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Pre-eclampsia (PE) is a multi-system disorder of pregnancy which constitute one of the leading causes of maternal and perinatal mortality worldwide. Dysfunction of trophoblast cells have been play an a significant role in the development and progression of PE. ELABELA (ELA), an endogenous apelin receptor (APJ) ligand, is a hormone secreted by the placenta into circulation, we previously identified ELA and its cognate apelin receptor (APJ) as proteins that are differentially expressed in the placentas of humans with PE. However, a fact known to few about the potential regulatory effects of ELA on the functions of trophoblast cells. In this study, our experiments showed that exogenous ELA did not effectively affect the proliferation and apoptosis of HTR-8/SVneo cells in higher concentrations but inhibited the invasion and migration capabilities. Studies have shown that the epithelial-mesenchymal transition (EMT) event of trophoblast cells is abnormal through regulate the P13K/AKT pathway in PE. First we confirmed APJ expression in HTR-8/SVneo cells and ELA suppressed P13K/AKT signalling pathway-related factors (AKT, phospho (p)-AKT) phosphorylation in HTR-8/SVneo cells in a concentration-dependent manner. Next, we found that treatment with higher concentrations of ELA or the P13K inhibitor LY294002 significantly increased the expression of β-catenin which is the classical epithelial marker relative to the control group. Moreover, treatment with both LY294002 and ELA more strongly affected the β-catenin expression and the HTR8/SVneo cells invasion and migration. These results demonstrate that ELA inhibits trophoblast cell functions by altering the β-catenin expression get though the PI3K/AKT signalling pathway in PE. Thus, this result might provide a new therapeutic target for the treatment of PE.

Placenta previa greatly contributes to severe antenatal and post-partum hemorrhage. Previous studies have mainly focused on the risk factors of placenta previa, with very few studies reporting which factors may affect the potential resolution of 28th-week previa. This study aimed to investigate the impact of maternal characteristics on potential resolution of placenta previa from the 28th-to the 36th-week of pregnancy.A retrospective longitudinal sub-cohort investigation was carried out among 368 pregnant women with 28th-week previa from the Longitudinal Placenta Previa Study (LoPPS). Logistic regression analysis was used to discover the connections between maternal covariates and the placental potential resolution. Multivariable linear regression analysis was used to detect the associations between perioperative characteristics and volume of intraoperative bleeding.Among pregnant women whose placenta completely or partially covered the internal os at the 28th-week of pregnancy, 37.5% were without placenta previa at the 36th-week and 25.8% converted into marginal placenta previa. There were significant correlation between placenta previa type and GHD (Beta: 2.808, 95% CI: 1.642, 7.138; p = 0.041), type of 28th-week previa (Beta: 6.767, 95% CI: 1.592, 18.767; p 0.001), and number of prior cesarean sections (Beta: 3.326, 95% CI: 1.580, 9.081; p 0.001).62.5% of the pregnant women with 28th-week placenta previa were still with previa at the 36 weeks of gestation (25.8% with marginal and 36.7% with partial/complete placenta previa). This proportion is even higher for 28th-week complete placenta previa.Chinese Clinical Trial Registry ChiCTR2100054068, December 8, 2021.

Background: Previous studies have shown that abnormal increases in autoimmune antibodies in pregnant women may increase the risk of maternal thrombosis. However, at our hospital, two pregnant women presented with umbilical artery thrombosis and positive maternal autoantibodies were detected in both, which led us to consider whether maternal autoantibodies also played a role in umbilical artery thrombosis. Case presentation: Case 1: Fetal ultrasound of a 34-year-old pregnant woman at 30+4 weeks gestation showed two umbilical arteries, with an inner diameter of approximately 0.15 cm for the smaller was artery. However, only a single umbilical artery blood flow signal was detected. Due to fetal distress, which was noted on abnormal cardiotocography and Doppler ultrasound, an emergency cesarean section was performed at 31+1 weeks gestation. The Apgar score of the newborn was 3-8-8. Umbilical cord examination detected thrombosis in the two umbilical arteries. Moreover, blood test results during pregnancy showed nRNP/Sm antibody (+) and SS antibody (+++). Case 2: The first systematic ultrasound of a 33-year-old twin pregnancy at 24+3 weeks gestation was normal, but routine fetal ultrasound at 27+1 weeks gestation showed only one umbilical artery between fetus A and the placenta. Blood test results showed that the patient was anti-nRNP/Sm antibody (+) in the rheumatoid immune activity test at 27+3 weeks gestation. An emergency cesarean section was performed at 34+6 weeks gestation because of the single umbilical artery and abnormal maternal coagulation. Both umbilical cords of fetus A and B blood test results showed anti-nRNP/Sm antibody (++). The pathological examination of the umbilical cord and placenta showed the presence of old thrombosis in one of the umbilical arteries of fetus A. Conclusions: Abnormal maternal autoantibodies may be a risk factor for umbilical artery thrombosis. For these pregnant women, anticoagulation therapy with heparin and aspirin was used in a timely manner, which could possibly have avoided the occurrence of adverse pregnancy outcomes.

