Development Of PE Research Articles

Risk Factors of Pulmonary Embolism in Long-Segment Posterior Thoracolumbar Fusion: Scoring System for Prophylactic Inferior Vena Cava Filter Placement

ObjectiveTo investigate the factors for PE development and the necessity of IVC filter placement. Specifically, propose a scoring system to identify patient populations who benefit from IVC filter placement. MethodsSingle-institution retrospective cohort study between 2010-2022. Inclusion criteria were open posterior thoracolumbar fusion, ≥ 7 segments, and adult patients ≥ 18 years old. Patients undergoing any surgical approach other than posterior were excluded. Risk factors such as smoking status, illicit drug use/type, body mass index (BMI), gender, age, anticoagulation history and status on presence of PE were reviewed. Results365 patients were identified; 170 (46.6%) patients were male, and 195 (53.4%) were female. 24 (6.6%) had IVC filters placed before the surgery. The overall rate of PE was 8 (2.2%), all in patients without IVC filter. Analysis showed that gender, age, and BMI did not affect incidence of PE. Smoking status, history of illicit drug use (cocaine/cannabis), and history of deep vein thrombosis/PE significantly increased the incidence of PE. Based on multivariate logistic regression, we developed a scoring system composed of aforementioned significant risk factors to determine risk of developing PE. Our scoring system stratified risk to low-risk (0-3 points), medium-risk (4-6 points), and high-risk (7-8 points). ConclusionRisk of PE is relatively low after long-segment posterior thoracolumbar fusion. Smoking (former and current), history of cocaine/cannabis use, and history of venous thromboembolism are risk factors in such patients. We recommend prophylactic IVC filter use only in high-risk subgroups and under discretion between physician and patient in medium-risk subgroups.

Combining widely targeted metabolomics and RNA-sequencing to reveal the function analysis of Phyllanthus emblica Linn. Juice-induced poultry macrophages

This study explored the functional effects of cultivated and wild Phyllanthus emblica Linn juice (PEJ) in HD11 poultry macrophage lines, with the aim of potentially developing cultivated PE and its fruit residue as poultry feed additives. RNA-Seq was used to evaluate the functional differences between cultivated and wild PEJ induced HD11 cells. Both cultivated and wild PEJ could regulate cell replication by histone H1/H2 family genes and host immune response by Toll-like receptor 7 regulation. Wild PEJ inhibited M1-type polarization of host macrophages, while cultivated PEJ promoted M2-type polarization. Metabolites of cultivated and wild PE were identified by widely targeted metabolomics based on liquid chromatography-tandem mass spectrometry. Of the 911 metabolites, 238 differed functionally between cultivated and wild PE. The data provide a theoretical basis for the subsequent development of PE as a functional feed additive in poultry.

Uterine Artery Doppler in the Second Trimester as a Predictor of Preeclampsia in High Risk Pregnancy

Abstract Background Preeclampsia is a multisystem disorder of pregnancy which is a major cause of maternal and fetal morbidity and mortality worldwide. The cardinal clinical features of the condition are hypertension and proteinuria occurring after 20 weeks gestation in women who were not previously known to be hypertensive. Aim of the Work The aim of the work was to evaluate the role of uterine artery Doppler in the second trimester as a predictor of preeclampsia in high risk pregnancy. Patients and Methods We included 80 pregnant females in the second trimester at high risk pregnancy in our study, uterine artery Doppler ultrasound was done in the second trimester and the patients were followed up in the third trimester for blood pressure measurement and diagnosis of PE. Results Our results revealed correlation between high indices of uterine arteries and development of PE. Conclusion Our study revealed that we can use uterine artery Doppler as a reliable method to predict preeclampsia.

Different Lengths of Gestational Exposure to Secondhand Smoke or e-Cigarette Vapor Induce the Development of Placental Disease Symptoms.

