PPARγ Regulates Triclosan Induced Placental Dysfunction

Exposure to the antibacterial agent triclosan (TCS) is associated with abnormal placenta growth and fetal development during pregnancy. Peroxisome proliferator-activated receptor γ (PPARγ) is crucial in placenta development. However, the mechanism of PPARγ in placenta injury induced by TCS remains unknown. Herein, we demonstrated that PPARγ worked as a protector against TCS-induced toxicity. TCS inhibited cell viability, migration, and angiogenesis dose-dependently in HTR-8/SVneo and JEG-3 cells. Furthermore, TCS downregulated expression of PPARγ and its downstream viability, migration, angiogenesis-related genes HMOX1, ANGPTL4, VEGFA, MMP-2, MMP-9, and upregulated inflammatory genes p65, IL-6, IL-1β, and TNF-α in vitro and in vivo. Further investigation showed that overexpression or activation (rosiglitazone) alleviated cell viability, migration, angiogenesis inhibition, and inflammatory response caused by TCS, while knockdown or inhibition (GW9662) of PPARγ had the opposite effect. Moreover, TCS caused placenta dysfunction characterized by the significant decrease in weight and size of the placenta and fetus, while PPARγ agonist rosiglitazone alleviated this damage in mice. Taken together, our results illustrated that TCS-induced placenta dysfunction, which was mediated by the PPARγ pathway. Our findings reveal that activation of PPARγ might be a promising strategy against the adverse effects of TCS exposure on the placenta and fetus.

A Preconception Paternal Fish Oil Diet Prevents Toxicant-Driven New Bronchopulmonary Dysplasia in Neonatal Mice

New bronchopulmonary dysplasia is a developmental lung disease associated with placental dysfunction and impaired alveolarization. Risk factors for new BPD include prematurity, delayed postnatal growth, the dysregulation of epithelial-to-mesenchymal transition (EMT), and parental exposure to toxicants. Our group previously reported that a history of paternal toxicant exposure increased the risk of prematurity and low birth weight in offspring. A history of paternal toxicant exposure also increased the offspring’s risk of new BPD and disease severity was increased in offspring who additionally received a supplemental formula diet, which has also been linked to poor lung development. Risk factors associated with new BPD are well-defined, but it is unclear whether the disease can be prevented. Herein, we assessed whether a paternal fish oil diet could attenuate the development of new BPD in the offspring of toxicant exposed mice, with and without neonatal formula feeding. We investigated the impact of a paternal fish oil diet preconception because we previously reported that this intervention reduces the risk of TCDD associated placental dysfunction, prematurity, and low birth weight. We found that a paternal fish oil diet significantly reduced the risk of new BPD in neonatal mice with a history of paternal toxicant exposure regardless of neonatal diet. Furthermore, our evidence suggests that the protective effects of a paternal fish oil diet are mediated in part by the modulation of small molecules involved in EMT.

An analysis of the pathological states of pregnant women in ante-intranatal fetal death in kharkov during 2016-2019

Background. In Ukraine among perinatal losses, a high proportion of stillbirth remains, the level of which depends on many factors, including the presence of somatic and genital pathology in a woman, pathological conditions during pregnancy, including eclampsia (PE), iron deficiency anemia of pregnant women (IDA), chorioamnionitis (CA). These conditions can be combined with each other, which increases the risk of fetal death during pregnancy or childbirth. Objective. To conduct a somatic and gynecological diseases, complications of pregnancy in pregnant women with preeclampsia (PE), iron deficiency anemia (IDA) and chorioamnionitis (CA), whose pregnancy ended in ante-intrapartum fetal death at 30-40 weeks of gestation. Methods. We investigated 58 cases of stillbirth at 30-40 weeks of gestation from pregnant women with PE (n = 16), IDA (n = 16), CA (n = 26) on the basis of the Communal non-profit enterprise "City Perinatal Center "Kharkov. The clinical data of the mothers, the protocols of the pathological examination of the placenta were studied. Results. Based on the study, it was found that in women whose pregnancy was complicated by PE and IDA, the most frequent types of somatic pathology were hypertensive disorders (32% and 12.5%, respectively) and chronic diseases of the digestive system. (25% and 12.5%, respectively), among gynecological diseases, uterine leiomyoma and endocervicosis were more common, among complications of pregnancy and childbirth - premature birth (50% each, respectively) pathology of the placenta (50% and 68.8%, respectively) and disorders of the content amniotic fluid (31.3% and 18.8%, respectively).The extragenital pathology in pregnant women with CA was presented with the infectious diseases (30.7%), an acute respiratory viral infections (19.2%), the cardiovascular pathology (11.5%), and the chronic inflammatory diseases of various localization (7.6%). The most frequency gynecological pathology were inflammatory genital diseases (23.21%). The pregnancy and labor were often complicated with the placental pathology (50%), premature birth (38.5%), preeclampsia (19.2%), and anemia (19.2%). During pregnancy, placental dysfunction diagnosed only in 31.3% of cases with PE, 25% with IDA and 3.8% with CA, but in pathological examination, morphological signs of placental insufficiency recorded in almost every case of all groups. Conclusion. In pregnancy, aggravated by PE, IDA or CA, the presence of extragenital pathology, gynecological diseases, and other complications of pregnancy were additional factors that increased the severity of placental insufficiency and fetal hypoxia, which was the cause of its death. Timely diagnosis of placental dysfunction and the implementation of therapeutic measures aimed at reducing the associated negative impact on the fetus can help reduce perinatal mortality.

