Recurrent pregnancy loss (RPL) is a common complication in obstetrics, affecting about 5% of women of childbearing age. An increase in the number of abortions results in escalation in the risk of miscarriage. Although concentrated research has identified numerous causes for RPL, about 50% of them remain unexplained. Pregnancy is a complex process, comprising fertilization, implantation, organ and tissue differentiation, and fetal growth, which is effectively controlled by a number of both maternal and fetal factors. An example is the immune response, in which T cells and natural killer cells participate, and inflammation mediated by tumor necrosis factor or colony-stimulating factor, which hinders embryo implantation. Furthermore, vitamin D affects glucose metabolism and inhibits embryonic development, whereas microRNA has a negative effect on the gene expression of embryo implantation and development. This review examines the causes of RPL from multiple perspectives, and focuses on the numerous factors that may result in RPL.
Abortion, Habitual ; Abortion, Spontaneous ; Colony-Stimulating Factors ; Embryo Implantation ; Embryonic Development ; Female ; Fertilization ; Fetal Development ; Gene Expression ; Glucose ; Humans ; Inflammation ; Killer Cells, Natural ; Metabolism ; MicroRNAs ; Obstetrics ; Pregnancy ; Proteomics ; T-Lymphocytes ; Tumor Necrosis Factor-alpha ; Vitamin D

Fetal growth restriction (FGR) is characterized by fetal compromise and delayed neurological maturation. We report 3 cases of early FGR in the 26th week of gestation, based on hemodynamic Doppler monitoring, conventional cardiotocography, and non-invasive fetal electrocardiography (NI-FECG). Fetal heart rate variability (HRV), beat-to-beat variations, and fetal autonomic brain age scores (fABASs) were normal despite the absence of umbilical diastolic flow in the first case and the pregnancy continued to 30 weeks. NI-FECG helped achieve better fetal maturity. Fetal HRV and fABASs were low in the second and third cases. Fetal demise occurred soon in both cases. We conclude that NI-FECG could be a prospective method for the detection of fetal distress in early FGR.
Brain ; Cardiotocography ; Electrocardiography ; Embryonic and Fetal Development ; Female ; Fetal Death ; Fetal Development ; Fetal Distress ; Fetus ; Heart Rate, Fetal ; Hemodynamics ; Methods ; Pregnancy ; Prospective Studies

The “Barker hypothesis” postulates that a number of organ structures and associated functions undergo programming during embryonic and fetal life, which determines the set point of physiological and metabolic responses that carry into adulthood. Hence, any stimulus or insult at a critical period of embryonic and fetal development can result in developmental adaptations that produce permanent structural, physiological and metabolic changes, thereby predisposing an individual to cardiovascular, metabolic and endocrine disease in adult life. This article will provide evidence linking these diseases to fetal undernutrition and an overview of previous studies in this area as well as current advances in understanding the mechanism and the role of the placenta in fetal programming.
Adult ; Chronic Disease ; Critical Period (Psychology) ; Embryonic and Fetal Development ; Endocrine System Diseases ; Fetal Development* ; Fetal Nutrition Disorders ; Humans ; Malnutrition ; Placenta

The study aims to investigate the embryo-fetus development toxicity of the novel PPAR-δ agonist HS060098 on SD rats. The pregnant rats that were randomly divided into the solvent control group (1% hydroxypropyl methyl cellulose water solution) and HS060098 suspension groups (10, 30 and 100 mg x kg(-1) xd(-1)) were orally administered with HS060098 suspension or vehicle during the gestation of 6 -15 days (GD6-15). At termination (GD20), female rats were sacrificed. The pregnant females were evaluated by corpora lutea count, implantation sites, existence and death of embryos. Fetal sex, weight, externals, variations and malformations of viscus and skeleton were observed. The results show that there were no significant abnormality in maternal general conditions and fetal appearance as well as viscera, but in the 100 mg x kg(-1) x d(-1) group, the maternal weight gain decreased greatly (P < 0.01) and the skeletal ossification delayed remarkably (P < 0.01); in the 30 mg x kg(-1) xd(-1) group, the fatal and litter number of incompletely ossified sternebrae II was higher than those of the control group (P < 0.05); the skeletal malformations occurred in all dose groups, which indicate that the novel PPAR-δ agonist HS060098 had maternal toxicity and adversely effected fetal skeletal development under the experimental conditions.
Animals ; Bone and Bones ; drug effects ; Embryonic Development ; drug effects ; Female ; Fetal Weight ; PPAR delta ; agonists ; Pregnancy ; Rats ; Toxicity Tests

OBJECTIVETo observe the toxicity of hyperoside in rat embryo-fetal development, in order to provide preference for safe use of drugs during gestation period.

