Showing papers on "Fetus published in 2015"
TL;DR: The definition, pathogenesis, grading and staging, and clinical significance of the most common lesions in placental disease are reviewed and diagrams of the mechanisms of disease are provided.
612 citations
TL;DR: The placenta is arguably the most important organ of the body, but paradoxically the most poorly understood, during its transient existence, it performs actions that are later taken on by diverse separate organs, including the lungs, liver, gut, kidneys and endocrine glands.
Abstract: The placenta is arguably the most important organ of the body, but paradoxically the most poorly understood. During its transient existence, it performs actions that are later taken on by diverse separate organs, including the lungs, liver, gut, kidneys and endocrine glands. Its principal function is to supply the fetus, and in particular, the fetal brain, with oxygen and nutrients. The placenta is structurally adapted to achieve this, possessing a large surface area for exchange and a thin interhaemal membrane separating the maternal and fetal circulations. In addition, it adopts other strategies that are key to facilitating transfer, including remodelling of the maternal uterine arteries that supply the placenta to ensure optimal perfusion. Furthermore, placental hormones have profound effects on maternal metabolism, initially building up her energy reserves and then releasing these to support fetal growth in later pregnancy and lactation post-natally. Bipedalism has posed unique haemodynamic challenges to the placental circulation, as pressure applied to the vena cava by the pregnant uterus may compromise venous return to the heart. These challenges, along with the immune interactions involved in maternal arterial remodelling, may explain complications of pregnancy that are almost unique to the human, including pre-eclampsia. Such complications may represent a trade-off against the provision for a large fetal brain.
402 citations
TL;DR: The major viral infections relevant to pregnancy are reviewed and potential mechanisms for the associated adverse pregnancy outcomes are offered.
Abstract: Viral infections during pregnancy have long been considered benign conditions with a few notable exceptions, such as herpes virus. The recent Ebola outbreak and other viral epidemics and pandemics show how pregnant women suffer worse outcomes (such as preterm labor and adverse fetal outcomes) than the general population and non-pregnant women. New knowledge about the ways the maternal-fetal interface and placenta interact with the maternal immune system may explain these findings. Once thought to be 'immunosuppressed', the pregnant woman actually undergoes an immunological transformation, where the immune system is necessary to promote and support the pregnancy and growing fetus. When this protection is breached, as in a viral infection, this security is weakened and infection with other microorganisms can then propagate and lead to outcomes, such as preterm labor. In this manuscript, we review the major viral infections relevant to pregnancy and offer potential mechanisms for the associated adverse pregnancy outcomes.
382 citations
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TL;DR: The placenta is a highly complex and fascinating organ as discussed by the authors, which acts as lungs, gut, kidneys, and liver of the fetus during the course of a pregnancy and has major endocrine actions that modulate maternal physiology and metabolism and provides a safe and protective milieu in which the fetus can develop.
207 citations
TL;DR: How adverse influences during fetal life and early development program an increased risk for cardiovascular disease including high blood pressure and the underlying mechanisms that contribute to the fetal origins of cardiovascular pathology are highlighted are highlighted.
Abstract: Low birth weight serves as a crude proxy for impaired growth during fetal life and indicates a failure for the fetus to achieve its full growth potential. Low birth weight can occur in response to numerous etiologies that include complications during pregnancy, poor prenatal care, parental smoking, maternal alcohol consumption, or stress. Numerous epidemiological and experimental studies demonstrate that birth weight is inversely associated with blood pressure and coronary heart disease. Sex and age impact the developmental programming of hypertension. In addition, impaired growth during fetal life also programs enhanced vulnerability to a secondary insult. Macrosomia, which occurs in response to maternal obesity, diabetes, and excessive weight gain during gestation, is also associated with increased cardiovascular risk. Yet, the exact mechanisms that permanently change the structure, physiology, and endocrine health of an individual across their lifespan following altered growth during fetal life are not entirely clear. Transmission of increased risk from one generation to the next in the absence of an additional prenatal insult indicates an important role for epigenetic processes. Experimental studies also indicate that the sympathetic nervous system, the renin angiotensin system, increased production of oxidative stress, and increased endothelin play an important role in the developmental programming of blood pressure in later life. Thus, this review will highlight how adverse influences during fetal life and early development program an increased risk for cardiovascular disease including high blood pressure and provide an overview of the underlying mechanisms that contribute to the fetal origins of cardiovascular pathology.