Seroprevalence of CMV in Women with Bad Obstetric History in Babil/Iraq

Placental dysfunction and or fetal central nervous system infestation caused by Human cytomegalovirus (HCMV) is the leading cause of congenital non-genetic neuro-developmental problems of the newborn, worldwide. Although the highest rates of congenital infection and CMV seroprevalence occurs in developing countries like Iraq, there remains a paucity of data from that part of the world. This descriptive case control study was undertaken in Babylon/ Iraq to determine the local seroprevalence of CMV in women of child bearing age, and to identify the socio-demographic factors associated with it. This study found a seropositivity peak amongst the 26-35 yr olds which declined in the 36 – 45 yr olds. However, the evidence of current infection was stable at 25% among the 26-35 yr olds and the 36 – 45 yr old women. Overall seropositivity was at 77.32%, a susceptibility rate was at 22.68%, and seropositivity for IgG was highest among the educated, those living in overcrowded settings, and those with poor obstetric histories. Our study concludes that CMV screening of women in the Al Hamza district in Babylon/Iraq and the availability of advice on how to prevent the infection can be beneficial for health outcomes.

MODERN DIAGNOSIS OF PLACENTAL DYSFUNCTION AND ITS COMPLICATIONS

The aim of the study was to improve the modern diagnosis of placental dysfunction and its complications. Materials and methods. The study involved a prospective survey of 70 pregnant women divided into the main group (pregnant women with placental dysfunction) (n = 50) and the control group (n = 20). The main group was divided into subgroups of pregnant women with placental dysfunction and fetal growth retardation (n = 30) and pregnant women with placental dysfunction without fetal growth retardation (n = 20). The control group comprised 20 pregnant women with physiological gestation. Apart from history taking, the study comprised obstetric and general clinical examination, evaluation of endothelium- dependent vasodilation, serum concentrations of soluble forms of vascular and platelet- endothelial molecules of cell adhesion 1, indicators of athrombogenicity of the vascular growth wall, uterine-placental-fetal blood circulation, pathomorphological and histometric examination of the placenta. Results. Based on the obtained clinical-morphological and endotheliotropic criteria, a personalized clinical algorithm for managing pregnant women with placental dysfunction was developed and implemented. Conclusions. Assessment of pregnancy results in a prospective clinical study showed that the proposed algorithm for personalization of the risk of perinatal abnormalities not only helped to avoid antenatal mortality, but also to prevent intranatal and early neonatal losses in patients with placental dysfunction and fetal growth retardation.

The impact of perfluoroalkyl substances on pregnancy, birth outcomes and offspring development: A review of data from mouse models

Per- and polyfluoroalkyl substances (PFASs) such as perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) are persistent in the environment and bioaccumulate in wildlife and humans, potentially causing adverse health effects at all stages of life. Studies from human pregnancy have shown that exposure to these contaminants are associated with placental dysfunction and fetal growth restriction; however, studies in humans are confounded by genetic and environmental factors. Here, we synthesize the available results from mouse models of pregnancy to show the causal effects of prenatal exposure to PFOA and PFOS on placental and fetal development and on neurocognitive function and metabolic disorders in offspring. We also propose gaps in the present knowledge and provide suggestions for future research studies.

ANALYSIS OF ANAMNESIS FEATURES IN PREGNANT WOMEN WITH PLACENTAL DYSFUNCTION

The article examines the analysis of the anamnesis of pregnant women with placental dysfunction, the results of the studies made it possible to conclude that with impaired uteroplacental blood flow from 18-22 weeks, showed a high level of development of late gestosis (84.7%). Timely treatment of placental insufficiency and prophylaxis of late gestosis made it possible to reduce the incidence of complications.