Preeclampsia (PE) is a leading cause of perinatal and maternal mortality. Considering that Nesfatin-1 was reported to be downregulated in serum of PE patients, we aimed to explore the functional role of Nesfatin-1 in trophoblast cells. Cell transfection was conducted to overexpress or inhibit Nesfatin-1, and its expression was measured by quantitative PCR. Cell proliferation, migration, and invasion abilities were determined employing CCK-8, flow cytometry, wound-healing, and transwell assays. Immunofluorescence assay was performed to detect E-cadherin and vimentin. ROS, MDA, and SOD levels were measured using their corresponding commercial kits. Western blot was used to identify the expression of vital kinases in PI3K/AKT/mTOR or GSK3β pathway and invasion-related proteins in trophoblast cells. Nesfatin-1 knockdown significantly suppressed proliferation, migration, and invasion and increased cell arrest in G1 phase, as well as downregulated expressions of MMP2/9 in HTR-8/SVneo cells. Besides, Nesfatin-1 knockdown promoted the expression of E-cadherin and reduced the expression of vimentin. Additionally, the levels of ROS, MDA, and SOD were elevated upon Nesfatin-1 knockdown. On the contrary, Nesfatin-1 overexpression exerted the opposite effects. Nesfatin-1 promoted the activation of PI3K/AKT/mTOR or GSK3β pathway, blocking of which reversed the promotive effects on trophoblast invasion and the inhibitory effects on oxidative stress of Nesfatin-1 in HTR-8/SVneo cells. In short, this study revealed that Nesfatin-1 promoted trophoblast cell proliferation, migration, invasion, and EMT and suppressed oxidative stress by activating PI3K/AKT/mTOR and AKT/GSK3β signaling pathway, laying the foundation for the development of therapeutic strategy for PE by targeting Nesfatin-1.

The objective of the study was to compare outcomes of women with placenta accreta spectrum(PAS) who underwent emergency cesarean hysterectomy with and without prophylactic intravascular balloon catheters.Outcome measures were not significantly different between the IIABOC group and the control group. IAABC plus hysterectomy resulted in a better outcome than hysterectomy alone, with less amount of estimated blood loss (EBL) during cesarean section (2000 vs 3000 ml,IAABC was more effective in emergency cesarean hysterectomy related to PAS disorders.

Introduction: Placenta previa contributes greatly to severe antenatal and post-partum hemorrhage in obstetrics. Previous studies have mainly focused on the risk factors of placenta previa, and very limited studies have reported which factors may affect the dynamic outcome of placenta previa in the second trimester. The aim of this study was to investigate the impact of maternal and neonatal characteristics on dynamic change of placenta previa from second trimester to delivery.Methods: A retrospective longitudinal sub-cohort investigation was carried out among 510 pregnant women with placenta previa in second trimester of pregnancy from the Longitudinal Placenta Previa Study (LoPPS). Logistic regression analysis was used to discover the connections between maternal covariates and dynamic change process of placenta. Multivariable linear regression analysis was used to detect the associations between perioperative characteristics and the volume of intraoperative bleeding. Results: Among the pregnant women with major placenta previa in the second trimester, 28.8% of them were without placenta previa at delivery, and 25.5% morphed into minor placenta previa. There was significant correlation between placenta previa type and pre-pregnancy BMI (Beta: 0.141, 95% CI: 0.046,0.235. p=0.003), gestational age (Beta: -0.355, 95% CI: -0.507, -0.204. pConclusion: 71.2% of the pregnant women with major placenta previa in the second trimester were still with placenta previa at delivery, and the proportion may be higher in pregnant women suffering previous cesarean section and with high pre-pregnancy BMI.