171 citations
TL;DR: This review describes the current landscape of clinical, biochemical, and engineering concepts associated with the mechanical function of the cervix during pregnancy and aims to develop a common translational language and inspire novel approaches to delineate normal and abnormal cervical function in pregnancy.
167 citations
TL;DR: It is suggested that each gestational week has significance for child’s subsequent neurodevelopment and risk for ADHD and showed that poor fetal growth increased the risk of ADHD.
Abstract: BACKGROUND: Previous studies have shown an association between prematurity and attention-deficit/hyperactivity disorder (ADHD). Results concerning late preterm infants are controversial, and studies examining fetal growth represented by weight for gestational age are scarce. Our objective was to examine the association between gestational age by each week of fetal maturity, weight for gestational age, and ADHD. METHODS: In this population-based study, 10 321 patients with ADHD, diagnosed according to the International Classification of Diseases and 38 355 controls individually matched for gender, date and place of birth, were identified from Finnish nationwide registers. Perinatal data were obtained from the Finnish Medical Birth Register. Conditional logistic regression was used to examine the association between gestational age, weight for gestational age, and ADHD after controlling for confounding factors. RESULTS: The risk of ADHD increased by each declining week of gestation. The associations were robust after adjusting for confounders. An elevated risk also was seen among late preterm and early term infants. As for fetal growth, the odds ratio showed a U-shaped curve with an increased risk seen when the weight for gestational age was 1 SD below and 2 SD above the mean. CONCLUSIONS: Our findings suggest that each gestational week has significance for child’s subsequent neurodevelopment and risk for ADHD. We also showed that poor fetal growth increased the risk of ADHD. This highlights the importance of taking into account both prematurity and poor fetal growth when planning the timing of birth as well as later follow-up and support policies.
167 citations
TL;DR: It is found that B cell development precedes T cell development and that repertoire maturation is both temporally and spatially regulated in the human fetus.
Abstract: Insights into the ontogeny of the human fetal adaptive immune system are of great value for understanding immunocompetence of the developing fetus. However, to date, this has remained largely uncharted territory, in large part because blood samples from healthy, early gestation fetuses have been hard to come by. In a comprehensive study, we analyzed levels of T cell receptor excision circles (TRECs), signal-joint κ receptor excision circles (sjKRECs), and intron recombination signal sequence–K-deleting element (iRSS-Kde) rearrangement, and T and B lymphocyte repertoire clonality in human fetuses from 12 to 26 weeks of gestational age. Using next-generation sequencing, we analyzed the diversity and complexity of T cell receptor β ( TRB ) and immunoglobulin heavy chain ( IGH ) repertoires in four fetuses at 12, 13, 22, and 26 weeks of gestation and in healthy full-term infants. We report the progressive increase of TREC, sjKREC, and iRSS-Kde levels over time and confirm that B cell development precedes T cell development in the human fetus. Temporally and spatially regulated maturation of B and T cell repertoire diversity and complexity during human fetal development was observed, including evidence that immunoglobulin somatic hypermutation and class switch recombination occur already during intrauterine life. Our results help define physiological levels of immunodeficiency in premature infants and may serve as a reference for future studies aimed at investigating the impact of intrauterine pathologies on fetal immune development and function.
141 citations
TL;DR: Oxidative stress in general, and more specifically fetal hemoglobin-induced oxidative stress, could play a key role in the pathology of preeclampsia seen both in the placenta and ultimately in the maternal endothelium.
