成人疾病发育起源的机制探讨

宫内生长发育是复杂的动态过程,这一过程受到胎儿本身遗传因素的控制和影响,只有当母亲营养充足,胎盘功能良好足以维持胎儿的高效增殖、生长和分化时,胎儿才能依其生长轨迹生长发育.健康和疾病发育起源或发育程序化概念的提出,反映了在生长发育关键时期的刺激或损伤可造成胎儿关键器官和组织长期的发育和生理性的改变.传统观念认为受到成人...     

宫内营养对胎儿心血管健康的远期影响

宫内生长发育是复杂的动态过程,这一过程受到胎儿本身遗传因素的控制和影响,只有当母亲营养充足,胎盘功能良好足以维持胎儿的高效增殖、生长和分化时,胎儿才能依其生长轨迹生长发育。能量和（或）蛋白质的摄入情况对胎儿发育起着重要的决定作用。宫内营养不均衡包括营养不足和营养过剩。越来越多的证据表明宫内营养不均衡对胎儿远期的心血管健康造成了负面影响。宫内营养不均衡直接影响子代的血管结构及功能并增加子代心血管代谢异常的危险,从而影响子代的血管健康。母体营养不良可能导致胎儿生长受限;同样,母体的代谢性疾病,如胰岛素抵抗、糖尿病、高血压、血脂异常也会增加子代发生动脉粥样硬化和心血管疾病的风险。     

定制出生体重标准在胎儿生长受限及小于胎龄儿诊断中的应用

胎儿发育受限（fetal growth restriction,FGR）是产科重要并发症之一,也是造成围产儿死亡的重要原因,胎儿在宫内的生长发育受到遗传、营养、子宫-胎盘血液灌流量及胎儿-胎盘功能等多因素的影响,任何因素影响了胎儿与胎盘间的母-儿血循环及物质交换,均可导致发生胎儿宫内生长受限。     

母体营养物质代谢与胎儿发育

孕妇的内分泌和代谢方面的改变是为维持妊娠、胎儿发育和产后哺乳准备适当条件.胎儿生长发育所需要的营养物质直接由母体供给,尤在妊娠后期胎儿发育迅速,需要的营养物质更多,母体的代谢改变也最明显.了解此阶段母体代谢的改变和营养需要,对保证胎儿正常发育生长,防止或治疗宫内生长迟缓有重要意义.本文介绍母体几种重要营养物质代谢及其与胎儿发育的关     

生殖道发育异常对女性生育的影响及其结局

正女性生殖道发育异常从简单到复杂多种多样。在女性胚胎发育时期,如受到某些内源性(如基因或染色体异常)或外源性因素(如使用性激素类药物)的影响,副中肾管或中肾旁管在形成、融合、再吸收过程中出现障碍,就可导致各种生殖道发育异常。生殖道发育异常对女性生育功能及妊娠结局都有重要影响,可能导致不孕、流产、胎位异常、胎儿发育异常、胎儿生长受限、胎盘早剥、产程异常、产后出血、胎盘滞留等一系列不良妊娠事件。其中子宫发育     

胰岛素样生长因子系统在胎儿生长发育中的作用

胰岛素样生长因子(insulin-like growth factors,IGFs)作为一类多功能的促生长调节因子,在细胞的增殖、分裂以及个体的生长、发育中具有重要的促进作用。IGFs分为1型和2型,主要通过与IGF-1受体结合,参与调控妊娠过程中滋养细胞侵袭、物质转运、胎盘血管重塑以及胎儿生长发育等一系列重要生理过程。其中,IGF-1、IGF-2及其相关受体的表达和功能异常可导致胎盘功能不全及胎儿功能生长受限。深入了解IGFs与胎儿生长发育之间的关系对研究胎盘功能代谢、物质转运、胎儿生长发育等具有重要意义。     

