linc01152 Regulates Cell Viability, Cell Migration and Cell Invasion of Breast Cancer via Regulating miR-320a and MTDH.

Breast cancer is a global disease and a cause of cancer-related deaths in women. Long non-coding RNAs (lncRNAs) perform important functions in biological processes. The aim of this study was to verify the functions and regulatory mechanisms of linc01152 in breast cancer. Relative expression of linc01152 was measured using RT-PCR. siRNAs targeting linc01152 were designed to inhibit its expression. Cell viability, cell invasion, and migration capacities were determined using CCK-8 and Transwell assays. Downstream targets, miRNAs, and mRNAs were predicted and validated using luciferase reporter assay. The expression of linc01152 in breast cancer cells was higher than that in normal breast cells, with BT474 and MDA-MB-468 cell lines presenting the highest expression levels of linc01152. The inhibition of linc01152 expression led to lower cell viability and attenuated cell migration and invasion. The regulatory network of linc01152-miR-320a-MTDH was validated using luciferase reporter assay. The inhibition of miR-320a expression reversed the effect of si-linc01152 on cell viability, migration, and invasion. Taken together, the linc01152-miR-320a-MTDH regulatory network is correlated with the pathogenesis of breast cancer.

miR-146b-5p downregulates IRAK1 and ADAM19 to suppress trophoblast proliferation, invasion, and migration in miscarriage†.

A large proportion of miscarriages are classified as unexplained miscarriages since no cause is identified. No reliable biomarkers or treatments are available for these pregnancy losses. While our transcriptomic sequencing has revealed substantial upregulation of miR-146b-5p in unexplained miscarriage villous tissues, its role and associated molecular processes have yet to be fully characterized. Our work revealed that relative to samples from normal pregnancy, miR-146b-5p was significantly elevated in villous tissues from unexplained miscarriage patients and displayed promising diagnostic potential. Moreover, miR-146b-5p agomir contributed to higher rates of embryonic resorption in ICR mice. When overexpressed in HTR-8/SVneo cells, miR-146b-5p attenuated the proliferative, invasive, and migratory activity of these cells while suppressing the expression of MMP9 and immune inflammation-associated cytokines, including IL1B, IL11, CXCL1, CXCL8, and CXCL12. Conversely, inhibition of its expression enhanced proliferation, migration, and invasion abilities. Mechanistically, IL-1 receptor-associated kinase-1 and a disintegrin and metalloproteinase 19 were identified as miR-146b-5p targets regulating trophoblast function, and silencing IL-1 receptor-associated kinase-1 had similar effects as miR-146b-5p overexpression, while IL-1 receptor-associated kinase-1 overexpression could partially reverse the inhibitory impact of this microRNA on trophoblasts. miR-146b-5p may inhibit trophoblast proliferation, migration, invasion, and implantation-associated inflammation by downregulating IL-1 receptor-associated kinase-1 and a disintegrin and metalloproteinase 19, participating in the pathogenesis of miscarriage and providing a critical biomarker and a promising therapeutic target for unexplained miscarriage.

Air pollution exposure and ovarian reserve impairment in Shandong province, China: The effects of particulate matter size and exposure window.

BACKGROUND: Lack of evidence exists on whether air pollution exposure may affect ovarian reserve, especially for Chinese women. OBJECTIVES: To explore the association between exposure to various air pollutants and anti-Müllerian hormone (AMH), a predictor of ovarian reserve, over different exposure windows in Shandong Province, China. METHODS: We enrolled 18,878 women who had AMH measurements in the Center for Reproductive Medicine, Shandong University during 2010-2019. Daily average concentrations of ambient particulate matter with diameters ≤1 µm/2.5 µm/10 µm (PM1, PM2.5, and PM10), nitrogen dioxide (NO2) and ozone (O3) were developed at a spatial resolution of 0.01° × 0.01°, and assigned to the residential addresses. Three exposure windows were considered, i.e., the process from primary to small antral follicle stage (W1), from primary to secondary follicle stage (W2), and from secondary to small antral follicle stage (W3). The air pollution-AMH association was fitted using the multivariable linear mixed effect model with adjustment for potential confounders. Stratified analyses were performed by age group, overweight status, residential region, and educational level. RESULTS: The level of AMH changed by -8.8% (95% confidence interval (CI): -12.1%, -5.3%), -2.1% (95% CI: -3.5%, -0.6%), -1.9% (95% CI: -3.3%, -0.5%), and -4.5% (95% CI: -7.1%, -1.9%) per 10 µg/m3 increase in PM1, PM2.5, PM10, and NO2, respectively, during W1. The effect estimates were significant during W2 for PM1, PM2.5 and NO2 while minimal association was observed in W3. Greater vulnerability for certain air pollutants were observed for women who lived in inland areas and were less educated. CONCLUSIONS: We found that ovarian reserve was negatively associated with air pollution exposure for women, particularly from the primary to secondary follicle stage. The effect estimate increased by the reduction in the diameter of PMs, which also varied across population sub-groups.