Abstract: Preeclampsia is a leading cause of pregnancy complications and affects 3-7% of pregnant women. This review summarizes the current knowledge of a new potential etiology of the disease, with a special focus on hemoglobin-induced oxidative stress. Furthermore, we also suggest hemoglobin as a potential target for therapy. Gene and protein profiling studies have shown increased expression and accumulation of free fetal hemoglobin in the preeclamptic placenta. Predominantly due to oxidative damage to the placental barrier, fetal hemoglobin leaks over to the maternal circulation. Free hemoglobin and its metabolites are toxic in several ways; (a) ferrous hemoglobin (Fe(2+)) binds strongly to the vasodilator nitric oxide (NO) and reduces the availability of free NO, which results in vasoconstriction, (b) hemoglobin (Fe(2+)) with bound oxygen spontaneously generates free oxygen radicals, and (c) the heme groups create an inflammatory response by inducing activation of neutrophils and cytokine production. The endogenous protein α1-microglobulin, with radical and heme binding properties, has shown both ex vivo and in vivo to have the ability to counteract free hemoglobin-induced placental and kidney damage. Oxidative stress in general, and more specifically fetal hemoglobin-induced oxidative stress, could play a key role in the pathology of preeclampsia seen both in the placenta and ultimately in the maternal endothelium.
127 citations
TL;DR: There is a biochemical basis for the increased risk of respiratory distress syndrome in male infants, and it is concluded that female infants had higher indexes of pulmonary maturity than did male Infants.
Abstract: It has been recognized that male infants are at greater risk of respiratory distress syndrome than are female infants. Amniotic fluid was obtained from 73 male and 76 female fetuses between 28 and 40 wk of gestation. To assess fetal pulmonary maturity, we determined the lecithin-sphingomyelin ratio and concentrations of saturated phosphatidyl choline and cortisol in all of these fluids. Analysis of covariance showed that female infants had higher indexes of pulmonary maturity than did male infants. The difference in degree of fetal pulmonary maturity was 1.2 to 2.5 wk, on the basis of these measurements, with females ahead of males. We conclude that there is a biochemical basis for the increased risk of respiratory distress syndrome in male infants.
117 citations
TL;DR: Sufficient fetal DNA in a maternal plasma sample is required for accurate aneuploidy detection via noninvasive prenatal testing, thus highlighting a need to understand the factors affecting fetal fraction.
Abstract: Objective
Sufficient fetal DNA in a maternal plasma sample is required for accurate aneuploidy detection via noninvasive prenatal testing, thus highlighting a need to understand the factors affecting fetal fraction.
Method
The MaterniT21™ PLUS test uses massively parallel sequencing to analyze cell-free fetal DNA in maternal plasma and detect chromosomal abnormalities. We assess the impact of a variety of factors, both maternal and fetal, on the fetal fraction across a large number of samples processed by Sequenom Laboratories.
Results
The rate of increase in fetal fraction with increasing gestational age varies across the duration of the testing period and is also influenced by fetal aneuploidy status. Maternal weight trends inversely with fetal fraction, and we find no added benefit from analyzing body mass index or blood volume instead of weight. Strong correlations exist between fetal fractions from aliquots taken from the same patient at the same blood draw and also at different blood draws.
Conclusion
While a number of factors trend with fetal fraction across the cohort as a whole, they are not the sole determinants of fetal fraction. In this study, the variability for any one patient does not appear large enough to justify postponing testing to a later gestational age. © 2015 John Wiley & Sons, Ltd.
TL;DR: BPA concentrations, BPA-specific metabolizing enzyme gene expression, and global DNA methylation were characterized across three matched tissues from elective pregnancy terminations of 2nd trimester human fetuses, suggesting organ-specific biological effects after fetal exposure.
TL;DR: In contrast to the response to acute hypoxemia, data show that there is a redistribution of blood flow to the adrenals and temporal lobe, but not the heart or whole brain, in chronically hypoxemic PR fetuses in late gestation.