Exposure to cigarette smoke is known to induce disease during pregnancy. Recent evidence showed that exposure to secondhand smoke (SHS) negatively impacts fetal and placental weights, leading to the development of intrauterine growth restriction (IUGR). Electronic cigarettes (eCigs) represent a phenomenon that has recently emerged, and their use is also steadily rising. Even so, the effects of SHS or eCigs during gestation remain limited. In the present study, we wanted to characterize the effects of SHS or eCig exposure at two different important gestational points during mouse pregnancy. C57/Bl6 mice were exposed to SHS or eCigs via a nose-only delivery system for 4 days (from 14.5 to 17.5 gestational days (dGA) or for 6 days (from 12.5 dGA to 17.5 dGA)). At the time of necropsy (18.5 dGA), placental and fetal weights were recorded, maternal blood pressure was determined, and a dipstick test to measure proteinuria was performed. Placental tissues were collected, and inflammatory molecules in the placenta were identified. Treatment with SHS showed the following: (1) a significant decrease in placental and fetal weights following four days of exposure, (2) higher systolic and diastolic blood pressure following six days of exposure, and (3) increased proteinuria after six days of exposure. Treatment with eCigs showed the following: (1) a significant decrease in placental weight and fetal weight following four or six days of exposure, (2) higher systolic and diastolic blood pressure following six days of exposure, and (3) increased proteinuria after six days of exposure. We also observed different inflammatory markers associated with the development of IUGR or PE. We conclude that the detrimental effects of SHS or eCig treatment coincide with the length of maternal exposure. These results could be beneficial in understanding the long-term effects of SHS or eCig exposure in the development of placental diseases.

Exploring altered free amino acids and metabolites: Insights into the metabolic landscape of preeclampsia

IntroductionPreeclampsia (PE) is a complex disease that poses a risk for maternal and perinatal morbidity and mortality. This study aimed to investigate the role of maternal serum amino acids (AAs) levels in PE. Materials and methodsA total of 56 pregnant women (26 with PE and 30 controls) were included in the study. The participants had a confirmed gestational age between 24 and 37 weeks. The mean body mass index (BMI) for the PE group was 33.1 kg/m2, while the control group had a mean BMI of 29.6 kg/m2. AAs levels were quantified, and statistical analyses were performed to identify significant differences between the two groups. Receiver Operating Characteristic (ROC) curve analysis was employed the diagnostic potential of specific AAs. ResultsWe observed significantly elevated levels of multiple AAs in the PE group, including citrulline, lysine, ethanolamine, ornithine and histidine. Citrulline exhibited exceptional predictive power for PE with 100.0% sensitivity and specificity at a cutoff of 7.79 µmol/L, reflected in an area under the curve (AUC) of 1.000. DiscussionOur study highlights the crucial involvement of altered amino acid levels, specifically in the urea cycle, disruptions in lysine and ethanolamine metabolism in PE development. Exploring these changes may reveal new therapeutic targets, providing insights into the disease's molecular mechanisms. Understanding amino acid metabolism in PE not only informs therapeutic strategies but also holds the potential to revolutionize early diagnosis and intervention.

OLFML3 suppresses trophoblast apoptosis via the PI3K/AKT pathway: A possible therapeutic target in preeclampsia

IntroductionPreeclampsia (PE) is a pregnancy complication that encompasses various pathogenic mechanisms. Shallow implantation of the placenta due to abnormal trophoblast behavior is considered an important mechanism underlying PE; however, its exact etiology remains unclear. MethodsThe expression of OLFML3 in the placenta and important clinical indicators were performed, followed by a correlation analysis. The effect of OLFML3 on the behavior of HTR-8/SVneo cells was examined, and the downstream molecular mechanisms of OLFML3 were investigated in HTR-8/SVneo cells. Additionally, a rat model of PE was generated by adenovirus injection via the tail vein to verify the role of OLFML3. ResultsOLFML3 is highly expressed in both syncytiotrophoblasts and cytotrophoblasts and deregulated in preeclamptic placentas. OLFML3 overexpression in HTR-8/SVneo cells promoted cell proliferation, migration, invasion, and impeded apoptosis, and triggered phosphorylation on ser473 of AKT. Conversely, OLFML3 knockdown exerted opposite effects. Furthermore, OLFML3 overexpression ameliorates CoCl2-induced apoptosis of HTR-8/SVneo cells. In a rat model, OLFML3 overexpression alleviates PE-associated maternal symptoms, leading to lower blood pressure, less severe proteinuria, improved fetal growth restriction, as well as upregulation of P-AKT and downregulation of Cleaved caspase3 and Bax. DiscussionOLFML3 may alleviate PE development by inhibiting extravillous trophoblast cell apoptosis through the PI3K/AKT pathway. Our findings indicated that OLFML3 may provide a possible therapeutic target for PE.