正常妊娠羊水表皮生长因子水平的变化及意义

胎儿、胎盘的生长、发育和成熟是一个极其复杂的过程,多种因子参与了这一过程的调节1。表皮生长因子（EGF）是一种多功能的生长激素,对维持正常妊娠和胎儿生长发育是必需的,EGF缺乏可导致胎儿丢失或生长迟缓[1-6]。羊水中的表皮生长因子通过胎儿的吞咽和呼吸样运动,与胎儿的消化道和呼吸道直接接触,但其变化规律以及对胎儿生长、器官发育和功能成熟的作用和意义尚未明确。作者检测136例妊娠13～42周正常孕妇的羊水表皮生长因子浓度,观察正常妊娠羊水表皮生长因子水平随孕周的变化;探讨羊水表皮生长因子的作用和意义。一、资料与方…     

大气污染对胎儿发育的影响

以往认为,胎儿由于受到母体气血屏障、子宫、胎盘屏障等多重保护,大气污染对胎儿发育过程的影响微乎其微,故未引起重视.但近年观察证实,大气污染物是导致胎儿发育异常、低出生体重(low brith weight,LBW)、早产等胎儿生长和出生异常的危险因素[1].     

胎盘发育机制的研究进展

胎盘是母体与胎儿之间重要的交流器官,其正常发育对胎儿的生长发育至关重要。胎盘的形成和发育受性别、表观遗传学及外界环境等诸多因素的影响,如不同性别胚胎会影响不同的性激素基因在各自胎盘中的表达,X染色体连锁基因中的性激素合成基因STS倾向于在女性胎儿的胎盘中表达;LHB-CGB基因簇的表达也倾向于女性胎儿的胎盘,其表达产物黄体生成激素、人绒毛膜促性腺激素(hCG)与胎盘的生长、侵袭、血管生成等密切相关。表观遗传学甲基化的重建过程影响胎盘的早期发育,如在胚胎发育早期抑制DNA的甲基化过程会破坏胎盘滋养层的增殖和迁移。另外,胎盘的生长需要充足的有氧环境,氧含量的下降会通过诱导缺氧诱导因子(HIF)活性的增加直接影响胎盘的体积、发育及成熟。综述胎盘发育过程中的一系列变化及这些变化对胎盘功能的影响,可为阐明胚胎发育机制提供必要的理论基础,同时也为母婴安全提供重要保障。     

胎盘发育机制的研究进展

胎盘是母体与胎儿之间重要的交流器官,其正常发育对胎儿的生长发育至关重要。胎盘的形成和发育受性别、表观遗传学及外界环境等诸多因素的影响,如不同性别胚胎会影响不同的性激素基因在各自胎盘中的表达,X染色体连锁基因中的性激素合成基因STS倾向于在女性胎儿的胎盘中表达;LHB-CGB基因簇的表达也倾向于女性胎儿的胎盘,其表达产物黄体生成激素、人绒毛膜促性腺激素(hCG)与胎盘的生长、侵袭、血管生成等密切相关。表观遗传学甲基化的重建过程影响胎盘的早期发育,如在胚胎发育早期抑制DNA的甲基化过程会破坏胎盘滋养层的增殖和迁移。另外,胎盘的生长需要充足的有氧环境,氧含量的下降会通过诱导缺氧诱导因子(HIF)活性的增加直接影响胎盘的体积、发育及成熟。综述胎盘发育过程中的一系列变化及这些变化对胎盘功能的影响,可为阐明胚胎发育机制提供必要的理论基础,同时也为母婴安全提供重要保障。     

Human fetal growth and organ development: 50 years of discoveries

Knowledge about human fetal growth and organ development has greatly developed in the last 50 years. Anatomists and physiologists had already described some crucial aspects, for example, the circulation of blood during intrauterine life through the fetal heart, the liver as well as the placenta. However, only in the last century physiologic studies were performed in animal models. In the human fetus, the introduction of ultrasound and Doppler velocimetry has provided data about the growth and development of the fetus and of the circulation through the different fetal districts. Moreover, in the last 2 decades we have learned about fetal oxygenation and fetal nutrient supply caused by the availability of fetal blood samples obtained under relatively steady state conditions. These studies, together with studies using stable isotope methodologies, have clarified some aspects of the supply of the major nutrients for the fetus such as glucose, amino acids, and fatty acids. At the same time, the relevance of placental function has been recognized as a major determinant of fetal diseases leading to intrauterine growth restriction. More recently, the availability of new tools such as 3-dimensional ultrasound and magnetic resonance imaging, have made possible the evaluation of the growth and development of fetal organs. This knowledge in the healthy fetus will improve the ability of clinicians to recognize abnormal phenotypes of the different fetal organs, thus allowing to stage fetal diseases.     

