Showing papers on "Fetus published in 2022"
10 Feb 2022
TL;DR: A case-based retrospective clinicopathologic analysis by a multinational group of 44 perinatal specialists from 12 countries of placental and autopsy pathology findings from 64 stillborns and 4 neonatal deaths having placentas testing positive for SARS-CoV-2 following delivery to mothers with COVID-19 was performed as mentioned in this paper .
Abstract: Perinatal death is an increasingly important problem as the coronavirus disease 2019 (COVID-19) pandemic continues, but the mechanism of death has been unclear.To evaluate the role of the placenta in causing stillbirth and neonatal death following maternal infection with COVID-19 and confirmed placental positivity for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).Case-based retrospective clinicopathologic analysis by a multinational group of 44 perinatal specialists from 12 countries of placental and autopsy pathology findings from 64 stillborns and 4 neonatal deaths having placentas testing positive for SARS-CoV-2 following delivery to mothers with COVID-19.Of the 3 findings constituting SARS-CoV-2 placentitis, all 68 placentas had increased fibrin deposition and villous trophoblast necrosis and 66 had chronic histiocytic intervillositis. Sixty-three placentas had massive perivillous fibrin deposition. Severe destructive placental disease from SARS-CoV-2 placentitis averaged 77.7% tissue involvement. Other findings included multiple intervillous thrombi (37%; 25 of 68) and chronic villitis (32%; 22 of 68). The majority (19; 63%) of the 30 autopsies revealed no significant fetal abnormalities except for intrauterine hypoxia and asphyxia. Among all 68 cases, SARS-CoV-2 was detected from a body specimen in 16 of 28 cases tested, most frequently from nasopharyngeal swabs. Four autopsied stillborns had SARS-CoV-2 identified in internal organs.The pathology abnormalities composing SARS-CoV-2 placentitis cause widespread and severe placental destruction resulting in placental malperfusion and insufficiency. In these cases, intrauterine and perinatal death likely results directly from placental insufficiency and fetal hypoxic-ischemic injury. There was no evidence that SARS-CoV-2 involvement of the fetus had a role in causing these deaths.
85 citations
TL;DR: This paper showed that SARS-CoV-2 infection during pregnancy primarily induces unique inflammatory responses at the maternal-fetal interface, which are largely governed by maternal T cells and fetal stromal cells.
Abstract: Pregnant women represent a high-risk population for severe/critical COVID-19 and mortality. However, the maternal-fetal immune responses initiated by SARS-CoV-2 infection, and whether this virus is detectable in the placenta, are still under investigation. Here we show that SARS-CoV-2 infection during pregnancy primarily induces unique inflammatory responses at the maternal-fetal interface, which are largely governed by maternal T cells and fetal stromal cells. SARS-CoV-2 infection during pregnancy is also associated with humoral and cellular immune responses in the maternal blood, as well as with a mild cytokine response in the neonatal circulation (i.e., umbilical cord blood), without compromising the T-cell repertoire or initiating IgM responses. Importantly, SARS-CoV-2 is not detected in the placental tissues, nor is the sterility of the placenta compromised by maternal viral infection. This study provides insight into the maternal-fetal immune responses triggered by SARS-CoV-2 and emphasizes the rarity of placental infection.
82 citations
TL;DR: A systematic review and meta‐analysis was conducted to determine the diagnostic yield of exome sequencing (ES) for prenatal diagnosis of fetal structural anomalies, where karyotype/chromosomal microarray (CMA) is normal.
Abstract: We conducted a systematic review and meta‐analysis to determine the diagnostic yield of exome sequencing (ES) for prenatal diagnosis of fetal structural anomalies, where karyotype/chromosomal microarray (CMA) is normal.
47 citations
TL;DR: It is suggested that delta-variant SARS-CoV-2 infection during pregnancy warrants vigilance for placental dysfunction and fetal compromise regardless of disease severity.
Abstract: Abstract There is limited information on the specific impact of maternal infection with the SARS-CoV-2 B.1.617.2 (delta) variant on pregnancy outcomes. We present 2 cases of intrauterine fetal demise and 1 case of severe fetal distress in the setting of maternal infection with delta-variant SARS-CoV-2. In all cases, fetal demise or distress occurred within 14 days of COVID-19 diagnosis. Evaluation revealed maternal viremia, high nasopharyngeal viral load, evidence of placental infection with delta-variant SARS-CoV-2, and hallmark features of SARS-CoV-2 placentitis. We suggest that delta-variant SARS-CoV-2 infection during pregnancy warrants vigilance for placental dysfunction and fetal compromise regardless of disease severity.