Novel cuproptosis-related prognostic gene profiles in preeclampsia

BackgroundPreeclampsia (PE) is a pregnancy-specific disorder with complex pathogenesis. Cuproptosis is a novel identified form of programmed cell death, however, the link between cuproptosis and clinical outcomes in PE is still not fully understood. In this study, we searched for cuproptosis-related genes (CRGs) in the placental tissues of normal and PE patients to clarify the importance of cuproptosis in the development of PE and provide potential predictive indicators for the occurrence of PE.MethodsUsing RNA sequencing data in the GEO database, we conducted functional enrichment analysis of Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Set Enrichment Analysis (GSEA), supported by linear regression model and operating characteristic curve (ROC) curve analysis, and summarized the role of CRGs in preeclampsia.ResultsA total of 2831 differentially expressed genes related to PE were screened through multiple database analyses. After further intersection with 19 reported CRGs, 5 CRGs have been closely associated with the pathogenesis of PE, including NFE2L2, PDHA1, PDHB, DLD and GLS. NFE2L2 was identified as a key central gene. Pearson correlation analysis showed that CRGs could be related to several maternal and fetal outcome factors, including the highest pregnancy blood pressure, placenta weight, umbilical blood flow pulsatility index (PI), and neonatal weight. Linear regression equation revealed that the expression of NFE2L2 is negatively correlated with the highest pregnancy blood pressure and umbilical blood flow PI but positively correlated with placental weight and neonatal weight. QRT-PCR showed that the expression of these CRGs was significantly lower in placental tissues.ConclusionsThis cuproptosis pattern may be a potential prognostic factor in patients with PE and could provide new insights into disease progression.

The targeting of DAPK1 with miR-190a-3p promotes autophagy in trophoblast cells.

Pre-eclampsia (PE) is a dangerous pathological status that occurs during pregnancy and is a leading reason for both maternal and fetal death. Autophagy is necessary for cellular survival in the face of environmental stress as well as cellular homeostasis and energy management. Aberrant microRNA (miRNA) expression is crucial in the pathophysiology of PE. Although studies have shown that miRNA (miR)-190a-3p function is tissue-specific, the precise involvement of miR-190a-3p in PE has yet to be determined. We discovered that miR-190a-3p was significantly lower and death-associated protein kinase 1 (DAPK1) was significantly higher in PE placental tissues compared to normal tissues, which is consistent with the results in cells. The luciferase analyses demonstrated the target-regulatory relationship between miR-190a-3p and DAPK1. The inhibitory effect of miR-190a-3p on autophagy was reversed by co-transfection of si-DAPK1 and miR-190a-3p inhibitors. Thus, our data indicate that the hypoxia-dependent miR-190a-3p/DAPK1 regulatory pathway is implicated in the development and progression of PE by promoting autophagy in trophoblast cells.

New Productivity in Higher Education: Enhancing University PE Teacher Growth and Development

New Productivity in Higher Education: Enhancing University PE Teacher Growth and Development

Progesterone-induced blocking factor blockade causes hypertension in pregnant rats.