Mersilene tape versus conventional sutures in transvaginal cervical cerclage: a systematic review and meta-analysis.

OBJECTIVE: This study aimed to assess the effectiveness of Mersilene tape versus alternative suture types in prolonging singleton pregnancies as well as other pregnancy and neonatal outcomes, in cases of history-, ultrasound-, and exam-indicated cervical cerclage. METHODS: A systematic review was conducted to identify relevant studies comparing different suture types in cervical cerclage procedures. The primary outcome of interest was preterm birth (PTB) rate < 37, <35, < 28, and < 24 weeks. Statistical analyses were performed to determine the relationship between suture type and various outcomes. RESULTS: A total of five studies, including three randomized controlled trials (RCTs) and two retrospective studies, with a combined participation of 2325 individuals, were included. The pooled analysis indicated no significant association between suture type and PTB at less than 37 weeks of gestation (RR: 1.02, 95% CI: 0.65-1.60, p < 0.01, I2 = 74%). Women who received Mersilene tape had a higher risk of PTB at 34-37 weeks (RR: 2.62, 95% CI: 1.57-4.37, p = 0.69, I2 = 0%), but a lower risk of PTB at less than 34 weeks (RR: 0.43, 95% CI: 0.28-0.66, p = 0.66, I2 = 46%). No statistically significant differences were observed for PTB before 28 weeks (RR: 1, 95% CI: 0.65-1.53, p = 0.70, I2 = 0%), before 24 weeks (RR: 0.86, 95% CI: 0.60-1.23, p = 0.33, I2 = 0%), incidence of chorioamnionitis (RR: 0.97, 95% CI: 020-4.83, p < 0.01, I2 = 95%), neonatal intensive care unit (NICU) admission (RR: 0.79, 95% CI: 0.28-2.22, p = 0.08, I2 = 67%) and neonatal death (RR: 1.00, 95% CI: 0.42-2.35, p = 0.17, I2 = 48%). CONCLUSION: Our findings suggest that Mersilene tape does not reduce the risk of PTB before 37, 28 or 24 weeks. We observed higher risk of preterm birth between 34 and 37 weeks with Mersilene tape but lower incidence before 34 weeks, a period with higher neonatal morbidity and mortality. Due to the limited number of studies, our results and their clinical significance should be interpreted with caution.

Upregulation of miRNA-26a Enhances the Apoptosis of Cerebral Neurons by Targeting EphA2 and Inhibiting the MAPK Pathway.

Neural tube defects (NTDs) constitute the second most common congenital malformation of the central nervous system. The pathogenesis of NTDs is not entirely clear. In recent years, microRNAs (miRNAs) have become a hot spot in genetic and developmental biology research. The present study aimed to explore the potential role of miRNA-26a in NTDs and the underlying pathogenesis thereof. First, we found significantly increased miRNA-26a expression in fetuses with NTDs (p < 0.0001), which significantly downregulated EphA2 and ERK1 mRNA and protein expression levels in fetuses with NTDs compared to normal controls (p < 0.01). In addition, a dual-luciferase reporter assay showed that miR-26a negatively regulated EphA2 by directly binding with the 3'-untranslated region of EphA2. Second, the upregulation of miRNA-26a expression increased caspase 3 and 9 protein expression levels (p < 0.01) and decreased EphA2 mRNA and protein expression levels (p < 0.01), as well as ERK1 and SRF protein expression levels (p < 0.01) in mouse neural stem cells (NE-4C) and human astroblastoma cells (U87MG). Furthermore, the upregulation of miRNA-26a inhibited cell proliferation and enhanced apoptosis of NE-4C and U87MG cells (p < 0.05). Similar results were observed with the MAPK inhibitor PD98059 (p < 0.01). These results suggest that miR-26a targets EphA2, modulates phosphorylation of the MAPK/ERK (MEK) pathway, regulates SRF, and participates in regulating nervous cell proliferation and apoptosis. Dysregulation of the aforementioned mechanism may be involved in the pathogenesis of NTDs.

MiR-135a-5p suppresses trophoblast proliferative, migratory, invasive, and angiogenic activity in the context of unexplained spontaneous abortion.

