胰岛素样生长因子—I与胎儿出生体重的关系

目的 了解胰岛素生长因子－Ｉ（ＩＧＦ－Ｉ）在胎儿生长发育中所起的作用,方法 选择１７１例产妇及其所分娩的新生儿１６４例,根据出生体重将新生儿分为大于胎龄儿（ＬＧＡ）组,产妇７７例,新生儿６４例,适于胎龄儿（ＡＧＡ）组：产妇５９例,新生儿５９例;小儿胎龄儿（ＳＧＡ）组：产妇３５例,新生儿４３例,用放射免疫法测定血清中ＩＧＦ－Ｉ的浓度。结果 母血中ＩＧＦ－Ｉ浓度均高于脐血,两者间存在浓度梯度（Ｐ〈０．     

胎儿胰岛素样生长因子-Ⅰ的检测及意义

目的评估胰岛素样生长因子Ⅰ（ＩＧＦⅠ）在胎儿、胎盘生长发育中的作用。方法用放射免疫分析法（ＲＩＡ）测定大于胎龄儿（ＬＧＡ）组３０例,适于胎龄儿（ＡＧＡ）组３６例及小于胎龄儿（ＳＧＡ）组３６例的脐血清ＩＧＦⅠ的水平。用线性相关分析法分析各组变量之间的相关关系。结果３组胎儿脐血清ＩＧＦⅠ与胎龄、胎儿体重、胎盘重量均呈显著正相关（ｒ＝０．３２,Ｐ＜０．００１;ｒ＝０．６８,Ｐ＜０．００１;ｒ＝０．７５,Ｐ＜０．０１）,其中与胎盘重量呈高度正相关。脐血清ＩＧＦⅠ水平,ＡＧＡ组为１４４５９±４６．７３μｇ／Ｌ;ＳＧＡ组为９０．８０μｇ／Ｌ（ｔ＝４．７,Ｐ＜０．００１）,ＬＧＡ组为２０９１７μｇ／Ｌ（ｔ＝７．９７,Ｐ＜０．００１）。结论ＩＧＦⅠ是胎儿、胎盘生长发育的重要调节因子,对巨大儿、小于胎龄儿的形成有重要作用。     

胎盘组织中胰岛素样生长因子 -Ⅰ的定位及定量分析

目的探讨胎盘组织中胰岛素样生长因子Ⅰ（ＩＧＦⅠ）定位，评估ＩＧＦⅠ在胎儿生长发育中的作用。方法用免疫组化法对妊娠胎盘组织中ＩＧＦⅠ细胞进行定位，并采用计算机医学图像分析系统，检测小于胎龄儿（ＳＧＡ）组２２例，适于胎龄儿（ＡＧＡ）组２５例及大于胎龄儿（ＬＧＡ）组２５例的ＩＧＦⅠ，并进行定量分析。用ｔ检验法进行各组间均数检验。结果（１）胎盘ＩＧＦⅠ主要位于绒毛小叶的合体滋养细胞及细胞滋养细胞。此外，也存在于Ｈｏｆｂａｕｅｒ细胞及平滑绒毛层，但染色较以上两种细胞明显减弱，胎膜的羊膜细胞及蜕膜细胞偶尔可见阳性，而绒毛小叶蜕膜细胞则未见阳性着色。（２）与ＡＧＡ组比较，ＳＧＡ组胎盘ＩＧＦⅠ的相对面积及平均吸光度均显著降低（ｔ＝４．６５，Ｐ＜０．００１、ｔ＝２．１５，Ｐ＜０．０５），而ＬＧＡ组胎盘ＩＧＦⅠ的相对面积及平均吸光度均显著升高（ｔ＝８．７２，Ｐ＜０．００１；ｔ＝７．８２，Ｐ＜０．００１）。结论胎盘组织中ＩＧＦⅠ主要定位于胎盘小叶的合体滋养细胞、细胞滋养细胞；胎盘组织合成和分泌ＩＧＦⅠ的多少，与发生ＬＧＡ及ＳＧＡ有关。     

表皮生长因子及其受体与胎儿出生体重的关系

目的探讨表皮生长因子（ＥＧＦ）及其受体与胎儿出生体重的关系。方法采用酶联免疫吸附测定法对正常非孕妇女１５例（对照组）、足月正常体重儿４０例（正常体重儿组）、ＩＵＧＲ儿４０例（ＩＵＧＲ儿组）、巨大儿２５例（巨大儿组）的母血清、脐血清及羊水中ＥＧＦ浓度进行测定,同时采用免疫组化方法对以上各组胎盘及胎膜上ＥＧＦ受体（ＥＧＦＲ）进行测定。结果各组母血、脐血及羊水中ＥＧＦ浓度明显高于对照组（Ｐ＜００５）。ＩＵＧＲ儿组母血、脐血及羊水中ＥＧＦ浓度低于正常体重儿组,差异有显著性。巨大儿组母血、脐血及羊水中ＥＧＦ浓度与正常体重儿组比较,差异无显著性。在ＩＵＧＲ儿组胎盘及胎膜上ＥＧＦＲ表达明显低于正常体重儿组（Ｐ＜０．０１）,巨大儿组胎盘上ＥＧＦＲ表达高于正常体重儿组。结论ＥＧＦ及其受体与ＩＵＧＲ的发生有关,在妊娠后期测定母血及羊水中ＥＧＦ浓度,对评价胎儿的生长发育具有重要意义。     