Metabolic requirements for fetal growth.

Table 1 outlines a metabolic balance sheet for the sheep fetus. It is clear that maternal substrate concentrations as well as placental function are important in assuring the provision of adequate substrate to meet fetal metabolic and growth requirements. It is intriguing that the fetus appears to use substrates not usually regarded as important in extrauterine diets (lactate) and to use substrates for catabolic purposes normally thought to be primarily anabolic substrates (amino acids). This information emphasizes the hazards of extrapolating metabolic and nutritional patterns seen in extrauterine life in reaching conclusions concerning the fetus. It likewise emphasizes the importance of ongoing studies in maternal and fetal nutrition and metabolism.     

Sinusoidal-like Fetal Heart Rate Tracing in a Case of Acute Fetomaternal Haemorrhage

EDITORIAL COMMENT: This case indicates that when fetomaternal haemorrhage is the cause of critical fetal reserve as observed by cardiotocography the fetus may be doomed in spite of prompt delivery by emergency Caesarean section, although there are reports of successful fetal outcome with immediate delivery in such cases. The moral of this case report is that cardiotocographic evidence of reduced fetal reserve of any degree indicates delivery when the pregnancy is at term, especially when there are other complications, such as fetal growth retardation.     

Intrauterine Growth Restriction (IUGR): Etiology and Diagnosis

Intrauterine growth restriction (IUGR) is associated with perinatal morbidity and mortality. IUGR is defined as fetus that fails to achieve his growth potential. Antenatal small for gestational age (SGA) is defined as fetus with weight <10th percentile. IUGR and SGA are commonly used interchangeably. The identification of IUGR is important. IUGR identification begins with assessment of risk factor(s), and the diagnosis is made by ultrasound using biometry when this confirms an estimated fetal weight (EFW) of <10th percentile. The common risk factors include maternal causes (hypertension, diabetes, cardiopulmonary disease, anemia, malnutrition, smoking, drug use), fetal causes (genetic disease including aneuploidy, congenital malformations, fetal infection, multiple pregnancies), and placental causes (placental insufficiency, placental infarction, placental mosaicism). Intrauterine growth determines the perinatal, postnatal, and adult life development. IUGR is associated with increased risk of development in adult life of metabolic diseases including but not limited to hypertension, diabetes, obesity, dyslipidemia, and the metabolic syndrome.     

Maternal serum activin A and the prediction of intrauterine growth restriction

BACKGROUND: Differentiating between the small healthy fetus and the high risk growth restricted fetus remains a significant obstetric challenge. It has been previously shown that maternal activin A levels are increased in association with fetal growth restriction. AIM: To evaluate maternal serum activin A as a marker of fetal growth restriction. METHODS: Prospective cohort study of 62 women referred for fetal assessment because of a clinical suspicion of a small for gestation fetus. Maternal serum levels of activin A were measured with an ELISA. RESULTS: Activin A levels, expressed as median (95% CI) MoMs, were similar in the women with a normal-sized fetus and in those with a healthy small for gestational age fetus, 1.14 (95% CI 1.0-1.5) and 1.31 (95% CI 0.8-2.1), respectively (P = 0.97). Compared to the women with a normal-sized fetus or a healthy small fetus, activin A levels were significantly elevated in the women who had an intrauterine fetal growth restriction fetus 2.37 (95% CI 1.6-3.7; P = 0.01 compared to normal and P = 0.04 compared to healthy small). CONCLUSIONS: These data confirm that circulating activin A is increased in association with fetal growth restriction. However, a single blood sample for activin A will not efficiently discern between healthy and compromised small fetuses.     

