胎儿额叶大脑皮质在发育过程中厚度变化的形态计量研究

本文以8个胎龄组的13例胎儿额叶大脑皮质为研究对象,通过对大脑皮质各层厚度及总厚度的测量,从形态计量的角度探讨人胎儿额叶大脑皮质发育规律。结果表明,随着所取胎龄组胎龄的逐渐增大,胎儿额叶大脑皮质各层厚度及总厚度均呈逐渐增大的趋势。     

胎心监护的合理应用

早期发现和处理胎儿缺氧并避免因缺氧而产生的不良影响是每个产科医生都感兴趣的问题,胎儿心率监护是最方便也是最有效的方法。高危孕妇应于32～34周开始评估胎儿健康状况,合并严重并发症应于26～28周开始监测。胎儿心率的调控机制：胎儿大脑皮质、皮质下、脑干的心脏调节中心、     

中孕期胎儿腹壁皮下组织厚度变化

目的 探讨中孕期(20～28周)胎儿腹壁皮下组织厚度(ASTT)的变化.方法 超声测量236例健康初产孕妇的胎儿ASTT,分析胎儿ASTT在中孕期的变化.结果 胎儿ASTT随孕周增长:20周为(1.69±0.25)mm,24周为(2.08±0.21) mm,28周为(2.59±0.42) mm (P＜0.05).孕26～27周可见胎儿ASTT增长较为迅速.结论 胎儿ASTT与孕周相关;孕26～27周可见胎儿ASTT增长较为迅速.胎儿ASTT可作为评测中孕期胎儿宫内营养发育的参考指标.     

新生小鼠大脑皮质神经细胞体外培养方法及鉴定

目的 探索用24 h内新生C57BL/6小鼠大脑皮质进行神经细胞体外培养的方法.方法 取出生24 h内新生C57BL/6小鼠大脑皮质,胰蛋白酶消化,等体积的基础培养基终止消化,机械性吹打通过细胞过滤器获得单细胞悬液,接种细胞,24 h后更换无血清培养基,每3～4 d半量换液.神经细胞特异性烯醇化酶(NSE)抗体免疫组化方法鉴定神经细胞的纯度.结果 细胞在培养12 h后开始贴壁,24 h开始分化生长成梭形.大部分神经细胞于第2天长出突起,第3天神经细胞间形成复杂的联系,第7天神经细胞发育基本成熟.经NSE鉴定,培养细胞中神经细胞纯度可达90%以上.结论 无血清体外原代神经细胞培养法简便易行,相对于有血清培养法具有较大的优越性.     

中孕中期胎儿动脉导管参考值范围的建立及其对胎儿先天性心脏病的诊断价值

目的探讨中孕中期(24~28周)胎儿动脉导管参考值范围及其对胎儿动脉导管依赖型先天性心脏病的诊断价值。方法 9026例进行产前筛查的孕妇,中孕中期8091例,同时进行胎儿心脏超声,测量动脉导管(DA)内径,统计各孕周DA内径参考值范围,分析动脉导管依赖型先天性心脏病与DA内径参考值的关系。结果中孕中期产前筛查的孕周内完成胎儿心脏超声检查共7931例观测到DA,显示率为98.0%。胎儿DA内径值呈正态分布,且DA内径值随孕周增长而增宽。24~28周胎龄胎儿DA内径值分别为(2.43±0.27)mm、(2.50±0.28)mm、(2.58±0.27)mm、(2.71±0.31)mm、(2.99±0.29)mm。DA增宽2例为完全型房室隔缺损、右室双出口和主动脉弓缩窄各1例;DA缩窄3例为三尖瓣下移畸形、法洛四联症以及完全性大动脉转位并肺动脉狭窄各1例。结论中孕中期能够观察到胎儿DA,并能进行管径测量,DA内径参考值的建立对早期发现DA异常及DA相关疾病有所帮助。     

超声心动图Tei指数联合脑钠肽评价妊娠期糖尿病孕妇胎儿心功能的研究

目的研究超声心动图Tei指数联合脑钠肽在评价妊娠期糖尿病孕妇胎儿心功能方面的作用效果。方法选取2017年9月1日～2019年6月30日我院收治的GDM孕妇60例为观察组,选取同一时间我院收治的健康孕妇60例作为对照组,分别于孕24～28周、29～35周、 35周采用多普勒超声仪检查两组孕妇胎儿心功能,比较两组的超声心动图Tei指数及脑钠肽的变化。结果对照组胎儿的左心室、右心室Tei指数随着孕周的增加,无显著性变化(P 0.05),观察组胎儿的左心室、右心室Tei指数随着孕周的增加呈升高趋势(P 0.05),且对应时间点显著高于对照组(P 0.05);两组组内孕妇不同孕周检测BNP浓度均随着孕周的增加而呈升高趋势(P 0.05),观察组各孕周检测的BNP浓度显著高于对照组(P 0.05);相关性分析结果显示,GDM孕妇BMP水平与Tei指数呈正相关(r_(左心室)=0.659,r_(右心室)=0.705,P 0.05)。结论超声心动图Tei指数联合脑钠肽在评价GDM孕妇胎儿心功能方面的效果显著,可反映GDM孕妇胎儿心功能的潜在损害,值得在早期诊断和治疗中进一步推广使用。     