Background: Fetal supraventricular tachyarrhythmia is a common reason for referral to fetal cardiology. Multiple antiarrhythmic transplacental medications can be used to treat these diseases. Debates remain regarding the standardized therapy. Methods: PubMed, EMBASE, Cochrane Library, Web of Science, Google Scholar, and ClinicalTrials.gov will be searched from inception to September 2020. A handsearching for gray literature, including unpublished conference articles, will be performed. The randomized control trials, case–control, and cohort studies will be accepted, no matter what the languages they were reported. We will first focus on the effectiveness of the therapy on fetal cardiac rhythm and/or heart rate. Then we will do further analysis of preterm delivery, fetal hydrops, intrauterine fetal demise, and maternal side effects. The Cochrane Risk of Bias Tool and the Newcastle–Ottawa scale will be used to assess the risk of bias of the randomized controlled trials, case–control, and cohort studies, respectively. Two independent reviewers will carry out literature identification, data collection, and study quality assessment. Discrepancies will be resolved by a third reviewer. Statistical analysis will be conducted using the STATA 13.0 software. Result: The results will provide helpful information about the effect of multiple antiarrhythmic transplacental therapies in pregnancies with supraventricular tachycardia or atrial flutter, and demonstrate which therapy is more effective. Conclusion: The conclusion drawn from this systematic review will benefit the patients with fetal supraventricular tachyarrhythmia.

The 2019 novel coronavirus disease (COVID-19), which is caused by the novel beta coronavirus, SARS-CoV-2, is currently prevalent all over the world, causing thousands of deaths with relatively high virulence. Like two other notable beta coronaviruses, severe acute respiratory syndrome coronavirus-1 (SARS-CoV-1) and Middle East respiratory syndrome coronavirus (MERS-CoV), SARS-CoV-2 can lead to severe contagious respiratory disease. Due to impaired cellular immunity and physiological changes, pregnant women are susceptible to respiratory disease and are more likely to develop severe pneumonia. Given the prevalence of COVID-19, it is speculated that some pregnant women have already been infected. However, limited data are available for the clinical course and management of COVID-19 in pregnancy. Therefore, we conducted this review to identify strategies for the obstetric management of COVID-19. We compared the clinical course and outcomes of COVID-19, SARS, and MERS in pregnancy and discussed several drugs for the treatment of COVID-19 in pregnancy.

Macrophages and their initiation of acute inflammation have been defined to be functionally important in tissue repair and regeneration. In injury-induced production of macrophage migration inhibitory factor (MIF), which has been described as a pleiotropic protein that participates in multiple cellular and biologic processes, it is unknown whether it is involved in the regulation of macrophage events during the epimorphic regeneration. In the model of gecko tail amputation, the protein levels of gecko MIF (gMIF) have been determined to be significantly increased in the nerve cells of the spinal cord in association with the recruitment of macrophages to the lesion site. gMIF has been shown to interact with the CD74 receptor to promote the migration of macrophages through activation of Ras homolog gene family member A and to trigger inflammatory responses through MAPK signaling pathways. The determination of microsphere phagocytosis also indicated that gMIF could enhance macrophage phagocytosis. gMIF-mediated recruitment and activation of macrophages have been found to be necessary for gecko tail regeneration, as evidenced by the depletion of macrophages using clodronate liposomes. The results present a novel function of MIF during the epimorphic regeneration, which is beneficial for insights into its pleiotropic property.-Wang, Y., Wei, S., Song, H., Zhang, X., Wang, W., Du, N., Song, T., Liang, H., Chen, X., Wang, Y. Macrophage migration inhibitory factor derived from spinal cord is involved in activation of macrophages following gecko tail amputation.

Background: To explore the genetic diversity and drug resistance status of MTB in Xuzhou, China. Methods: A total of 325 clinical MTB strains were genotyped by spacer-oligonucleotide typing (spoligotyping) and mycobacterial interspersed repetitive unit variable number of tandem repeats (MIRU-VNTR). Phenotypic resistance was assessed by drug susceptibility testing (DST). Result: Based on the spoligotyping method, 325 MTB isolates were classified into 5 known genotypes and 12 unknown genotypes, and the largest branch comprised 268 strains belonging to the Beijing family. Based on the 15-loci VNTR typing method, 325 MTB isolates were divided into 35 clusters and 220 unique patterns. Compared to the low discriminatory power of spoligotyping genotyping (HGDI = 0.3444), 15-loci VNTR genotyping had a significantly higher discriminatory power for all strains (HGDI = 0.9980), particularly for the Beijing family strains (HGDI = 0.9892). When spoligotyping and 15-loci VNTR methods were used together, the discriminatory power increased to 0.9991. The Beijing family strain presented increased risks for developing multi-drug resistance TB (P < 0.05). Conclusion: The Beijing family isolates is the most prevalent strains in Xuzhou. Spoligotyping, in combination with 15-loci MIRU-VNTR, is useful for epidemiological analysis of MTB transmission in Xuzhou.