Amniotic fluid assessment

The mysterious environment surrounding the fetus for much of his or her life is now being explored with increasing fervor. Assessment of amniotic fluid in the early portion of pregnancy is now possible for fetal karyotype determination. This may permit early diagnosis of abnormal fetuses, increasing the options for patients. As pregnancy progresses, high-resolution ultrasound assessment of amniotic fluid volume is integral to the management of pregnancies at risk for oligohydramnios. Such pregnancies include those who are postdate and those with suspected intrauterine growth retardation. Additional evaluation and ultrasonography are recommended for evaluation of the fetus in this clinical situation. With either hydramnios or oligohydramnios, careful ultrasound assessment of the fetus is essential to rule out significant congenital malformations. Finally, the use of ultrasound-directed amniocentesis in later pregnancy permits an assessment of fetal lung maturity and of the fetus at risk for Rhesus immunization. Attention to detail should increase chances of a successful pregnancy outcome while decreasing neonatal morbidity and mortality.     

胎儿死亡的胎盘病理

人类胎盘是一个妊娠期的临时器官,对胎儿发育和正常妊娠的维持起重要作用。妊娠期间,胎盘在母体和胎儿间建立沟通的桥梁,为胎儿提供营养物质,进行气体交换和废物清除,并建立免疫耐受环境,保障半异体胎儿不被母体排斥;胎盘还可作为妊娠期重要的内分泌器官,协调胎儿发育及母体多器官的妊娠适应性应答。胎盘发育不良往往导致胎儿生长异常及多种妊娠并发症,严重情况下可导致胎儿死亡。文章阐述了生理状况下人类胎盘的结构和功能,描述了因胎儿生长受限(FGR)、子痫前期(PE)、妊娠期糖尿病(GDM)等造成胎儿死亡的胎盘病理特征,进而展望通过靶向胎盘干预妊娠期疾病的可能前景。     

Role of fetal catecholamines before and during birth

It is true that developing fetus in uterus may be mostly influenced by maternal conditions. However, there is little evidence to prove the existence of nervous connection between fetus and mother. The biochemical and physiological phenomena of fetus in utero may be controlled mainly by fetal autonomy with nutritional supply from mother. The sympathoadrenal system of fetus has received much attention with the technical progress of catecholamine assays. Fetal plasma catecholamine concentrations during birth are remarkably higher than those in adult life. The function of those high catecholamine concentrations has been shown to control fetal circulation during hypoxia, to maintain glucose supply to the heart and brain, and to prepare the lung for ventilation. So it may be said that fetal plasma catecholamine surge at birth is essential to neonatal adaptation. Amniotic fluid catecholamines and their metabolites were higher in intrauterine growth retarded fetus, which consumed own catecholamine reserve in adrenal medulla before parturition. It is possible to estimate the fetal condition by measuring the concentration of catecholamines and their metabolites in amniotic fluid. The amniotic norepinephrine, epinephrine and particularly dopamine concentration has been found to increase toward term. The rise in dopamine has been assumed to stimulate intrauterine synthesis of prostaglandins. We demonstrated that L-dopa was metabolized to dopamine in fetal kidney and that dopamine in amniotic fluid was originated from fetal urine.     

Review: Alterations in placental glycogen deposition in complicated pregnancies: Current preclinical and clinical evidence

Normal placental function is essential for optimal fetal growth. Transport of glucose from mother to fetus is critical for fetal nutrient demands and can be stored in the placenta as glycogen. However, the function of this glycogen deposition remains a matter of debate: It could be a source of fuel for the placenta itself or a storage reservoir for later use by the fetus in times of need. While the significance of placental glycogen remains elusive, mounting evidence indicates that altered glycogen metabolism and/or deposition accompanies many pregnancy complications that adversely affect fetal development. This review will summarize histological, biochemical and molecular evidence that glycogen accumulates in a) placentas from a variety of experimental rodent models of perturbed pregnancy, including maternal alcohol exposure, glucocorticoid exposure, dietary deficiencies and hypoxia and b) placentas from human pregnancies with complications including preeclampsia, gestational diabetes mellitus and intrauterine growth restriction (IUGR). These pregnancies typically result in altered fetal growth, developmental abnormalities and/or disease outcomes in offspring. Collectively, this evidence suggests that changes in placental glycogen deposition is a common feature of pregnancy complications, particularly those associated with altered fetal growth.