胎儿心脏二尖瓣前叶附着点与三尖瓣隔叶附着点间距离Z值曲线建立的研究

目的应用超声心动图技术研究分析胎儿心脏二尖瓣前叶附着点与三尖瓣隔叶附着点间距离(MTD)与胎儿生物学参数的相关性,探讨Z值曲线建立的临床价值。方法孕中期至晚期胎儿453例,据孕周20～23+6周,24～27+6周,28～31+6周,32～35+6周,36～40周分为5组,应用超声技术分别测量胎儿MTD及双项径(BPD)、头围(HC)、腹围(AC)、股骨长度(FL)、体质量等生物学参数,分析MTD与生物学参数间的相关性。结果胎儿MTD与其生物学参数间呈显著线性相关(P<0.01),其中FL与MTD相关性最高(R2=0.933),并建立MTD与FL相关Z值曲线图。结论建立孕中期至晚期胎儿MTD与FL相关Z值曲线图,为临床提供准确、快速判断胎儿心脏三尖瓣下移畸形和心内膜垫发育情况的参考依据。     

围生期细菌感染症的诊断

围生期细菌感染症是指胎儿及新生儿在宫内、产程中、出生后至28天内细菌感染而致病。新生儿败血症的发病率为1～10‰,病死率为13～45%。细菌感染是胎儿及新生儿死亡及严重后遗症的主要原因之一。本文就围生期细菌感染症的诊断综述如下:一、病史1.羊水早破与感染Daikoku 等报告孕周<28周羊水早破的发生率为31%,29～32周为47%,33～36周为43%。Thibceult 指出     

大鼠脑缺血再灌注后神经细胞凋亡的动态变化

目的观察大鼠脑缺血再灌注后大脑皮质和纹状体神经细胞凋亡的动态变化。方法采用大鼠脑缺血2h,再灌注1h,6h,12h,24h和48h的脑缺血再灌注模型。用HE染色体和TUNEL标记的方法,观察大鼠大脑皮层和纹状体神经细胞凋亡的变化。结果在脑缺血再灌注早期有部分神经细胞发生凋亡,随再灌注时间的延长,凋亡细胞数目逐渐增多。24～48h达高峰。结论在脑缺血再灌注损伤时神经细胞凋亡起着重要作用。     

透明压膜保持器与Hawley保持器临床效果及牙周健康的比较

颈项透明层是指胎儿颈后部皮下组织内液体积聚的厚度，反映在声像图上，即为胎儿颈后部皮下组织的无回声层。这一名称由Nieolaides等于1992年提出，用来描述早孕期胎儿颈部皮下的无回声带。一般认为在孕11～14周测量胎儿颈项透明层较好，此时头臀长相当于45～84mm。标准测量平面为胎儿正中矢状切面，面部向上背部在后，胎体呈自然俯屈位，也即头臀长切面。     

Perchloroethylene-Induced Reduction in Glial and Neuronal Cell Marker Proteins in Rat Brain

Abstract: Rats were exposed to continous inhalation of 300 and 600 p.p.m. of perchloroethylene for 4 and 12 weeks. Exposure to 600 p.p.m. for 4 to 12 weeks resulted in a slower increase in brain weight. Brain region weights, total proteins and DNA were decreased in frontal cerebral cortex and brain stem but not in hippocampus after exposure to 600 p.p.m. for 12 weeks. Four marker proteins were measured to monitor the specific neurotoxic effects of perchloroethylene: S-100 protein and glial fibrillary acidic protein as glial cell markers and neurone specific enolase and neurofilament 68 kD polypeptide as neuronal markers. The concentrations of glial and neuronal cytoskeletal proteins (glial fibrillary acidic protein and neurofilament 68 kD polypeptide) were reduced in frontal cerebral cortex. The total tissue contents of glial proteins (S-100 protein and glial fibrillary acidic protein) were decreased in all 3 brain regions investigated (frontal cerebral cortex, hippocampus and brain stem). Neurone specific enolase was unchanged by perchloroethylene exposure. These results indicate that exposure to perchloroethylene reduces the number of brain cells, possibly glial cells, and interferes with the metabolism of cytoskeletal elements in both glial and neuronal cells.     