Certain regenerative vertebrates such as fish, amphibians and reptiles are capable of regenerating spinal cord after injury. Most neurons of spinal cord will survive from the injury and regrow axons to repair circuits with an absence of glial scar formation. However, the underlying mechanisms of neuronal anti-apoptosis and glia-related responses have not been fully clarified during the regenerative process. Gecko has becoming an inspiring model to address spinal cord regeneration in amniotes. In the present study, we investigated the regulatory roles of Snail family members, the important transcriptional factors involved in both triggering of the cell migration and cell survival, during the spontaneous spinal cord regeneration. Both Snail1 and Snail3 have been shown to promote neuronal survival and astrocytic migration via anti-apoptotic and GTPases signaling following gecko tail amputation. Transforming growth factor-beta (TGFβ), together with other cytokines were involved in inducing expression of Snail protein. Our data indicate a conserved function of Snail proteins in embryonic development and tissue regeneration, which may provide clues for CNS repair in the mammals.

The Wingless/Integrated (Wnt) signaling pathway plays important roles in central nervous system (CNS) development and regeneration, and β-catenin, the central component, has been considered in association with adult neurogenesis. To decipher its roles on spontaneous spinal cord regeneration, we cloned β-catenin from Gekko japonicus and examined its function in regenerating spinal cord. The protein was localized in the neurons and oligodendrocytes and maintained a stable expression levels during the spinal cord regeneration. The temporal pattern of expression has been found to be completely distinct with those of glycogen synthase kinase 3β (GSK3β). Experiments of gain-of-function by overexpression of full length β-catenin or stabilized ΔN90-β-catenin revealed that the accumulated protein attenuates the elongation of neurites and oligodendrocyte process. Knockdown of endogenous β-catenin, however, decreased proliferation of oligodendrocytes by affecting expression of downstream lef1 and c-jun. The upregulated extracellular matrix fibronectin in injured cord was found to be inefficient in regulation of β-catenin expression. Our results suggest that a tightly regulated stable expression of β-catenin is required for the spontaneous spinal cord regeneration.

Reactive oxygen species (ROS) participate in various physiological and pathological functions following generation from different types of cells. Here we explore ROS functions on spontaneous tail regeneration using gecko model. ROS were mainly produced in the skeletal muscle after tail amputation, showing a temporal increase as the regeneration proceeded. Inhibition of the ROS production influenced the formation of autophagy in the skeletal muscles, and as a consequence, the length of the regenerating tail. Transcriptome analysis has shown that NADPH oxidase (NOX2) and the subunits (p40phox and p47phox) are involved in the ROS production. ROS promoted the formation of autophagy through regulation of both ULK and MAPK activities. Our results suggest that ROS produced by skeletal muscles are required for the successful gecko tail regeneration.

Brown planthopper (BPH, Nilaparvata lugens Stal) is one of the most serious rice insect pests in Chinaand the world. Exploiting new resistance genes and breeding advanced genetic stocks are important for breeding resistance varieties. In this study, more than 1 200 accessions of common wild rice ( Oryza rufipogon Griff.), were evaluated for the resistance to several biotypes of BPH. 30 resistant accessions were obtained and 6 of them showed broad spectrum resistance to 5 or all of the 6 BPH biotypes, i.e. biotypes 1 and 2, Bangladesh, Mekong (Vietnam), Cuulong (Vietnam) and Pantnagar (India), which are spreading most rice growing regions in the world. Genetic analysis was turned out that the BPH resistance in these stocks was controlled by two pairs of recessive genes with duplicate interaction against biotypes 2 and Cuulong, but the resistance to the biotype Pantnagar was controlled by one pair of recessive gene. This indicated different genetic mechanism of reaction against BPH biotypesin the resistant sources. The two recessive genes existing in the entry 2183 might be new discovered genes as no BPH resistance gene has been reported in these chromosome regions. They were tentatively designated asbph18 (t) and bph19 (t), respectively. A total of 143 entries of advanced genetic stocks resistant to BPH and 6promising resistance lines or hybrid combinations with high yield or good quality were bred. These resistant advanced genetic stocks set a solid foundation for breeding new resistance varieties.