49例早发型重度子痫前期的临床分析

目的探讨早发型重度子痫前期的临床特点及治疗。方法对山西医科大学第一临床医学院妇产科2006-1~2008-12收治的213例重度子痫前期患者(其中早发型49例,即24~34孕周发病者;晚发型164例,即≥34孕周发病者)及其新生儿228例进行回顾性分析,观察指标包括一般情况、并发症、合并症及母婴结局。结果早发型重度子痫前期患者分娩孕周较晚发型早(P0.01)、治疗时间较晚发型长(P0.05),其临床症状及并发症/合并症较晚发型严重,母婴结局明显较晚发型严重,母婴结局明显较晚发型差。结论早发型重度子痫前期病情严重,围生儿预后不佳,应根据母胎情况,严格选择病例进行保守治疗,同时密切监测母胎病情变化。     

幼年大鼠溺水应激后胰岛素信号传导变化及外源胰岛素治疗反应

Objective To explore the alteration of insulin signal transduction in drowning-induced stress hyperglycemia and to investigate therapeutic effect of insulin on it.Methods Stress hyperglycemia model was induced by drowning.Thirty-two infant rats were randomized into control,drowning,air resuscitation and air-insulin resuscitation groups.Insulin was injected abdominally into the air-insulin resuscitation rats.Fasting serum glucose and insulin were determined routinely,and protein expressions and serine phosphorylation levels of insulin receptor substrate 1(IRS-1) in muscle tissue were detected by Western blot and immunoprecipitation.The expressions of glucose transporter 4(GLUT4) in the intracellular and plasma membranes of muscle tissue were detected by Western blot.Results In the drowning group,insulin resistance index(HOMA-IR) increased significantly as compared with that of the control group,but the level of IRS-1 had no significantly change as compared with the other three groups.As compared with that of the drowning group(0.71±0.12),IRS-1 serine phosphorylation levels of the two resuscitation groups decreased significantly(0.56±0.13 and 0.46±0.08 respectively).The intracellular GLUT4 expression in the two resuscitation groups(1.82±0.11 and 1.96±0.28 respectively)increased significantly in contrast to that of the drowning group(1.45±0.15),and the air-insulin resuscitation groups showed an especially high increase of intracellular GLUT4 expression.Conclusion During the drowning-induced stress hyperglycemia,the alteration of serine phosphorylation and GLUT4 distribution is one of the important mechanism of insulin resistance.Insulin may decrease the blood glucose through decreasing serine phosphorylation levels of IRS-1 and increasing the intracellular GLUT4 expressions.     

磁共振弥散加权成像在早产儿脑室周围白质软化早期的预测价值

目的 探讨磁共振弥散加权成像(DWI)早期评价和预测早产儿脑室周围白质软化(PVL)的作用及意义.方法 回顾分析2005年8月至2007年4月,在我院新生儿科住院,且经头部MRI确诊的12例PVL早产儿生后7 d内、2 w和4 w的DWI及常规MRI资料.结果 初次检查(平均生后4.5 d)全部病例DWI均显示双侧脑室周围脑白质对称性、弥漫性高信号,常规MRI基本正常;出生后2周DWI示脑白质内不规则高、低混杂信号,而常规MRI则显示相应部位小片状或点状T1WI高信号,T2WI稍低信号;出生后4W DWI示侧脑室后角、枕部三角区大小不等的囊性低信号,常规MRI显示相应病灶的T1WI低信号,T2WI高信号(即囊性PVL改变);出生后4个月常规MRI示囊腔逐渐变小、消失,脑白质减少、脑室扩大.结论 DWI显示的双侧脑室周围白质对称性弥漫性高信号是PVL的最早期表现;所提供的影像学异常变化与晚期常规MRl所证实PVL发生的高度相关性,表明了DWI可能是早期评价脑白质损伤及预测早产儿PVL发生的重要检测手段.     

慢性肺疾病早产鼠的肺组织中HoxB5 mRNA表达及其对肺发育的影响

目的 探讨高氧致慢性肺疾病(CLD)早产鼠的肺组织HoxB5基因表达规律及其对肺发育抑制的影响机制.方法 将孕21 d剖宫取出的新生鼠(即早产鼠)80只随机分为实验组及对照组(每组均为40只),采用高浓度氧诱导早产鼠CLD模型,分别于实验后1、3、7、14、21 d采集肺组织,应用反转录聚合酶链反应(RT-PCR)等技术,测定肺组织HoxB5、AQP-5、SP-B mRNA水平,并同期观察肺发育的评价指标放射状肺泡计数(RAC)的变化.结果 生后1 d和3 d,实验组和对照组的HoxB5、AQP-5及SP-B mRNA水平和RAC均差异无统计学意义(P＞0.05);生后7 d,与对照组比较,实验组RAC开始减少(6.35±0.83vs.7.67 ±0.52),HoxB5(0.98±0.14vs.1.20±0.16)及AQP-5(0.78±0.11vs1.04±0.19)mRNA也明显降低(P＜0.05)、SP-B(1.34±0.04vs1.04±0.11)反而明显升高(P＜0.05);生后14 d,实验组RAC逐渐减少,HoxB5及AQP-5 mRNA持续下降,21 d,HoxB5(0.64±0.11vs.1.18±0.13)及AQP-5(0.67±0.12vs.0.97±0.01)mRNA降至最低(P＜0.01),而SP-B(1.43±0.07vs.1.12±0.09)mRNA升至最高(P＜0.01);实验组肺组织HoxB5 mRNA水平及RAC呈明显正相关(γ=0.685,P＜0.01).结论 暴露高氧中早产鼠的肺组织HoxB5基因呈低水平表达,其表达降低可能导致的Ⅱ型肺泡上皮细胞向Ⅰ型肺泡上皮细胞的分化障碍与CLD肺发育停滞密切相关.     