Preeclampsia (PE) is a multisystem disorder characterized by new onset hypertension in mid-late gestation and can include multi-organ dysfunction with or without proteinuria. It affects 5%-7% of all pregnancies in the U.S., making PE a major contributor to maternal and fetal morbidity and mortality. Currently, there is no cure for this pregnancy complication except for early delivery of the placenta and fetus. Moreover, the therapeutic options to treat PE are very limited. One potential trigger for the development of PE is progesterone deficiency-induced imbalance between T Helper 1(Th1)/Th2 cells, an increase in cytolytic natural killer (NK) cells and inflammatory cytokines that in turn leads to endothelial dysfunction, intrauterine growth restriction (IUGR) and hypertension. Importantly, progesterone signals the synthesis of progesterone-induced blocking factor (PIBF) which has anti-inflammatory effects and could promote the regulation of inflammation balance during pregnancy. However, the role of progesterone and PIBF in the pathophysiology of PE is still not fully understood. Thus, this current study was designed to test the hypothesis that inhibition of PIBF causes signs of PE in pregnant Sprague Dawley rats. In order to address our hypothesis, rabbit anti-PIBF IgG (0.25, low dose-LD or 0.50mg/mL, high dose-HD) was administered intraperitoneally on gestation day (GD) 15 to normal pregnant Sprague Dawley (NP) rats. On GD 18, carotid catheters were inserted and on GD 19 mean blood pressure (MAP) and samples were collected for further analysis. MAP in normal pregnant rats (NP) rats (n=7) was 99±3mmHg, which increased to 116±2 mmHg in NP+ anti-PIBF LD (n=10) and 113±4mmHg in NP+ anti-PIBF HD (n=4), p<0.05. Plasma TNF-alpha levels were 35±8 pg/mL in NP rats and increased to 84±21 pg/mL in NP+ Anti-PIBF HD (n=4), p<0.05. Plasma IL-4 and IL-10 levels were 22±5 and 25+6 pg/mL in NP (n=5), which decreased to 6±1 and 8±1 pg/mL in NP+ Anti-PIBF LD (n=6, p<0.05) and 16±4 and 15±5 pg/mL in NP+ Anti-PIBF HD (n=4). Circulating total NK cells were 67±11 % gatein NP rats (n=3), which decreased to 28±7% gate in NP+ Anti-PIBF LD and 45±6% gate in NP+ Anti-PIBF HD. Cytolytic NK cells were increased in NP+ Anti-PIBF HD, p<0.05. Moreover, circulating NO levels were significantly decreased while renal cortex PPET-1 levels increased NP+ Anti-PIBF HD. Our study demonstrates that PIBF blockade causes hypertension, inflammation and signs of endothelial dysfunction, all of which are associated with PE, thus indicating the importance of progesterone signalling pathways during a healthy pregnancy.

Luteolin prevents TNF-α-induced NF-κB activation and ROS production in cultured human placental explants and endothelial cells

IntroductionPreeclampsia (PE) is a serious hypertensive pregnancy disorder and a leading cause of maternal and perinatal morbidity and mortality. Despite the prevalence and complications, there are no approved therapeutics to relieve PE symptoms. Inflammation, oxidative stress, and angiogenic imbalance have been shown to contribute to the PE pathophysiology, though there is a lack of understanding in how best to target these pathways in PE. We recently demonstrated that the bioflavonoid luteolin is a potent inhibitor of the anti-angiogenic and pro-hypertensive soluble fms-like tyrosine kinase 1 (sFlt-1), and here we aimed to determine if luteolin was also capable of reducing inflammation and oxidative stress pathways. MethodsTumor necrosis factor (TNF)-α, which is upregulated in PE, was utilized to stimulate these pathways in human placental explants and endothelial cells. Endothelin-1 (ET-1) and interleukin (IL)-6 in the media from explants and cells were measured via ELISA, and NF-κB localization and reactive oxygen species were detected via fluorescence microscopy. ResultsPretreatment with luteolin demonstrated significant reductions in NF-κB activation, reactive oxygen species, superoxide, and IL-6 and ET-1 expression in endothelial cells. We also saw a significant reduction in phosphorylation of NF-κB in human placental explants. DiscussionThese data demonstrate that luteolin inhibits pathways implicated in the development of PE and should be explored further for its potential as a PE therapeutic.

Biological Function of Rab11-Family Interacting Protein 4 in the Development of Preeclampsia and Their Underlying Mechanism

To elucidate the biological function of Rab11-FIP4 in the development of preeclampsia, as well as its clinical significance and underlying mechanism. Relative levels of Rab11-FIP4, IL-6 and TNF-α in placental tissues of PE pregnant women and healthy pregnant women were detected by qRT-PCR. The correlation between Rab11-FIP4 and IL-6 or TNF-α was assessed by Pearson correlation test. After constructing overexpression lentivirus targeting Rab11-FIP4, its influences on biological characteristics of HTR-8/SVneo cells and expression levels of inflammatory cytokines were examined. Rab11-FIP4 was highly expressed in placental tissues of PE pregnant women. Overexpression of Rab11-FIP4 enhanced migratory and invasive capacities of trophoblasts, and upregulated inflammatory proteins. Rab11-FIP4 aggravates the development of PE by upregulating inflammatory proteins, and stimulating migratory and invasive capacities of trophoblasts.