Limbic muscarinic cholinergic and benzodiazepine receptor changes with chronic intravenous morphine and self-administration

Muscarinic cholinergic and benzodiazepine receptor affinities and densities were evaluated in membranes from seven brain regions of rats intravenously self-administering morphine and in littermates receiving yoked-morphine or yoked vehicle infusions to identify neuronal systems potentially involved in mediating opiate reinforcement processes. Passive morphine infusion resulted in increases in muscarinic cholinergic receptor densities in the pyriform cortex and in decreases in the cingulate cortex while benzodiazepine receptor densities were decreased in both the hippocampal formation and entorhinal-subicular cortex compared to littermates receiving passive infusions of vehicle. Morphine self-administration resulted in decreased muscarinic cholinergic receptor densities in the frontal and entorhinal-subicular cortices and increases in the amygdaloid complex compared to littermates receiving yoked passive drug. These data are in agreement with acetylcholine turnover rate measurements in these animals and support the proposed role of cholinergic innervations of the frontal and entorhinal-subicular cortices and amygdaloid complex in opiate reinforcement processes.     

Quantitative autoradiographic studies of relaxin binding in rat atria, uterus and cerebral cortex: characterization and effects of oestrogen treatment.

The binding characteristics of the relaxin receptor in rat atria, uterus and cortex were studied using a [33P]-labelled human gene 2 relaxin (B33) and quantitative receptor autoradiography. The binding kinetics of [33P]-human gene 2 relaxin (B33) were investigated in slide-mounted rat atrial sections. The binding achieved equilibrium after 60 min incubation at room temperature (23+/-1 degrees C) and dissociated slowly. The association and dissociation rate constants were 4.31+/-0.34x10(8) M(-1) x min(-1) and 1.55+/-0.38x10(-3) min(-1) respectively. Thus, the kinetic dissociation constant was 3.46+/-0.59 pM. Binding was saturable to a single population of non-interacting sites throughout atria, in uterine myometrium and the 5th layer of cerebral cortex. The binding affinities (pK(D)) of [33P]-human gene 2 relaxin (B33) were 8.92+/-0.09 in atrial myocardium and 8.79+/-0.04 in cerebral cortex of male rats, and 8.79+/-0.10 in uterine myometrium. Receptor densities in the cerebral cortex and atria were higher than in uterine myometrium, indicating that relaxin also has important roles in non-reproductive tissues. In male rats, treatment with 17beta-oestradiol (20 microg in 0.1 ml sesame oil s.c., 18-24 h) significantly decreased the density of relaxin receptors in atria and cerebral cortex. Identical treatment in female rats had no significant effect in atria and cerebral cortex, but it significantly increased the density of relaxin receptors in uterine myometrium. Relaxin binding was competitively displaced by porcine and rat native relaxins. Porcine native relaxin binds to the relaxin receptor in male rat atria (8.90+/-0.02), and cerebral cortex (8.90+/-0.03) and uterine myometrium (8.89+/-0.03) with affinities not significantly different from human gene 2 (B33) relaxin. Nevertheless, rat relaxin binds to the receptors with affinities (8.35+/-0.09 in atria, 8.22+/-0.07 in cerebral cortex and 8.48+/-0.06 in uterine myometrium) significantly less than human gene 2 (B33) and porcine relaxins. Quantitative receptor autoradiography is the method of choice for measurement of affinities and densities of relaxin receptor in atria, uterine myometrium and cerebral cortex. High densities were found in all these tissues. 17beta-oestradiol treatment produced complex effects where it increased the densities of relaxin receptors in uterus but decreased those in atria and cerebral cortex of the male rats, and had no effect on the atria and cerebral cortex of the female rats.     

Nefiracetam improves the impairment of local cerebral blood flow and glucose utilization after chronic focal cerebral ischemia in rats

In this study we investigated the effects of nefiracetam (DM-9384) on local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCMR(glc)) in the chronic phase after middle cerebral artery (MCA) occlusion in rats. Nefiracetam (10 mg/kg) was administered orally once a day for 2 weeks from day 15 after MCA occlusion. On day 28 after MCA occlusion, LCBF and LCMR(glc) were measured by an autoradiographic image-processing method. In MCA-occluded rats, LCBF and LCMR(glc) in the ischemic side of seven regions including the frontal cortex were significant decreased compared with those of the nonischemic side. Nefiracetam significantly improved the impairment of LCBF in the frontal cortex, parietal cortex, caudate putamen, ventral thalamus, amygdaloid nucleus and hippocampus. It also improved the decrease of LCMR(glc) in the frontal cortex, ventral thalamus and hippocampus. These results suggested that nefiracetam has ameliorating effects on chronic disorders of LCBF and LCMR(glc) induced by MCA occlusion.     