46 citations
TL;DR: In this article , the effect of SARS-CoV-2 infection on placental function is not well understood, but placentas from two mothers with symptomatic COVID-19 whose pregnancies resulted in adverse outcomes for the fetuses contained high levels of viral Alpha variant RNA.
43 citations
TL;DR: Grossman et al. as mentioned in this paper report the experiences from two urban, inner-city healthcare systems in Texas after state-level legislation on abortion has encroached on access to reproductive care with disproportionate effects on underserved communities.
41 citations
TL;DR: In this article , the authors investigated biological pathways and intermediate biomarkers underlying the association between serum PFAS and fetal growth using high-resolution metabolomics in a cohort of pregnant African American women in the Atlanta area, Georgia.
41 citations
TL;DR: In this article, the authors investigated biological pathways and intermediate biomarkers underlying the association between serum PFAS and fetal growth using high-resolution metabolomics in a cohort of pregnant African American women in the Atlanta area.
40 citations
TL;DR: In this paper , the authors explored whether the antecedents for neurodevelopmental disabilities might begin in utero, and analyzed whether fetal brain volume predicted subsequent neuro developmental outcome in children with CHD.
Abstract: Background: Neurodevelopmental impairment is common in children with congenital heart disease (CHD), but postnatal variables explain only 30% of the variance in outcomes. To explore whether the antecedents for neurodevelopmental disabilities might begin in utero, we analyzed whether fetal brain volume predicted subsequent neurodevelopmental outcome in children with CHD. Methods: Fetuses with isolated CHD and sociodemographically comparable healthy control fetuses underwent fetal brain magnetic resonance imaging and 2-year neurodevelopmental evaluation with the Bayley Scales of Infant and Toddler Development, Third Edition (Bayley-III) and the Adaptive Behavior Assessment System, Third Edition (ABAS-3). Hierarchical regression evaluated potential predictors of Bayley-III and ABAS-3 outcomes in the CHD group, including fetal total brain volume adjusted for gestational age and sex, sociodemographic characteristics, birth measures, and medical history. Results: The CHD group (n=52) had lower Bayley-III cognitive, language, and motor scores than the control group (n=26), but fetal brain volumes were similar. Within the CHD group, larger fetal total brain volume correlated with higher Bayley-III cognitive, language, and motor scores and ABAS-3 adaptive functioning scores ( r =0.32–0.47; all P <0.05), but this was not noted in the control group. Fetal brain volume predicted 10% to 21% of the variance in neurodevelopmental outcome measures in univariate analyses. Multivariable models that also included social class and postnatal factors explained 18% to 45% of the variance in outcome, depending on developmental domain. Moreover, in final multivariable models, fetal brain volume was the most consistent predictor of neurodevelopmental outcome across domains. Conclusions: Small fetal brain volume is a strong independent predictor of 2-year neurodevelopmental outcomes and may be an important imaging biomarker of future neurodevelopmental risk in CHD. Future studies are needed to support this hypothesis. Our findings support inclusion of fetal brain volume in risk stratification models and as a possible outcome in fetal neuroprotective intervention studies.
33 citations
TL;DR: In this article , 21 emerging and legacy per-polyfluoroalkyl substances (PFASs) accumulated in mothers can be transferred to newborns through placenta and/or breastfeeding, causing potential health risks.
31 citations
TL;DR: In this article , a review of the existing literature on preeclampsia can be found in Section 5.1.1, where the authors delineate the physiological hemodynamic changes that occur in normal pregnancy and those that are observed with the pathologic processes associated with preeclampia.
TL;DR: In this paper , fetal, endothelial, hematopoietic, and trophoblast-specific genetic manipulations in the mouse were used to demonstrate that endothelial and fetus-derived IGF2 is required for the continuous expansion of the fetoplacental microvasculature in late pregnancy.
TL;DR: The use of routine monitoring of donor-derived cell-free DNA (dd-cfDNA) after kidney transplant may allow clinicians to identify subclinical allograft injury and intervene prior to development of clinically evident graft injury as mentioned in this paper .
TL;DR: A review of the literature about the diagnosis, antepartum surveillance, and time of delivery of fetuses suspected to be small for gestational age or growth restricted is presented in this article .
TL;DR: The placenta is a transient fetal organ that plays a critical role in the health and wellbeing of both the fetus and its mother as discussed by the authors , and is the primary cause of common disorders of pregnancy, including recurrent miscarriage, fetal growth restriction, pre-eclampsia and stillbirth.