Abstract: In the fetus, there is a redistribution of cardiac output in response to acute hypoxemia, to maintain perfusion of key organs, including the brain, heart, and adrenal glands. There may be a similar redistribution of cardiac output in the chronically hypoxemic, intrauterine growth-restricted fetus. Surgical removal of uterine caruncles in nonpregnant ewe results in the restriction of placental growth (PR) and intrauterine growth. Vascular catheters were implanted in seven control and six PR fetal sheep, and blood flow to organs was determined using microspheres. Placental and fetal weight was significantly reduced in the PR group. Despite an increase in the relative brain weight in the PR group, there was no difference in blood flow to the brain between the groups, although PR fetuses had higher blood flow to the temporal lobe. Adrenal blood flow was significantly higher in PR fetuses, and there was a direct relationship between mean gestational PaO2 and blood flow to the adrenal gland. There was no change in blood flow, but a decrease in oxygen and glucose delivery to the heart in the PR fetuses. In another group, there was a decrease in femoral artery blood flow in the PR compared with the Control group, and this may support blood flow changes to the adrenal and temporal lobe. In contrast to the response to acute hypoxemia, these data show that there is a redistribution of blood flow to the adrenals and temporal lobe, but not the heart or whole brain, in chronically hypoxemic PR fetuses in late gestation.
TL;DR: It is unknown whether the sex of the fetus differentially alters the maternal immune milieu, potentially contributing to the observed differences.
Abstract: Problem
Several pregnancy complications have disparities based on the sex of the fetus It is unknown whether the sex of the fetus differentially alters the maternal immune milieu, potentially contributing to the observed differences
Method of study
Using maternal plasma collected during 38 uncomplicated pregnancies (19 males, 19 females), we compared levels of cytokines, sex hormones, and angiogenic factors throughout gestation and postpartum
Results
Male fetal sex was associated with higher levels of proinflammatory cytokines (G-CSF, IL-12p70, IL-21, and IL-33) and angiogenic factors (PlGF and VEGF-A) compared with female fetal sex at multiple timepoints Female fetal sex was associated with higher levels of regulatory cytokines (IL-5, IL-9, IL-17, and IL-25) IL-27 increased throughout pregnancy regardless of fetal sex There was no fetal sex-based difference in analyte concentrations at the postpartum measurement
Conclusion
Women carrying a male fetus exhibit a more proinflammatory/proangiogenic immune milieu than women carrying a female fetus
TL;DR: HCQ reduces neonatal morbidity in women with SLE by significantly decreasing the rate of prematurity and intrauterine growth restriction.
Abstract: ObjectiveThe aim of this study was to evaluate the effect of hydroxychloroquine (HCQ) on fetal preterm delivery and intrauterine growth restriction (IUGR) in a cohort of pregnant women with systemic lupus erythematosus (SLE).MethodsOver an 11-year period (January 1, 2001 to December 31, 2011), all women with SLE and admitted to deliver after 22 weeks of gestation to Bordeaux University Hospital (France), were retrospectively enrolled in the present study. The population was then split into two groups based on the treatment they received: HCQ exposed (HCQ+) versus HCQ non-exposed (HCQ−) group.Results118 pregnancies were included, 41 in the HCQ+ group and 77 in the HCQ− group. The rate of adverse fetal outcome was significantly lower in the HCQ+ group (p = 0.001), particularly in terms of preterm delivery, 15.8 % versus 44.2 % (p = 0.006), and IUGR, 10.5 % versus 28.6 % (p = 0.03). No adverse outcomes were reported in the HCQ+ group.ConclusionHCQ reduces neonatal morbidity in women with SLE by significantly...
TL;DR: If the infant commences breathing, aerates its lungs and increases pulmonary blood flow before the umbilical cord is clamped, then pulmonary venous return can immediately take over the supply of left ventricular preload upon cord clamping, and there is no intervening period of reduced preload and cardiac output and the large swings in arterial pressures and flows are reduced leading to a more stable circulatory transition.
Abstract: Umbilical cord clamping at birth has a major impact on an infant's cardiovascular system that varies in significance depending upon whether the infant has commenced breathing. As umbilical venous return is a major source of preload for the left ventricle during fetal life, recent experimental evidence has shown that clamping the umbilical cord severely limits cardiac venous return in the absence of pulmonary ventilation. As a result, cardiac output greatly reduces and remains low until breathing commences. Once the infant begins breathing, aeration of the lung triggers a large increase in pulmonary blood flow, which replaces umbilical venous return as the source of preload for the left ventricle. As a result, cardiac output markedly increases, as indicated by an increase in heart rate immediately after birth. Thus, infants born apnoeic and hypoxic and have their cords immediately clamped, are likely to have a restricted cardiac output combined with hypoxia. As increased cardiac output is a major physiological defence mechanism that counteracts the effects of hypoxaemia, limiting the increase in cardiac output exposes the infant to ischaemia along with hypoxia. However, if the infant commences breathing, aerates its lungs and increases pulmonary blood flow before the umbilical cord is clamped, then pulmonary venous return can immediately take over the supply of left ventricular preload upon cord clamping. As a result, there is no intervening period of reduced preload and cardiac output and the large swings in arterial pressures and flows are reduced leading to a more stable circulatory transition.