胰岛素样生长因子-Ⅰ辅助促排卵的实验研究

目的探讨胰岛素样生长因子Ⅰ（ＩＧＦⅠ）辅助促排卵的作用。方法建立小白鼠排卵障碍动物模型,将排卵障碍性小白鼠分为３组,分别于每只小白鼠腹腔内一次性注射ＩＧＦⅠ１μｇ加人绝经期促性腺激素（ｈＭＧ）５ＩＵ（ＩＧＦⅠ加ｈＭＧ组）、ＩＧＦⅠ２μｇ（ＩＧＦⅠ组）和ｈＭＧ１０ＩＵ（ｈＭＧ组）,观察阴道脱落细胞涂片的周期性变化和输卵管内卵母细胞数。结果ＩＧＦⅠ加ｈＭＧ组、ＩＧＦⅠ组和ｈＭＧ组阴道脱落细胞涂片呈周期性变化者分别为８０％、２０％和６０％,ＩＧＦⅠ加ｈＭＧ组高于ＩＧＦⅠ组和ｈＭＧ组（Ｐ＜０．０１和Ｐ＜０．０５）,ＩＧＦⅠ组与ｈＭＧ组比较,差异无显著性（Ｐ＞０．０５）。输卵管内卵母细胞数,ＩＧＦⅠ加ｈＭＧ组平均为１２．３个,ｈＭＧ组平均为９．２个,两组比较,差异有显著性（Ｐ＜０．０５）。ＩＧＦⅠ组阴道脱落细胞呈周期性变化的小白鼠,输卵管内未见卵母细胞。结论ＩＧＦⅠ可作为辅助促排卵剂。     

胎儿生长迟缓孕妇淋巴细胞姐妹染色单体的互换频率

目的：了解胎儿生长迟缓（ＩＵＧＲ）孕妇外周血及新生儿脐血姐妹染色单体互换（ＳＣＥ）频率的变化。方法：应用姐妹染色单体互换技术，对１４例单纯性ＩＵＧＲ孕妇（ＩＵＧＲ组）及９０例正常孕妇（对照组）的外周血及其所分娩新生儿脐血ＳＣＥ频率进行测定。结果：ＩＵＧＲ组外周血及脐血ＳＣＥ频率分别为１０．５３±２．６９，７．２５±１．３４；对照组外周血及脐血ＳＣＥ频率分别为７．５８±０．３２，５．０５±０．２９；两组比较，差异有极显著性（Ｐ均＜０．０１）。ＩＵＧＲ组外周血及脐血ＳＣＥ频率全部异常。结论：ＩＵＧＲ与遗传物质损伤有关，ＳＣＥ频率有可能作为一项诊断ＩＵＧＲ的新指标。     

适于胎龄儿与小于胎龄儿血浆氨基酸浓度的比较

目的：了解正常胎儿血浆氨基酸谱，探讨小于胎龄（ＳＧＡ）儿的发病机理。方法：用经腹脐静脉穿刺术和剖宫产术采脐静脉血，测定３０例不同胎龄正常胎儿血浆氨基酸浓度，并用配对的方法比较１０对出生后适于胎龄（ＡＧＡ）和ＳＧＡ母、儿血浆氨基酸浓度的差异。结果：ＡＧＡ儿脐血１５种氨基酸浓度高于其母血，脐血与母血血浆氨基酸浓度显著相关；胎儿与母体氨基酸总浓度及其比值均恒定。ＳＧＡ儿必需氨基酸浓度下降，尤以支链氨基酸和赖氨酸下降明显，ＳＧＡ儿与其母体的必需氨基酸和支链氨基酸比值亦下降，差异均有显著性，但ＳＧＡ孕妇必需氨基酸和支链氨基酸浓度无显著变化。结论：胎盘功能和母体营养供给是维持胎儿正常生长发育的重要因素，ＡＧＡ母、儿双方氨基酸维持相对稳定和平衡；ＳＧＡ儿存在氨基酸代谢紊乱，某些ＳＧＡ儿氨基酸浓度降低并不是因其母体氨基酸浓度低所致。     