TL;DR: In this article , a systematic search was performed to understand the potential involvement of SARS-CoV-2 in preeclampsia onset using the databases, PubMed and Web of Science until 31 January 2022.
Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the coronavirus disease 2019 (COVID-19) disease that has rapidly spread worldwide, causing hundreds of thousand deaths. Normal placentation is characterized by many processes strictly regulated during pregnancy. If placentation is impaired, it can lead to gestational disorders, such as preeclampsia that is a multisystem disorder that occurs in 2-8% of pregnancies worldwide.We performed a systematic search to understand the potential involvement of SARS-CoV-2 in preeclampsia onset using the databases, PubMed and Web of Science until 31 January 2022.SARS-CoV-2 infection not only causes damage to the respiratory system but also can infect human placenta cells impairing pivotal processes necessary for normal placenta development. The inflammatory response trigged by COVID-19 disease is very similar to that one found in preeclampsia pregnancies suggesting a possible link between SARS-CoV-2 infection and preeclampsia onset during pregnancy.Some studies showed that pregnancies affected by COVID-19 had higher incidence of preeclampsia compared with SARS-CoV-2-negative ones. However, increased blood pressure found in COVID-19 pregnancies does not allow to associate COVID-19 to preeclampsia as hypertension is a common factor to both conditions. At present, no diagnostic tools are available to discriminate real preeclampsia from preeclampsia-like syndrome in patients with SARS-CoV-2 infection. Thus, new specific diagnostic tools are necessary to assure an appropriate diagnosis of preeclampsia in these patients, especially in case of severe COVID-19 disease.
TL;DR: The placenta is a highly metabolically active organ fulfilling the bioenergetic and biosynthetic needs to support its own rapid growth and that of the fetus as discussed by the authors , but its causal relationship to the pathophysiology is unclear.
TL;DR: Kanker et al. as mentioned in this paper found evidence of the presence of black carbon particles in cord blood, confirming the ability of these particles to cross the placenta and enter the fetal circulation system.
TL;DR: In this article , the benefits and main clinical applications of CTC and ctDNA analysis in solid tumors are summarized in the field of liquid biopsy and their recent findings in the literature are summarized.
TL;DR: This paper showed that pre-gestational hyperglycaemia renders the offspring more vulnerable to glucose intolerance and showed that the expression of TET3 dioxygenase, responsible for 5-methylcytosine oxidation and DNA demethylation in the zygote, is reduced in oocytes from a mouse model of hyper glycaemia (HG mice) and humans with diabetes.
Abstract: Diabetes mellitus is prevalent among women of reproductive age, and many women are left undiagnosed or untreated1. Gestational diabetes has profound and enduring effects on the long-term health of the offspring2,3. However, the link between pregestational diabetes and disease risk into adulthood in the next generation has not been sufficiently investigated. Here we show that pregestational hyperglycaemia renders the offspring more vulnerable to glucose intolerance. The expression of TET3 dioxygenase, responsible for 5-methylcytosine oxidation and DNA demethylation in the zygote4, is reduced in oocytes from a mouse model of hyperglycaemia (HG mice) and humans with diabetes. Insufficient demethylation by oocyte TET3 contributes to hypermethylation at the paternal alleles of several insulin secretion genes, including the glucokinase gene (Gck), that persists from zygote to adult, promoting impaired glucose homeostasis largely owing to the defect in glucose-stimulated insulin secretion. Consistent with these findings, mouse progenies derived from the oocytes of maternal heterozygous and homozygous Tet3 deletion display glucose intolerance and epigenetic abnormalities similar to those from the oocytes of HG mice. Moreover, the expression of exogenous Tet3 mRNA in oocytes from HG mice ameliorates the maternal effect in offspring. Thus, our observations suggest an environment-sensitive window in oocyte development that confers predisposition to glucose intolerance in the next generation through TET3 insufficiency rather than through a direct perturbation of the oocyte epigenome. This finding suggests a potential benefit of pre-conception interventions in mothers to protect the health of offspring.
TL;DR: In this article , the authors analyzed 50 placentas from COVID-19-positive unvaccinated mothers and found massive placental damage associating trophoblastic necrosis, fibrinous deposits, intervillositis, as well as extensive hemorrhagic changes due to SARS-CoV-2 infection probably responsible of intrauterine fetal death.
TL;DR: In this article , two different laboratories performed in vitro experiments that applied an identical experimental procedure and used cells and FBS from the same suppliers, and the results they obtained were very different.