TL;DR: In this article, the effects of prenatal maternal life stressors on neonatal birth outcomes, neurobehavioral development, and stress-related hormones levels were investigated, and the findings showed that maternal life-stressors during pregnancy negatively affect fetal birth outcomes and affect neonates' cord plasma ACTH, cortisol, norepinephrine, and epinephrine.
Abstract: Background Relatively few studies have been made on neurobehavioral outcomes of prenatal maternal stress during the newborn period, and little research has focused on umbilical cord stress hormones including cortisol, adrenocorticotropic hormone (ACTH), norepinephrine, and epinephrine. Our objective was to investigate the effects of prenatal maternal life stressors on neonatal birth outcomes, neurobehavioral development, and stress-related hormones levels. Methods Participants were 142 mothers and their infants; 71 were selected as the prenatal life stressor exposed group and 71 as the control group matched on maternal age, gestational week, delivery type, socioeconomic and education status, and newborns' sex. Maternal life stressors during pregnancy were determined using the Life Events Scale for Pregnant Women. Neonatal neurobehavioral development was assessed with the Neonatal Behavioral Neurological Assessment. Umbilical cord plasma stress-related hormones, including ACTH, cortisol, norepinephrine, and epinephrine were measured using an enzyme-linked immunosorbent assay. Results In the prenatal life stressors exposed group, newborns had significantly lower birth weight, smaller head circumference ( p p p p p Conclusion Prenatal maternal stress may negatively affect fetal birth outcomes, neurobehavioral development and affect neonates' cord plasma ACTH, cortisol, norepinephrine, and epinephrine.
TL;DR: Placentas from pregnancies complicated by fetal HLHS are characterized by abnormal parenchymal morphology, suggesting immature structure may be due to vascular abnormalities, and increased leptin expression may indicate an attempt to compensate for these vascular abnormalities.
01 Oct 2015
TL;DR: This work is distributed under the terms of the License http://creativecommons.org/licenses/by-nc/3.0/.
Abstract: License. The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. Permissions beyond the scope of the License are administered by Dove Medical Press Limited. Information on how to request permission may be found at: http://www.dovepress.com/permissions.php Research and Reports in Biology 2015:6 171–189 Research and Reports in Biology Dovepress
TL;DR: This work focuses on the interrelationships between adipocyte classification, anatomical location, and impact of diet in early life together with the extent to which fat development differs between the major species examined.
Abstract: There are three different types of adipose tissue (AT)-brown, white, and beige-that differ with stage of development, species, and anatomical location. Of these, brown AT (BAT) is the least abundant but has the greatest potential impact on energy balance. BAT is capable of rapidly producing large amounts of heat through activation of the unique uncoupling protein 1 (UCP1) located within the inner mitochondrial membrane. White AT is an endocrine organ and site of lipid storage, whereas beige AT is primarily white but contains some cells that possess UCP1. BAT first appears in the fetus around mid-gestation and is then gradually lost through childhood, adolescence, and adulthood. We focus on the interrelationships between adipocyte classification, anatomical location, and impact of diet in early life together with the extent to which fat development differs between the major species examined. Ultimately, novel dietary interventions designed to reactivate BAT could be possible.
TL;DR: Leptin appears to play a major role in organogenesis, which may adversely affect the risk of developing a number of diseases in adulthood, and greater understanding of the role of leptin during development may assist in the prevention and treatment of anumber of disease states that occur in adulthood.