Predictors of 30-day mortality, unplanned related readmission and reoperation among isolated closed femoral shaft fractures

BackgroundIsolated, closed, femoral shaft fractures are dangerous injuries that commonly occur in the setting of high energy trauma or among older patients with significant comorbidities. Despite their prevalence, relatively little data exists connecting patient independent risk factors to the time to 30-day mortality, unplanned reoperations and unplanned readmissions in these fractures. MethodsUsing National Surgical Quality Improvement Program (NSQIP) database, isolated close femoral shaft fractures were identified using ICD-10 codes. Patient demographics, perioperative course and adverse events were identified. Categorical and binary variables were analyzed among procedure cohorts using Chi2 analysis. Univariate and multivariate analysis were conducted to identify independent risk factors associated with primary outcomes. ResultsBetween 2010 and 2019, 1346 closed isolated femoral shaft fracture patients with a mean age of 66.7 were identified, of whom 30.6% and 69.4% were male and female, respectively. Surgical procedures included: 915 (68.0%) intramedullary nail (IMN); 428 (31.8%) open reduction internal fixation (ORIF); and 3 (0.2%) external fixator (Ex-fix). Patients who underwent ORIF reported 3.19 (OR: 3.19; CI: 1.45–7.03; p = 0.004) and 2.12 (OR: 2.12; CI: 1.10–4.09; p = 0.024) increased odds of mortality and unplanned related readmission compared to patients who received IMN. Transfusion, DVT, and PE rates were 34.2%, 1.4%, and 1.1%, respectively. Furthermore, 50% of mortality cases occurred within 6 days of surgery. Patients requiring reintubation reported 61.8 (OR: 61.8; CI: 15.7–242.40; p < 0.001) increased odds of mortality compared to patients not requiring reintubation. ConclusionPatients with femoral shaft fractures who require reintubation have increased odds of mortality than those successfully extubated. In addition to precautions prior to extubation, patients with femoral shaft fractures should also be carefully monitored for the development of DVT or PE, and they should be definitively fixed with IMN whenever possible.

POSSIBILITIES OF CORRECTING CELLULAR-HUMORAL IMMUNE DISORDERS AND CYTOKINE STATUS IN HIGH-RISK PREGNANT WOMEN FOR THE DEVELOPMENT OF PREECLAMPSIA

POSSIBILITIES OF CORRECTING CELLULAR-HUMORAL IMMUNE DISORDERS AND CYTOKINE STATUS IN HIGH-RISK PREGNANT WOMEN FOR THE DEVELOPMENT OF PREECLAMPSIA

ANTIOXIDANT DEFICIENCY AS PREECLAMPSIA RISK FACTOR

The aim – to study the state of the processes of lipid peroxidation (LPO) and theantioxidant system (AOS) of protection in pregnant women with different degrees ofpreeclampsia severity(PE).Materials and methods. LPO and AOS indicators were studied at 24-26 and 34-36 weeksof pregnancy in 20 healthy women with a physiological course of pregnancy (controlgroup) and in 34 women with PE (main group). 20 of them- with moderate PE (groupI) and 14 – with severe PE (group II).The results. When studying the processes of POL-AOS in pregnant women of all groups,a reliable increase in POL was found, which was more significant in the main group(Р˂0.001). In response to the activation of LPO processes in the control group, the activationof the AOS components of blood protection occurred, as evidenced by an increase in thelevel of glutathione (Р˂0.02) and glutathione peroxidase (Р˂0.05). This contributes to theneutralization of POL products. In pregnant women of the I group, at 24-26 weeks, the levelof glutathione and glutathione- peroxidase increased (Р˂0.02 and Р˂0.01, respectively), andat 34-36 weeks, these indicators did not differ from the control (Р&gt;0.05). In women of theII group, against a background of an increase in the level of lipoperoxidation products, theindicator of glutathione peroxidase did not increase reliably (Р&gt;0.05). The level of glutathionein 24-26 weeks also did not increase (Р&gt;0.05), and in 34-36 – significantly decreased.Conclusions. In women with moderate PE at 34-36 weeks of pregnancy, there is anantioxidant deficiency and a decrease in compensatory and adaptive mechanisms.Exhaustion of the body’s antioxidant defense system was found in pregnant women withsevere PE. Violation of AOS function against a background of hyperproduction of lipidhydroperoxides can lead to oxidative stress, disruption of compensatory and adaptivemechanisms and the development of pathological conditions in the mother and fetus.Preclinical diagnosis and correction of disorders of POL-AOS processes will give anopportunity to prevent the development of severe PE.

