下注射低分子肝素联合治疗,比较治疗前后两组患者血清中甘油三酯(triglyceride,TG)、总胆固醇(total cholesterol,TC)及低密度脂蛋白胆固醇(low-density lipoprotein cholesterol,LDH-C),炎性因子的水平变化及心功能的改变情况。结果 与治疗前相比较,治疗后对照组和观察组患者血清TG、TC及LDH-C水平均降低,炎性因子TNF-α,IL-1β,CRP,IL-6的水平均降低,患者的左心室后壁厚度、左心室舒张末期内径均有降低,射血分数升高;而与对照组治疗后相比较,治疗后观察组患者血清TG、TC及LDH-C水平进一步降低,炎性因子TNF-α,IL-1β,CRP,IL-6的水平进一步降低,患者的左心室后壁厚度、左心室舒张末期内径均降低,而射血分数升高,差异有统计学意义。结论 氯吡格雷联合低分子量肝素可通过降低血清中血脂的水平,抑制AMI过程中的炎症反应,减少炎性因子的释放,提高患者的心功能,改善患者的病情。

Objective To explore the effects of clopidogrel combined with low molecular weight heparin on serum lipids and inflammatory factors in elderly patients with acute myocardial infarction, and provide reference for clinical treatment of AMI. Methods 112 elderly patients with AMI admitted to the First Affiliated Hospital of Xinxiang Medical University from October 2016 to November 2019 were randomly divided into control group and observation group,56 cases in each group.The control group was treated with clopidogrel alone, and the observation group was treated with clopidogrel combined with low molecular weight heparin. The levels of serum TG, TC and LDH-C, inflammatory factors and cardiac function were compared between the two groups before and after treatment. Results Compared with before treatment, the levels of serum TG, TC and LDH-C decreased, and the levels of inflammatory factors TNF-α, IL-1β, CRP and IL-6 decreased in the observation group and the control group after treatment. The left ventricular posterior wall thickness and LVEDD decreased, but LVEF increased in the observation group and control group after treatment. Compared with control group after treatment, the levels of serum TG, TC and LDH-C decreased, and the levels of inflammatory factors TNF-α, IL-1β, CRP and IL-6 decreased, the left ventricular posterior wall thickness and LVEDD decreased, but LVEF increased further in observation group after treatment. Conclusion Clopidogrel combined with low molecular weight heparin may improve the patient's cardiac function, then improve the patient's condition through reducing the level of serum lipids, inhibit the inflammatory reaction in AMI, reduce the release of inflammatory factors.

目的 分析重症流感相关性脑病患儿的临床特点及诊治要点。方法 回顾性分析2017年5月—2020年4月收入我院PICU的17例重症流感相关性脑病患儿的临床资料进行回顾性分析。结果 17例患儿中男性10例、女性7例,起病年龄3(2～5)岁。所有患儿均出现发热,1(0～3.5)天后出现神经系统症状,包括惊厥发作(88%)和昏迷(88%)。头颅影像学检查病变主要分布在丘脑、脑干、髓质脑室周围白质,呈对称性和多灶性改变。经颅多普勒检查出现脑血流速度减慢呈震荡波、钉子波的5例患儿均死亡。16例患儿予机械通气,2例予连续性肾替代治疗,死亡8例,存活者出院前均遗留不同程度神经系统损害。结论 儿童重症流感相关性脑病以发热、惊厥和昏迷为主要表现,头颅影像学及脑电图、经颅多普勒等检查有助于早期诊断和预后判断,早期联合应用甲强龙冲击及IVIG的有效性仍需进一步研究。

Objective To analyze the characteristics, diagnosis and treatment of severe influenza-associated encephalopathy in children. Methods The clinical data of 17 children with severe influenza-associated encephalopathy admitted to PICU from May 2017 to April 2020 were retrospectively analyzed. Results Among the 17 cases, 10 were male and 7 were female, and the onset age was 3 (2-5) years old. All children developed fever, and neurological symptoms 1 (0-3.5) days later, including seizures (88%) and coma (88%). The lesions were mainly distributed in the thalamus, brainstem and medullary ventricular white matter, showing symmetry and multifocal changes. All the 5 cases with slowed cerebral blood flow velocity and presented shock wave or nail wave died. 16 children were on mechanical ventilation, 2 with continuous renal replacement therapy, and 8 died. All the survivors had varying degrees of neurological damage before discharge. Conclusion Severe influenza-associated encephalopathy of childhood is mainly characterized by fever, convulsions and coma. Cranial imaging, EEG, TCD and other examinations are helpful for early diagnosis and prognosis judgment. The effectiveness of early combined application of methylprednisolone and IVIG still needs further study.