Abstract: Emerging research has highlighted the importance of leptin in fetal growth and development independent of its essential role in the maintenance of hunger and satiety through the modulation of neuropeptide Y and proopiomelanocortin neurons. Alterations in maternal-placental-fetal leptin exchange may modify the development of the fetus and contribute to the increased risk of developing disease in adulthood. In addition, leptin also plays an important role in reproductive functions, with plasma leptin concentrations rising in pregnant women, peaking during the third trimester. Elevated plasma leptin concentrations occur at the completion of organogenesis, and research in animal models has demonstrated that leptin is involved in the development and maturation of a number of organs, including the heart, brain, kidneys, and pancreas. Elevated maternal plasma leptin is associated with maternal obesity, and reduced fetal plasma leptin is correlated with intrauterine growth restriction. Alterations in plasma leptin during development may be associated with an increased risk of developing a number of adulthood diseases, including cardiovascular, metabolic, and renal diseases via altered fetal development and organogenesis. Importantly, research has shown that leptin antagonism after birth significantly reduces maturation of numerous organs. Conversely, restoration of the leptin deficiency after birth in growth-restricted animals restores the offspring's body weight and improves organogenesis. Therefore, leptin appears to play a major role in organogenesis, which may adversely affect the risk of developing a number of diseases in adulthood. Therefore, greater understanding of the role of leptin during development may assist in the prevention and treatment of a number of disease states that occur in adulthood.
TL;DR: Data on the DEHP metabolite indicate possible interference with human male fetal gonadal function, and considering the DiNP metabolite, cannot exclude (nor statistically confirm) an association with hypospadias and, less strongly, with cryptorchidism.
Abstract: Prenatal exposure to phthalates may pose a threat to human male reproduction. However, additional knowledge about the in vivo effect in humans is needed, and reported associations with genital abnormalities are inconclusive. We aimed to study prenatal di(2-ethylhexyl) phthalate (DEHP) and diisononyl phthalate (DiNP) exposure in relation to cryptorchidism, hypospadias, and human fetal Leydig cell function.
TL;DR: Overall, it is shown that prenatal vitamin D-deficiency leads to alterations in fetal mouse brain morphology and genes related to neuronal survival, speech and language development, and dopamine synthesis.
TL;DR: It is speculated that increased placental size promotes glucose delivery to these fetuses, because maternal fasting glucose levels and placental glucose transport capacity were not increased in obese women delivering larger infants.
TL;DR: The fetal fraction was affected by fetal aneuploidy, maternal BMI, and the number of gestation, and maternal preexisting of hypertension appeared to reduce fetal fraction.
Abstract: To study factors that influence the concentration of cell-free fetal DNA (fetal fraction) using a large clinical data set of pregnancies with male fetus. A retrospective analysis of 23 067 pregnancies that received noninvasive prenatal testing from January 2012 to October 2013, including 22 650 normal singleton pregnancies (control group) and 417 pregnancies with aneuploidy, twin pregnancy, or various maternal conditions including preexisting hypertension, preexisting diabetes, hyperthyroidism, and carrier of the surface antigen of the hepatitis B virus (HBsAg; study group). Multiples of the median (MoM) analysis was performed in the control group to derive gestation and body mass index (BMI)-corrected fetal fraction. The effects of study group conditions on fetal fraction were examined by calculating the ratio of MoM (RMoM) values. Fetal fraction showed a positive correlation with gestational age (r2 = .10, P < .001) and increased rapidly after the 21 weeks of gestation (r2 = .26, P < .001). Negative association with maternal BMI was found with fetal fraction (r2 = .04, P < .001). In study group, fetal fraction was higher among pregnant women with a trisomy 21 fetus (RMoM = 1.24, P < .001) and lower among trisomy 18 (RMoM = 0.84, P < .001). A 1.6-fold incensement of fetal fraction was observed in twin fetuses comparing to singleton pregnancy (RMoM = 1.62, P < .001). Women with preexisting hypertension had significantly lower fetal fraction (RMoM = 0.85, P = .02). Preexisting diabetes, hyperthyroidism, or carrier of HBsAg did not affect fetal fraction. The fetal fraction was affected by fetal aneuploidy, maternal BMI, and the number of gestation. Maternal preexisting of hypertension appeared to reduce fetal fraction.
TL;DR: Amniotic mesenchymal stem cells can induce partial or complete coverage of experimental spina bifida after concentrated intra-amniotic injection, and Trans-amniotics stem cell therapy (TRASCET) may become a practical option in the prenatal management of spina Bifida.