Identification of novel first-trimester serum biomarkers for early prediction of preeclampsia

BackgroundPreeclampsia (PE) is a leading cause of maternal and perinatal mortality and morbidity worldwide, but effective early prediction remains a challenge due to the lack of reliable biomarkers.MethodsBased on the extensive human biobank of our large-scale assisted reproductive cohort platform, the first-trimester serum levels of 48 cytokines, total immunoglobulins (Igs), anti-phosphatidylserine (aPS) antibodies, and several previously reported PE biomarkers [including placental growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1), and activin A] were measured in 34 women diagnosed with PE and 34 matched normotensive controls.ResultsThe PE group has significantly higher first-trimester serum levels of interleukin (IL)-2Rα, IL-9, tumor necrosis factor-β (TNF-β), RANTES, hepatocyte growth factor (HGF), total IgM, and total IgG, and aPS IgG optical density (OD) value, as well as lower first-trimester serum levels of PlGF and total IgA and aPS-IgG immune complexes (IC) OD value than the control group. Combining top five first-trimester serum biomarkers (total IgM, total IgG, PlGF, aPS IgG, and total IgA) achieved superior predictive value [area under the curve (AUC) and 95% confidence interval (CI) 0.983 (0.952–1.000), with a sensitivity of 100% and a specificity of 94.1%] for PE development compared to PlGF and PlGF/sFlt-1 independently [AUC and 95% CI 0.825 (0.726–0.924) and 0.670 (0.539–0.800), respectively].ConclusionWe identified novel first-trimester serum biomarkers and developed an effective first-trimester prediction model using immune-related factors and PlGF for PE, which could facilitate the development of early diagnostic strategies and provide immunological insight into the further mechanistic exploration of PE.

Maternal-derived galectin-1 shapes the placenta niche through Sda terminal glycosylation: Implication for preeclampsia.

Placental abnormalities cause impaired fetal growth and poor pregnancy outcome (e.g. preeclampsia [PE]) with long-lasting consequences for the mother and offspring. The molecular dialogue between the maternal niche and the developing placenta is critical for the function of this organ. Galectin-1 (gal-1), a highly expressed glycan-binding protein at the maternal-fetal interface, orchestrates the maternal adaptation to pregnancy and placenta development. Down-regulation or deficiency of gal-1 during pregnancy is associated with the development of PE; however, the maternal- and placental-derived gal-1 contributions to the disease onset are largely unknown. We demonstrate that lack of gal-1 imposes a risk for PE development in a niche-specific manner, and this is accompanied by a placental dysfunction highly influenced by the absence of maternal-derived gal-1. Notably, differential placental glycosylation through the Sda-capped N-glycans dominates the invasive trophoblast capacity triggered by maternal-derived gal-1. Our findings show that gal-1 derived from the maternal niche is essential for healthy placenta development and indicate that impairment of the gal-1 signaling pathway within the maternal niche could be a molecular cause for maternal cardiovascular maladaptation during pregnancy.

“Reflective practice” in physical education

Physical education (PE) is rooted in a historically evolved subject culture that goes largely unquestioned in everyday teaching and learning. It is characterized by a normative primacy of movement practices, placing it in a precarious relationship with the intellectual practices required by sports pedagogy and school curricula. The present case study is based on praxeological classroom research and examines how didactic interferences between intellectual reserves and movement reserves are represented in the principle of “reflective practice” in PE. To reconstruct key orientations toward the interfering practices of teaching and learning that guide teachers’ actions, we conducted six expert interviews in a PE development project in North Rhine-Westphalia (Germany) and analyzed the interview data based on the coding procedure of grounded theory. The reconstructed orientations guiding PE teachers’ actions can be described according to three key dimensions: On the temporal level, one key interference is the scarcity of time for movement. On the spatial level, the space of the gymnasium often stands in the way of establishing and routinizing intellectual practices. On the media level, the use of written forms in PE classes appears to be regarded as a requirement that is imposed upon teachers and that should be kept to a minimum. The results are particularly relevant to research on the institutional professionalization of PE teachers.