Bolus maternal cocaine administration does not produce a large increase in fetal sheep cerebral cortical glutamate concentration

Human cocaine use during pregnancy may result in postnatal neurologic dysfunction and abnormal behavior. L-Glutamate, the major excitatory neurotransmitter in the brain, plays an important role in cerebral cortical development. An optimal level of glutamate is required for normal neuronal development. We tested whether acute cocaine exposure produces large increases in glutamate release in the intact cerebral cortex of the near-term fetal sheep. Cocaine 3.0 mg kg(-1) IV bolus produced the expected increase in maternal and fetal mean arterial pressure, increase in fetal heart rate, decrease in uterine blood flow, and decrease in fetal arterial blood pO2 (N = 5). The percentage increases in extracellular glutamate concentration in the fetal cerebral cortex measured by in utero microdialysis were 7%, 15%, 17%, 17%, and 43% in each fetus (upper 95% confidence bound for the median = 43%). We conclude that if cocaine increases glutamate concentration in the developing cerebral cortex, the increase in magnitude is small relative to the changes produced by other interventions such as ethanol or umbilical cord occlusion. Mechanisms other than increases in cerebral cortical glutamate concentration probably contribute to the neurologic injury associated with prenatal cocaine exposure.     

Effect of prolonged co-dergocrine mesylate treatment on choline acetyltransferase levels in rat cerebral cortex after lesioning of the nucleus basalis magnocellularis (of Meynert)

The effects of monolateral lesions of the nucleus basalis magnocellularis (of Meynert) and of 1 or 4 weeks of co-dergocrine mesylate treatment (0.1 or 0.6 mg/kg) on choline acetyltransferase activity in rat frontal, parietal and occipital cortex were studied. According to the literature, ibotenic acid-induced lesions of the nucleus basalis magnocellularis cause a significant decrease in choline acetyltransferase activity in frontal and parietal cortex, but had no effect on enzyme activity in the occipital cortex or cortical areas controlateral to the lesion. Co-dergocrine administration caused, after 4 weeks of treatment, a dose related increase of choline acetyltransferase activity in the frontal and parietal cortex in the lesioned side. In contrast, it had no effect on the enzyme activity in the other cortical regions studied. The possible significance of the increased choline acetyltransferase activity elicited by co-dergocrine mesylate in cerebral cortex areas sensitive to nucleus basalis magnocellularis lesions is discussed.     

Regulation of m1 muscarinic receptors and nNOS mRNA levels by autoantibodies from schizophrenic patients

In this paper we demonstrate that, circulating antibodies from schizophrenic patients interacting with cerebral M1 muscarinic acetylcholine receptors (M1 mAChRs), can act as an inducer of m1 mAChR-mRNA, and neuronal nitric oxide synthase (nNOS) mRNA gene expression of rat frontal cortex. The different signaling pathways involved in the autoantibody's actions, were characterized. As previously reported serum autoantibodies from schizophrenic patients reacted against neural cells surface inhibiting the binding of the specific mAChR radioligand to rat cerebral frontal cortex membrane. Moreover, by ELISA using M1 synthetic peptide (with identical aminoacid sequence to human M1 mAChR) as coating antigen we demonstrated the reactivity against the second extracellular loop of human cerebral M1 mAChR. The corresponding affinity-purified anti M1 peptide IgG (anti M1 peptide IgG) from schizophrenic patients by stimulation of M1 mAChR exerted an increase in m1 mAChR-mRNA and nNOS-mRNA levels, that significantly correlated with the accumulation of phosphoinositides (IPs) and activation of NOS (alpha = 0.05). All these effects were blunted by pirenzepine and mimicked the action of the authentic agonist. Concurrent analysis of the effects of nNOS, phospholipase C (PLC) and calcium/calmodulin (CaM) inhibition on both, m1 mAChR-mRNA and nNOS-mRNA levels, showing that antibody up-regulation mRNA level is under the control of endogenous nitric oxide (NO) signaling system. On the basis of our results, the activation of M1 mAChR by schizophrenic autoantibody appears to induce nNOS-mRNA expression and reciprocally, the activation of NOS up-regulates m1 mAChR gene expression. These results gave support to the participation of an autoimmune process in a particular group of chronic schizophrenic patients.