TL;DR: Fetal bone development and serum mineral regulation are dependent upon parathyroid hormone and PTH-related protein, but not calcitriol, fibroblast growth factor-23, calcitonin, or the sex steroids.
TL;DR: Results showed that oxidised multi-walled carbon nanotubes (oMWCNTs) crossed the placental barrier and entered the foetus body, and histology and vascular endothelial growth factor/reactive oxygen species content in the placenta showed that oMWC NTs narrowed the blood vessel and decreased the number of blood vessels in the Placenta.
Abstract: The mechanism by which nanoparticles cross the placental barrier was studied by using isotopic tracers. The abortion rates and other related data were counted and analysed in pregnant mice with different pregnancy times. Results showed that oxidised multi-walled carbon nanotubes (oMWCNTs) crossed the placental barrier and entered the foetus body. The abortion rates in the pregnant mice depended on pregnancy times. The abortion rates in the first-time, second-time and fourth-time pregnant mice were 70%, 40% and 50%, respectively. The maternal body weight gain was inhibited until gestational ages of 13, 10 and 11 d. oMWCNTs decreased the serum progesterone level and increased the serum oestradiol level in a dose- and time-dependent manner. However, this effect decreased with gestational age. The histology and vascular endothelial growth factor/reactive oxygen species content in the placenta showed that oMWCNTs narrowed the blood vessel and decreased the number of blood vessels in the placenta.
Journal Article•
TL;DR: Changes of the development, anatomy and function of the placenta in the environment of abnormal glucose metabolism which can establish the maternal-placental-fetal interface dysfunction as a potential source of adverse pregnancy outcomes are reviewed.
Abstract: Nowadays, the continuous rise of maternal obesity is followed by increased gestational diabetes mellitus incidence. GDM is associated with adverse fetal and neonatal outcome that often presents with macrosomia, birth trauma, neonatal hypoglycemia, and respiratory distress syndrome. Inclusion of GDM into 'the great obstetrical syndromes' emphasizes the role of the placenta in interactions of the maternal and fetal unit. The placenta acts as a natural selective barrier between maternal and fetal blood circulations. Placenta is sensitive to the hyperglycemic milieu and responses with adaptive changes of the structure and function. Alteration of the placental development and subsequent vascular dysfunction are presented in 6 out of 7 women with all ranges of diabetic severity. Most placentas from GDM pregnancies present typical histological findings such as villous immaturity, villous fibrinoid necrosis, chorangiosis, and increased angiogenesis. The type of dysfunction depends on how early in pregnancy glycaemia disorders occurred. Generally, if impaired glucose metabolism is diagnosed in the early pregnancy, mainly structural dysfunctions are observed. GDM that is detected in late gestation affects placental function to a greater extent. Moreover many studies suggest that diabetic placental changes are associated with inflammation and oxidative stress that can lead to the chronic fetal hypoxia. This article aims to review particular changes of the development, anatomy and function of the placenta in the environment of abnormal glucose metabolism which can establish the maternal-placental-fetal interface dysfunction as a potential source of adverse pregnancy outcomes. A detailed sequence of events that leads from hyperglycemia to placental dysfunction and subsequent pregnancy complications may become an important issue for further studies.
TL;DR: In preeclampsia, there is an increased systemic inflammatory response compared to normal pregnancy, which can influence fetal status at birth.
Abstract: Objective To evaluate the systemic inflammatory response in preeclampsia compared to normal pregnancy. Materials and methods The following serum parameters were determined in three groups of patients: leukocytes, neutrophils, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), C-reactive protein (CRP), and certain markers of oxidative stress. Fetal status was assessed based on the gestational age at which birth occurred, on the Apgar score, and on fetal weight. Results In preeclampsia, a higher systemic inflammatory status was found compared to normal pregnancy. Gestational age at birth, fetal weight, and Apgar score were significantly lower in the group with preeclampsia compared to normal pregnancy. Conclusion In preeclampsia, there is an increased systemic inflammatory response compared to normal pregnancy, which can influence fetal status at birth.