Downregulated DUXAP8 lncRNA impedes trophoblast cell proliferation and migration by epigenetically upregulating TFPI2 expression

BackgroundPreeclampsia (PE), a pregnancy complication characterized by new-onset hypertension and proteinuria during the second trimester, is the leading cause of neonatal and maternal morbidity and mortality. In the etiology of PE, failure of uterine spiral artery remodeling may be related to functioning abnormally of trophoblast cells, leading to the occurrence and progression of PE. Recently, long noncoding RNAs (lncRNAs) have been reported to play critical roles in PE nowadays. This study aimed to investigate the expression and functions of the TFPI2 pathway-related lncRNA DUXAP8.MethodsDUXAP8 expression in the placenta from pregnancies was examined using qPCR. Then, the in vitro functions of DUXAP8 were investigated through MTT, EdU, colony, transwell, and flow cytometry experiments. The downstream gene expression profiles were assessed using RNA transcriptome sequencing analysis and verified using qPCR and western blot. Furthermore, Immunoprecipitation (RIP), chromatin immunoprecipitation (CHIP) and fluorescence in situ hybridization (FISH) were used to detect the interaction between lncDUXAP8/EZH2/TFPI2.ResultsThe expression of lncRNA DUXAP8 in placenta of patients with eclampsia was significantly decreased. After knockout of DUXAP8, the proliferation and migration of trophoblasts were significantly decreased, and the percentage of apoptosis was increased. Flow cytometry showed that low expression of DUXAP8 increased the accumulation of cells in G2/M phase, while overexpression of DUXAP8 had the opposite effect. We also proved that DUXAP8 epigenetically inhibited TFPI2 expression by recruiting EZH2 and mediating H3K27me3 modification.ConclusionTogether, these resulting data clarify that aberrant expression of DUXAP8 is involved in the potential PE development and progress. Unraveling the role of DUXAP8 will provide novel insights into the pathogenesis of PE.

Serum uric acid to creatinine ratio and risk of preeclampsia and adverse pregnancy outcomes.

Preeclampsia is one of the most severe diseases among the hypertensive disorders of pregnancy (HDP) and the leading cause of maternal and fetal morbidity and mortality. It is of crucial importance to early identify women at a high risk for preeclampsia to implement appropriate preventive strategies. In our study, we aimed to test the hypothesis that serum uric acid to creatinine ratio (SUA/sCr) is related to the development of preeclampsia and maternal and neonatal complications. We searched for uric acid and creatine values in the medical records of 269 women who consecutively attended our HDP Clinic from December 2018 to December 2022. We compared the baseline characteristics of participants with normotensive pregnancy ( n = 57), to those with HDP without preeclampsia (HDP-non-PE) ( n = 100) and those with preeclampsia ( n = 112), and we performed adjusted logistic regression analysis to test the associations between SUA/sCr and the development of preeclampsia and maternal and neonatal complications. SUA/sCr was consistently higher in women with preeclampsia in all trimesters of pregnancy. Higher SUA/sCr at the third trimester was associated with an increased odd of developing preeclampsia [odds ratio (OR) 1.29, confidence interval (CI) 1.15-1.50, P = 0.001], preterm birth (OR 1.23, CI 1.05-1.45, P = 0.011), and composite neonatal outcome (OR 1.33, CI 1.12-1.59, P = 0.001), after adjustment for age, BMI before pregnancy, nulliparity, antihypertensive therapy, and acetylsalicylic acid therapy during pregnancy. Having higher SUA/sCr during pregnancy is associated with the development of PE and adverse pregnancy outcomes. Controlled prospective studies are warranted to clarify the predictive power of this novel marker during pregnancy.