33 例非免疫性胎儿水肿临床特征及转归

目的探讨非免疫性胎儿水肿(NIHF)临床特征及转归。方法回顾分析2014年1月—2016年12月收治的33例NIHF新生儿的临床资料,将其分为死亡组和治愈组,进行两组间各因素的比较分析。结果 33例患儿中,男16例、女17例,中位胎龄33.4周(31.2～35.1周),出生体质量(2 714±712)g,死亡20例。死亡组出生体质量、1分钟及5分钟Apgar评分低于治愈组,差异均有统计学意义(P0.05)。新生儿产时复苏插管组和未插管组的母亲孕期合并症发生率及宫内干预率的差异有统计学意义(P0.05)。宫内干预是导致新生儿需产时复苏的独立危险因素(OR=15.30,95%CI:2.46～95.19);1分钟Apgar评分是NIHF疾病转归的独立危险因素(OR=1.75,95%CI:1.20～2.53),评分越低、死亡率越高。结论宫内干预与产时需要复苏有关,而1分钟Apgar评分是影响NIHF结局的重要因素。     

不同干预方法缓解新生儿疼痛效果的对比研究

目的对比不同干预方法缓解新生儿疼痛的效果,探索有效缓解新生儿疼痛的方法。方法选用N-PASS量表(neonatalpain,agitationandsedationscale)对120例住院新生儿进行疼痛评分,按随机原则分3组:未干预组(对照组)、应用非营养性吸吮(NNS)组和给予体位支持组,每组40例。分别于针刺足跟后1,5min进行疼痛程度评分。结果3组间的疼痛评分在刺激后1,5min各组间评分差异有显著性(F值=22.13,P<0.05;F值=22.44,P<0.05)。疼痛程度方面,不同的干预方法在1min的轻、中度疼痛的镇痛效果之间存在明显差异(χ2值=9.67,P<0.05;χ2值=7.85,P<0.05),对重度疼痛和5min时疼痛的缓解效果,各种干预方法之间无显著差异。结论新生儿对急性、短暂性疼痛很敏感;不同的干预方法对缓解新生儿疼痛的近期效果不同,NNS在短期内缓解疼痛的效果优于体位支持组;非药物疼痛干预方法对新生儿轻、中度疼痛效果好,在短时间内作用显著;应重视对新生儿疼痛的管理。     

新生儿锁骨骨折的护理评估及干预

新生儿锁骨骨折是新生儿产伤性骨折中最常见的一种,多发生在分娩过程中,常见于胎儿出肩困难时助产处理不当或臀位牵引拉肩部用力过重而造成,偶尔也可见于自然分娩的新生儿[1]。因其症状和体征不明显,易漏诊而导致医疗纠纷,应引起临床重视。1994年1月-2005年3月,对新生儿科收治的28例新生儿锁骨骨折进行了观察与分析,总结相关护理评估要点与干预措施,现报道如下。临床资料1.一般资料。1994年1月-2005年3月,在新生儿科收治的锁骨骨折新生儿28例,男17例,女11例。早产儿1例,过期产儿1例,足月儿26例。体重2 790~5 960 g(<3 500 g 5例,≥3 500 g 2…     

syndecan-4对碱性成纤维细胞生长因子诱导人肾小球系膜细胞增殖及细胞外基质分泌的影响

目的 研究syndecan-4对碱性成纤维细胞生长因子（bFGF）诱导人肾小球系膜细胞(HMC)增殖及细胞外基质（ECM）分泌的影响,并探讨syndecan-4-蛋白激酶Cα（PKCα）途径在其中的作用。 方法 免疫荧光方法观察syndecan-4在HMC上的表达。筛选有效的syndecan-4-siRNA转染HMC,噻唑蓝（MTT）比色法检测HMC在bFGF不同作用时间下的增殖差异;ELISA法检测细胞上清液中的Ⅰ、Ⅳ型胶原和纤连蛋白（FN）含量;荧光定量PCR观察syndecan-4和PKCα含量的变化。 结果　syndecan-4蛋白在HMC有表达。bFGF可促进HMC的增殖及FN、Ⅳ型胶原的分泌,使得每百万看家基因中PKCα拷贝数明显增加。转染syndecan-4 siRNA后,显著降低了HMC的增殖速度（48~60 h时点,P < 0.01）、ECM分泌（FN：24 h时点,P < 0.01,48~96 h,P < 0.05;Ⅳ型胶原：72~96 h时点,P < 0.05）及PKCα含量 （0 h时点,P < 0.05,12 ~48 h时点,P < 0.01）。 结论 syndecan-4参与调控bFGF诱导HMC的增殖及ECM分泌过程。syndecan-4-PKCα途径可能在其中扮演重要作用。     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.     

病毒感染与小儿短暂性滑膜炎关系的研究

探讨小儿短暂性滑膜炎与病毒感染 ,特别是柯萨奇B组病毒 (CVB)感染的关系。方法 :采用酶联免疫吸附试验 (ELISA)对 16 2例小儿髋关节短暂性滑膜炎患儿静脉血和其中的 2 1例关节腔液进行病毒IgM抗体检测 ,柯萨奇病毒B组 (CVB)阳性者进行血清学分型及病毒分离。结果 :在 16 2例静脉血样本中病毒IgM阳性 6 2例 ,占总检数的 38.2 7% ,CVB -IgM2 6例占 16 .0 5 % ,AdV -IgM 19例占 11.73% ,CMV -IgM 10例占 6 .17% ,RSV -IgM 4例占 2 .4 7% ;在关节腔液中检出 9例CVB阳性 ,血清学分型 8例为CVB3,1例为CVB4 ,并分离出 1例CVB3。结论 :CVB和腺病毒 (AdV)是小儿髋关节短暂性滑膜炎感染的主要病毒 ,而且以CVB3为主。     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.     

细胞因子对脐血单个核细胞端粒酶活性的影响

目的研究集落刺激因子对脐血单个核细胞(CBMC)端粒酶活性的影响。方法体外培养3例足月正常新生儿的CBMC,并加入集落刺激因子IL?3、SCF、GM?CSF及其组合,培养5d后用TRAP?ELISA法测定每份标本的端粒酶活性。结果CBMC培养前有较弱的端粒酶活性,加入集落刺激因子体外培养后端粒酶活性均有不同程度的上调,以加入IL?3、SCF、GM?CSF组最为显著;CBMC与PBMC培养前端粒酶活性差异无显著性,培养后比较差异有显著性(P<0.01)。结论IL?3、SCF、GM?CSF的组合对CBMC端粒酶活性有明显影响;集落刺激因子对CBMC和PBMC均有扩增作用,但CBMC具有更高扩增潜能。     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.