Abstract: Description Ethical and possible reproducibility issues arise when using fetal bovine serum in cell culture media Fetal bovine serum [FBS, also known as fetal calf serum (FCS)] is a popular supplement to the basal medium used in cell and tissue culture. FBS is sourced from unborn calves at the slaughterhouse, raising ethical concerns about animal welfare. Recently, two different laboratories performed in vitro experiments that applied an identical experimental procedure and used cells and FBS from the same suppliers (1). The results they obtained were very different. Further analyses revealed that one cause for the difference in cell response was the supplementation of the cell culture medium with FBS, which had originated from different batches. Given the ubiquitous use of cell culture throughout research, it is important to ensure reproducibility as well as ethical sourcing of research products, such as the development of synthetic media.
TL;DR: In this paper , the authors investigated the mechanisms that cause miscarriage and found that aneuploidy originating in oocytes during meiosis drives the age-related risk of miscarriage.
TL;DR: In this article , an integrated model of the maternal-placental-fetal array that delineates the commensality among the constituent parts, showing how a disruption in any component or nexus may lead to the multifaceted syndrome of preeclampsia and how the latter resembles the changes associated with cardiac disease states.
TL;DR: Preeclampsia is a common hypertensive disorder of pregnancy associated with considerable neonatal and maternal morbidities and mortalities as discussed by the authors , and it is generally accepted that abnormal placentation resulting in the release of soluble antiangiogenic factors, coupled with increased oxidative stress and inflammation, leads to systemic endothelial dysfunction and the clinical manifestations of the disease.
TL;DR: In this article , Nafion byproduct 2 (NBP2) was recently detected in surface water, drinking water, and human serum samples from monitoring studies in North Carolina, USA.
TL;DR: In this paper , mesenchymal stromal cell-derived extracellular vesicles (MEx) were used to improve developmental lung injury in experimental preeclampsia, using the heme oxygenase-1−/−) model.
Abstract: In preeclamptic pregnancies, a variety of intrauterine alterations lead to abnormal placentation, release of inflammatory and/or antiangiogenic factors, and subsequent fetal growth restriction with significant potential to cause a primary insult to the developing fetal lung. Thus, modulation of the maternal intrauterine environment may be a key therapeutic avenue to prevent preeclampsia-associated developmental lung injury. A biologic therapy of interest is mesenchymal stromal cell–derived extracellular vesicles (MEx), which we have previously shown to ameliorate preeclamptic physiology through intrauterine immunomodulation. To evaluate the therapeutic potential of MEx to improve developmental lung injury in experimental preeclampsia, using the heme oxygenase-1–null mouse (Hmox1−/−) model, preeclamptic pregnant dams were administered intravenous antenatal MEx treatment during each week of pregnancy followed by analysis of fetal and postnatal lung tissues, amniotic fluid protein profiles, and lung explant and amniotic fluid cocultures in comparison with control and untreated preeclamptic pregnancies. We first identified that a preeclamptic intrauterine environment had a significant adverse impact on fetal lung development, including alterations in fetal lung developmental gene profiles in addition to postnatal alveolar and bronchial changes. Amniotic fluid proteomic analysis and fetal lung explant and amniotic fluid cocultures further demonstrated that maternally administered MEx altered the expression of multiple inflammatory mediators in the preeclamptic intrauterine compartment, resulting in the normalization of fetal lung branching morphogenesis and developmental gene expression. Our evaluation of fetal and postnatal parameters overall suggests that antenatal MEx treatment may provide a highly valuable preventative therapeutic modality for amelioration of lung development in preeclamptic disease.
TL;DR: In this article , the authors evaluated the transplacental transfer of mRNA vaccine products and functional anti-SARS-CoV-2 antibodies during pregnancy and early infancy in a cohort of 20 individuals vaccinated during late pregnancy.
Abstract: Abstract Studies are needed to evaluate the safety and effectiveness of mRNA SARS-CoV-2 vaccination during pregnancy, and the levels of protection provided to their newborns through placental transfer of antibodies. Here, we evaluate the transplacental transfer of mRNA vaccine products and functional anti-SARS-CoV-2 antibodies during pregnancy and early infancy in a cohort of 20 individuals vaccinated during late pregnancy. We find no evidence of mRNA vaccine products in maternal blood, placenta tissue, or cord blood at delivery. However, we find time-dependent efficient transfer of IgG and neutralizing antibodies to the neonate that persists during early infancy. Additionally, using phage immunoprecipitation sequencing, we find a vaccine-specific signature of SARS-CoV-2 Spike protein epitope binding that is transplacentally transferred during pregnancy. Timing of vaccination during pregnancy is critical to ensure transplacental transfer of protective antibodies during early infancy.