METHODHealthy pregnant rats were randomly divided into hyperosid groups (30, 175, 1000 mg x kg(-1) x d(-1)), the positive control group (cyclophosphamide, 7 mg x kg(-1) x d(-1)) and the solvent control group (1% aqueous carboxymethylcellulose). These rats were orally administered with hyperosid or vehicle during 6-15 d after gestation and subcutaneously injected with cyclophosphamide during 11-13 d. Maternal clinical sign, abortions, premature deliveries and body weight were monitored throughout gestation. At termination (gestation days 20), pregnant females were evaluated for clinical symposiums, weight change, corpora lutea count, existence and death of embryos; live fetuses were examined for gender, external, visceral and skeletal malformation and variations.

RESULTAll pregnant rats showed no significant abnormality in appearance, viscera and skeletal development. However, there was a difference between the high-dose group of hyperoside and negative control group in the fetus body weight, the length of the embryos and the length of tail (P < 0.05).

CONCLUSIONPregnant women are suggested to cautiously use hyperoside because it shows certain impact on development of fetal rats under the experimental conditions.

Abelmoschus ; chemistry ; Animals ; Drugs, Chinese Herbal ; toxicity ; Embryonic Development ; drug effects ; Female ; Fetal Development ; drug effects ; Litter Size ; drug effects ; Male ; Pregnancy ; Quercetin ; analogs & derivatives ; toxicity ; Rats ; Rats, Wistar

The safety of human exposure to an ever-increasing number and diversity of electromagnetic field (EMF) sources both at work and at home has become a public health issue. To date, many in vivo and in vitro studies have revealed that EMF exposure can alter cellular homeostasis, endocrine function, reproductive function, and fetal development in animal systems. Reproductive parameters reported to be altered by EMF exposure include male germ cell death, the estrous cycle, reproductive endocrine hormones, reproductive organ weights, sperm motility, early embryonic development, and pregnancy success. At the cellular level, an increase in free radicals and [Ca2+]i may mediate the effect of EMFs and lead to cell growth inhibition, protein misfolding, and DNA breaks. The effect of EMF exposure on reproductive function differs according to frequency and wave, strength (energy), and duration of exposure. In the present review, the effects of EMFs on reproductive function are summarized according to the types of EMF, wave type, strength, and duration of exposure at cellular and organism levels.
Animals ; DNA Breaks ; Electromagnetic Fields ; Embryonic Development ; Estrous Cycle ; Female ; Fetal Development ; Free Radicals ; Germ Cells ; Homeostasis ; Humans ; Magnets ; Male ; Organ Size ; Pregnancy ; Public Health ; Reproduction ; Sperm Motility

The safety of human exposure to an ever-increasing number and diversity of electromagnetic field (EMF) sources both at work and at home has become a public health issue. To date, many in vivo and in vitro studies have revealed that EMF exposure can alter cellular homeostasis, endocrine function, reproductive function, and fetal development in animal systems. Reproductive parameters reported to be altered by EMF exposure include male germ cell death, the estrous cycle, reproductive endocrine hormones, reproductive organ weights, sperm motility, early embryonic development, and pregnancy success. At the cellular level, an increase in free radicals and [Ca2+]i may mediate the effect of EMFs and lead to cell growth inhibition, protein misfolding, and DNA breaks. The effect of EMF exposure on reproductive function differs according to frequency and wave, strength (energy), and duration of exposure. In the present review, the effects of EMFs on reproductive function are summarized according to the types of EMF, wave type, strength, and duration of exposure at cellular and organism levels.
Animals ; DNA Breaks ; Electromagnetic Fields ; Embryonic Development ; Estrous Cycle ; Female ; Fetal Development ; Free Radicals ; Germ Cells ; Homeostasis ; Humans ; Magnets ; Male ; Organ Size ; Pregnancy ; Public Health ; Reproduction ; Sperm Motility

OBJECTIVETo investigate the potential developmental toxicity of Radix Ophiopogonis decoction in SD rats.