新生儿允许性高碳酸血症的研究现状

目前允许性高碳酸血症(PHC)正逐渐应用于临床,与传统的机械通气相比,应用PHC通气策略可以提高先天性膈疝新生儿的生存率,然而有关PHC在新生儿领域的定义、临床可接受的允许值范围及其对发育中重要器官的功能影响等诸多问题均需进一步研究和证实.     

超声引导下22G套管针辅助新生儿颈内静脉穿刺术

目的探讨超声引导下22G套管针辅助新生儿颈内静脉穿刺置管的可行性。方法选择沧州市中心医院2016年7月至2017年9月在全身麻醉下手术需要中心静脉置管的新生儿60例,随机分为观察组和对照组,每组30例。观察组在彩超引导下采用22G套管针进行穿刺置管,对照组在彩超引导下采用原穿刺针进行穿刺置管。结果观察组一次穿刺成功率、置导丝成功率、置管成功率均高于对照组,穿刺时间明显短于对照组,并发症明显低于对照组,2组比较差异有统计学意义(P 0. 05)。结论超声引导下22G套管针进行新生儿颈内静脉穿刺术能够极大地提高穿刺置管成功率,为临床麻醉及围术期管理提供支持。     

提纯血清和腹水中IgG的一种简单非层析技术

几年前，Chanutin与Curnirh报道：在酸性条件下，短链脂肪酸如正辛酸可沉淀血浆中不同蛋白。根据这一理论，Stelnbuch与Audran研究了用正辛酸提纯哺乳动物血清中IgG的方法，而Russo等报道了这一方法在提纯小鼠腹水中McAb的应用。     

胃癌单抗MG5相应抗原的纯化及分析

作者报告鼠抗人胃癌单克隆抗体MG5相应抗原的纯化和初步鉴定，首先收集胃癌患者转移性腹水癌细胞。制备可溶性抗原提取液。用concanavalin A(Con A)Sepharose 4B亲和层析法分离提取胃癌细胞糖蛋白成份后，再甩MG5-Sepharose 4B免疫亲和层析法纯化单抗MG5相应抗原。经高碘酸氧化，电泳脂蛋白染色SDS-PAGE和免癌印渍等实验分析，证实MG5相应抗原是一种含3个亚单位的糖蛋白，分子量分别为68kD、52kD和44kD，抗原决定簇存在于糖链上．免疫分析提示MG5相应抗原是一种新的胃癌相关抗原。     

幼年大鼠溺水应激后胰岛素信号传导变化及外源胰岛素治疗反应

Objective To explore the alteration of insulin signal transduction in drowning-induced stress hyperglycemia and to investigate therapeutic effect of insulin on it.Methods Stress hyperglycemia model was induced by drowning.Thirty-two infant rats were randomized into control,drowning,air resuscitation and air-insulin resuscitation groups.Insulin was injected abdominally into the air-insulin resuscitation rats.Fasting serum glucose and insulin were determined routinely,and protein expressions and serine phosphorylation levels of insulin receptor substrate 1(IRS-1) in muscle tissue were detected by Western blot and immunoprecipitation.The expressions of glucose transporter 4(GLUT4) in the intracellular and plasma membranes of muscle tissue were detected by Western blot.Results In the drowning group,insulin resistance index(HOMA-IR) increased significantly as compared with that of the control group,but the level of IRS-1 had no significantly change as compared with the other three groups.As compared with that of the drowning group(0.71±0.12),IRS-1 serine phosphorylation levels of the two resuscitation groups decreased significantly(0.56±0.13 and 0.46±0.08 respectively).The intracellular GLUT4 expression in the two resuscitation groups(1.82±0.11 and 1.96±0.28 respectively)increased significantly in contrast to that of the drowning group(1.45±0.15),and the air-insulin resuscitation groups showed an especially high increase of intracellular GLUT4 expression.Conclusion During the drowning-induced stress hyperglycemia,the alteration of serine phosphorylation and GLUT4 distribution is one of the important mechanism of insulin resistance.Insulin may decrease the blood glucose through decreasing serine phosphorylation levels of IRS-1 and increasing the intracellular GLUT4 expressions.