目的 探讨miR-148a对大鼠急性胰腺炎细胞模型中细胞自噬的影响。方法 选取培养AR42J细胞,细胞分为4组,即正常对照组、模型组、miR-148a mimics组及miR-148a阴性对照组。利用Lipofectamine 2000转染miR-148a mimics及阴性对照miR-148a至AR42J细胞,继续培养48 h后,利用浓度为200 μmol的牛磺胆酸钠盐(TLCs)刺激以上两组及模型组AR42J细胞20 min,正常对照组不做处理,然后提取各组细胞蛋白及RNA。利用RT-qPCR检测各组细胞中miR-148a的表达;利用CCK8实验检测各组细胞的活性;利用ELISA法检测各组细胞培养液中炎性因子IL-6,IL-1β及TNF-α的含量;利用Western blot检测自噬相关的基因Beclin1、LC3Ⅰ、 LC3Ⅱ的表达。结果 RT-qPCR结果显示,与正常对照组相比较,模型组心肌细胞中miR-148a mRNA的表达降低,而miR-148a mimics组细胞中miR-148a mRNA的表达显著升高;CCK-8实验结果显示,转染miR-148a mimics至细胞后,可提高模型细胞的活性;ELISA实验结果显示,与模型组相比较,转染miR-148a mimics至细胞后,细胞培养液中炎性因子IL-6,IL-1β及TNF-α的含量显著降低;Western blot结果显示,与模型组相比较,转染miR-148a mimics至细胞后,可降低细胞中Beclin1的表达,降低LC3Ⅱ/LC3Ⅰ的比率。结论 利用miR-148a mimics提高TLCs刺激的细胞模型中的miR-148a表达后,细胞中Beclin1的表达降低,LC3Ⅱ/LC3Ⅰ的比率降低,抑制了细胞自噬,降低了炎性因子IL-6、IL-1β、TNF-α的释放,从而提高了细胞的活性,miR-148a可通过调节模型细胞的自噬而发挥细胞保护作用。

Objective To investigate the effect of miR-148a on autophagy in rat acute pancreatitis cell model. Methods AR42J cells were cultured and divided into 4 groups: normal control group, model group, miR-148a mimics group and miR-148a negative control group. miR-148a mimics and miR-148a negative control were transfected to AR42J cells with Lipofectamine 2 000, then cells were cultured for 48 h. The AR42J cells were stimulated with sodium taurocholate (TLCs) at a concentration of 200 μmol for 20 min, the normal control group was not treated, then the protein and RNA were extracted in each group. The expression of miR-148a was detected by RT-qPCR in each group. The activity of cells was detected by CCK8 assay in each group. The contents of IL-6, IL-1β and TNF-α in the cell culture medium were detected by ELISA. Western blot was used to detect the expression of autophagy related genes Beclin1, LC3Ⅰ and LC3Ⅱ. Results RT-qPCR results showed that the expression of miR-148a mRNA in model group was significantly lower than that in normal control group, while the expression of miR-148a mRNA in miR-148a mimics group was significantly higher than that in normal control group. The results of CCK-8 assay showed that miR-148a could significantly increase the activity of model cells stimulated by TLCs. The results of ELISA showed that the contents of IL-6, IL-1β and TNF-α in cell culture medium were significantly decreased after miR-148a mimics transfection, compared with the model group. Western blot showed that miR-148a mimics could significantly decrease the expression of Beclin1 and the ratio of LC3Ⅱ/LC3Ⅰ, compared with the model group. Conclusion miR-148a mimics was used to enhance the expression of miR-148a in cells model stimulated by TLCs, the expression of Beclin1 and the ratio of LC3Ⅱ/LC3Ⅰ were decreased, and the autophagy was inhibited. The release of IL-6, IL-1β and TNF-α was decreased and the activity of cells was increased. miR-148a plays a cellular protective role by regulating autophagy in model cells.

目的 总结一个以心脏损害为首发症状的假肥大肌营养不良症家系的遗传学及临床特征。方法 对先证者和家系成员进行临床观察、并收集其血清酶、胸片、心电图、 心脏彩色超声、肌肉组织活检及抗肌萎缩蛋白基因突变检测等结果。结果 先证者及家系成员患者符合假肥大肌营养不良症诊断,但以心脏扩大为首发症状,表现为心肌酶谱异常,心电图异常,心彩超提示扩张型心肌病,同时骨骼肌受累不明显,基因检测提示先证者及家系成员患者携带抗肌萎缩蛋白基因外显子40的无义突变[c.5632C>T, p(Gln1878^*)]。结论 该家系成员患者符合X连锁扩张型心肌病诊断,患者存在新发的抗肌萎缩蛋白基因无义突变。

Objective To summarize the genetic and clinical characteristics of a family with Duchenne muscular dystrophy (DMD) with cardiac damage as the first symptom. Methods The results of clinical observations, laboratory tests, chest radiographs, electromyography, echocardiography, muscle tissue biopsies, and DMD gene mutations were collected. Results Patients with probands and family members met the diagnosis of DMD. However, cardiac enlargement was the first symptom, presenting as abnormal myocardial enzyme spectrum, abnormal electrocardiogram, and dilated cardiomyopathy in echocardiography, while skeletal muscle involvement was not obvious. One nonsense pathogenic mutation c.5632C>T, p(Gln1878^*) of exon 40 in the DMD gene was identified in the patients with probands and family members. Conclusion The patients of this family met the diagnosis of x-linked dilated cardiomyopathy, and a new nonsense pathogenic mutation of DMD gene was identified in this family.