METHODTimed-pregnant SD rats were given Radix Ophiopogonis decoction (26.9 g x kg(-1)) or vehicle (distilled water) by gavage on gestation days 6-17. Maternal clinical sign, abortions, premature deliveries, and body weight were monitored throughout gestation. At termination (gestation days 20) pregnant females were evaluated for clinical status and gestational outcome; live fetuses were examined for gender, external, visceral and skeletal malformation and variations.

RESULTNo deaths, premature deliveries or dose-related clinical signs were attributed to Radix Ophiopogonis decoction. Maternal body weight and body weight gain were not affected. There were no effects on fetus weight and viability, incidences of fetal malformation and variation.

CONCLUSIONThese results demonstrated that Radix Ophiopogonis decoction had no detectable adverse effects in either the treated F0 female rats or the fetuses.

Animals ; Body Weight ; drug effects ; Drugs, Chinese Herbal ; administration & dosage ; adverse effects ; Embryonic Development ; drug effects ; Female ; Fetal Development ; drug effects ; Fetal Weight ; drug effects ; Humans ; Male ; Models, Animal ; Ophiopogon ; chemistry ; Pregnancy ; Random Allocation ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo observe the effect of Cinnabaris on mouse embryos after pregnant mice were treated by Cinnabaris in different periods of pregnancy.

METHODTwo separate experiments were performed: First, Cinnabaris was orally given into pregnant mice at the doses of 0.08, 0.4, 4.0 g x kg(-1) from D6 to D19 after pregnancy; Second, Cinnabaris was orally given into mice at the same doses mentioned above from D14 prior to pregnancy until D19 after pregnancy. All animals were sacrificed on D 20 of pregnancy by caesarean section. The numbers of survival, dead and absorbed fetuses were calculated and the survival fetus weight was measured. The survival fetuses were treated by two methods: One third survival fetuses were fixed and stained by Bouin solution for organ examination and the remaining two thirds fetuses were stained for skeleton examination.

RESULTNo obvious embryo toxicity was observed in the first experiment at Cinnabaris dose levels of 0.08, 0.4, or 4 g x kg(-1) x d(-1). There was no significant effect on embryonic development and the numbers of the survival, dead and absorbed fetus. No obvious malformations on appearance, organ, and skeleton examination of fetuses were found. The second experiment showed that the rates of abortion and absorbed fetus in 0.4, 4 g x kg(-1) x d(-1) Cinnabaris group were higher but without statistical significance compared with control group. Appearance and organ examination of Cinnabaris groups fetus showed no obvious malformation, but skeleton malformation was found in 0.4, 4 g x kg(-1) x d(-1) groups (the rates of skeleton malformation were 46.7% and 77.8%, respectively).

CONCLUSIONNo obvious embryonic development toxicity was observed when Cinnabaris was orally given in intermediate and late pregnant period, but the embryos in the early stage of pregnancy was more sensitive to Cinnabaris. When Cinnabaris was given prior to pregnancy until the whole period of pregnancy, it may be harmful for the fetuses at above the dose level 0.08 g x kg(-1) x d(-1) (equivalent to 5 times clinical intake dose), both in a dose-dependent manner.

Animals ; Drugs, Chinese Herbal ; toxicity ; Embryo, Mammalian ; Embryonic Development ; drug effects ; Female ; Fetal Development ; drug effects ; Mice ; Mice, Inbred ICR ; Models, Animal ; Pregnancy

The "Barker hypothesis" postulates that a number of organ structures and associated functions undergo programming during embryonic and fetal life, which determines the set pont of physiological and metabolic responses that carry into adulthood. Hence, stimulus or insult at a critical period of embryonic and fetal development, can result in developmental adaptations that produce permanent structural physiological, and metabolic changes, thereby predisposing an individual to cardiovascular, metabolic and endocrine disease in adult life. This article will provide an evidence linking these disease to fetal undernutrition and an overview of previous studies in this area, the current advances in understanding the mechanism and the role of the placenta in fetal programming.
Adult ; Critical Period (Psychology) ; Embryonic and Fetal Development ; Endocrine System Diseases ; Fetal Development* ; Humans ; Malnutrition ; Placenta