胎儿宫内发育迟缓时胎盘病理改变与孕妇血及脐血中一氧化氮水平的关系

目的了解胎儿宫内发育迟缓（ＩＵＧＲ）时胎盘病理改变与母血及脐血中一氧化氮（ＮＯ）水平的关系。方法对１９９７年１１月～１９９８年１０月３８例妊娠合并胎儿宫内发育迟缓（ＩＵＧＲ组）及３０例正常孕妇（对照组）分娩后的胎盘及胎儿附属物进行分析。用隔还原显色法测定母血及脐血ＮＯ水平。结果ＩＵＧＲ组中２６例有胎盘、脐带病理改变（６８．４２％）。主要表现为绒毛发育迟缓及绒毛炎;对照组中５例有胎盘病理改变（１６．６７％）,两组比较差异有极显著性（Ｐ＜０．０１）;ＩＵＧＲ组中母血及脐血ＮＯ水平均低于对照组（Ｐ＜０．０５,Ｐ＜０．０１）;ＩＵＧＲ组中２６例胎盘病理改变明显,其母血及脐血ＮＯ水平低于胎盘无明显病理改变者（Ｐ＜０．０５,Ｐ＜０．０５）;两组脐血ＮＯ水平均高于母血ＮＯ水平（Ｐ＜０．０１,Ｐ＜０．０５）,两组脐血与母血ＮＯ水平均有相关性（ｒ＝０．５４７５,ｒ＝０．８５０６）;脐血ＮＯ水平与新生儿体重在ＩＵＧＲ组未发现明显相关性（ｒ＝０．２８３８）。结论ＩＵＧＲ时,胎盘发生明显病理变化,导致母血及脐血中ＮＯ的水平降低。     

胎盘组织中胰岛素样生长因子—I的定位及定量分析

目的 探讨胎盘组织中胰岛素样生长因子－Ｉ（ＩＧＦ－Ｉ）定位,评估ＩＧＦ－Ｉ在胎儿生长发育中的作用。方法 用免疫组化法对对妊娠胎盘组织中ＩＧＦ－Ｉ细胞进行定位,并采用计算机医学图像分析系统,检测小于胎龄儿（ＳＧＡ）组２２例,适于胎龄儿（ＡＧＡ）组２５例及大于胎龄儿（ＬＧＡ）组２５例的ＩＧＦ－１,并进行定量分析,用ｔ检验法进行各组间均数检验。结果 （１）胎盘ＩＧＦ－Ｉ主要位于绒毛小叶的合体滋养细胞滋养     

IUGR脐血中表皮生长因子水平的研究

目的：从内分泌因素的角度对胎儿生长发育及其异常进行研究，以探讨ＩＵＧＲ与脐血中表皮生长因子（ＥＧＦ）水平的关系。方法：选择伴有ＩＵＧＲ的孕妇２２例及正常孕妇３８例，于分娩时抽取脐血，用放射免疫测定法（ＲＩＡ）测定ＥＧＦ水平，同时测定胎儿体重与胎盘重量，比较两组的差异。结果：正常体重儿（３４０９．１±２８４．７９ｇ）组的脐血ＥＧＦ水平（６２４．６４±７３．９０μｇ／Ｌ）明显高于低体重儿（２４０３．３±２７７．４１ｇ）组（２１７．９０±５４．５２μｇ／Ｌ）（Ｐ＜０．０５）；ＩＵＧＲ组胎盘重量３５４．３±９２．６４ｇ亦明显低于正常组的５４２．１±７８．３２ｇ（Ｐ＜０．０１）。结论：脐血中低ＥＧＦ水平是ＩＵＧＲ的相关因素之一，对妊娠过程中ＥＧＦ的作用及其机制进行研究有助于探讨ＩＵＧＲ病因及临床治疗。     

Nutrition and Fetal Growth

Fetal nutrition is the major regulator of fetal growth in late gestation. However, the relationship between nutrition and fetal growth in human pregnancy has not been widely recognized by clinicians for a number of reasons. The balance and timing of maternal nutritional in take may have complex and interactive effects on fetal and placental growth. There is a need to distinguish fetal nutrition from maternal nutrition, and to distinguish fetal growth from birthweight. The effects of nutrition on fetal growth may be indirect through their influence on the fetal endocrine status or direct by modifying the substrate supply. Finally, the effect of nutrition on fetal growth may be evident over the life-time of the individual and over more than one generation. All of these factors must be considered in assessing the role of nutrition in the regulation of fetal growth.     

Early Fetal Growth Delay

It has been reported that the congenital anomalies frequently observed in offspring of diabetic women may be predicted by first-trimester ultrasound findings that reveal diminution in growth of the embryo/fetus. The aim of the current study was to examine the relationship between early growth delay and congenital anomalies in pregnancies complicated by diabetes.

We conducted a retrospective study of 38 patients with insulin-requiring pregestational diabetes mellitus and 81 control pregnancies who had first-trimester ultrasound examinations. A cross-sectional survey of all patients revealed a congenital anomaly rate of 18.4% among the diabetic pregnancies compared to 4.9% among controls (P < 0.02). Early fetal growth delay was defined as a difference of six or more days between the menstrual gestational age and the sonographic gestational age (menstrual age minus ultrasound age).

Early growth delay was exhibited in fifteen control pregnancies (18.5%) and eleven insulin-requiring pregestational diabetic pregnancies (28.9%) (P = 0.02). However the incidence of congenital anomalies in these two groups was significantly different, but there was no difference between groups with and without growth delay. The longitudinal growth of two anomalous fetuses of the diabetic group and three anomalous fetuses from the control group was studied. Both groups of fetuses remained within the normal growth range for their respective groups.

This study described herein fails to confirm the association of early fetal growth delay with the occurrence of congenital malformations in insulin-requiring pregestational diabetic pregnancies.