BACKGROUND: Spontaneous abortions (SA) is amongst the most common complications associated with pregnancy in humans, and the underlying causes cannot be identified in roughly half of SA cases. We found miR-135a-5p to be significantly upregulated in SA-associated villus tissues, yet the function it plays in this context has yet to be clarified. This study explored the function of miR-135a-5p and its potential as a biomarker for unexplained SA. METHOD: RT-qPCR was employed for appraising miR-135a-5p expression within villus tissues with its clinical diagnostic values being assessed using ROC curves. The effects of miR-135a-5p in HTR-8/SVneo cells were analyzed via wound healing, Transwell, flow cytometry, EdU, CCK-8, and tube formation assays. Moreover, protein expression was examined via Western blotting, and interactions between miR-135a-5p and PTPN1 were explored through RIP-PCR, bioinformatics analyses and luciferase reporter assays. RESULTS: Relative to normal pregnancy (NP), villus tissue samples from pregnancies that ended in unexplained sporadic miscarriage (USM) or unexplained recurrent SA (URSA) exhibited miR-135a-5p upregulation. When this miRNA was overexpressed in HTR-8/SVneo cells, their migration, proliferation, and cell cycle progression were suppressed, as were their tube forming and invasive activities. miR-135a-5p over-expression also downregulated the protein level of cyclins, PTPN1, MMP2 and MMP9. In RIP-PCR assays, the Ago2 protein exhibited significant miR-135a-5p and PTPN1 mRNA enrichment, and dual-luciferase reporter assays indicated PTPN1 to be a bona fide miR-135a-5p target gene within HTR-8/SVneo cells. CONCLUSION: miR-135a-5p may suppress trophoblast migratory, invasive, proliferative, and angiogenic activity via targeting PTPN1, and it may thus offer value as a biomarker for unexplained SA.

Placental transcriptome sequencing combined with bioinformatics predicts potential genes and circular RNAs associated with hemoglobin Bart's hydrops fetalis syndrome.

AIM: Hemoglobin Bart's hydrops fetalis syndrome (BHFS) is the most severe form of α-thalassemia. Histological alternations can be observed in placenta, but placental transcriptome profile and circular RNAs have not been studied in this disease. The aim of this study was to define the placental transcriptional changes and find relevant circular RNAs in BHFS. METHODS: We performed high-throughput RNA sequencing to detect placental samples from fetuses affected by BHFS (n = 5) and normal fetuses (NF, n = 5), quantitative reverse transcription polymerase chain reaction (RT-qPCR), and Sanger sequencing to validate the differentially expressed circRNAs and their potentially related miRNAs (BHFS, n = 22; NF, n = 11). Bioinformatics methods were performed for further analysis. RESULTS: Our results showed 152 differentially expressed genes (DEGs), 112 circRNAs, and 45 microRNAs that were differentially expressed. DEGs were found to be involved in Gene Ontology terms related to gas transport, cell adhesion, oxidative stress, organ development, hemopoiesis, and others. RT-qPCR results showed that hsa_circ_0003961 and hsa_circ_0006687 were upregulated (p < 0.05). The competing endogenous RNA and co-expression networks showed that hsa_circ_0003961 and hsa_circ_0006687 were connected with 3 miRNAs and some DEGs, including cell adhesion genes (e.g., CLDN19), hemoglobin related genes (e.g., SOX6 and HBZ) and angiogenesis related genes (e.g., EPHB2). Downregulations of hsa-miR-1299 and hsa-miR-625-5p in ceRNA network were also validated by RT-qPCR. Gene set enrichment analysis results for the two circRNAs showed that some gene sets associated with cell adhesion, hematopoietic system and apoptosis were significantly enriched. CONCLUSIONS: Our study characterized the placental transcriptome of BHFS. The circRNAs hsa_circ_0003961 and hsa_circ_0006687 in placenta may be relevant to BHFS.

Circulating noncoding RNAs as early predictive biomarkers in preeclampsia: a diagnostic meta-analysis.

BACKGROUND: We designed a meta-analysis to evaluate the clinical significance and efficacy of circulating noncoding RNAs (ncRNAs) in the early prediction of preeclampsia. METHODS: PubMed, Embase and the Cochrane Library were used to search for literature. The combined prediction performance was evaluated by calculating the area under the summary receiver operator characteristic (SROC) curve. The potential sources of heterogeneity were analysed by meta-regression analysis and subgroup analysis. All statistical analyses and mapping were performed by RevMan 5.3 and Stata 12.0. RESULTS: A total of 41 studies from 14 articles, including 557 preeclampsia patients and 842 controls, were included in our meta-analysis. All studies collected blood before onset. NcRNAs in blood performed relatively well in predicting preeclampsia. The combined sensitivity was 0.71, the specificity was 0.84, and the area under the SROC curve (AUC) was 0.86. Peripheral blood mononuclear cell (PBMC) samples showed the best diagnostic accuracy. The combined AUC was 0.93. Combined detection was better than single detection, and miRNA was better than circRNA. The heterogeneity of the study was determined by sample size, lncRNA characteristics, lncRNA source and race. CONCLUSION: Circulating ncRNAs can be valuable biomarkers used as candidates for noninvasive early predictive biomarkers of preeclampsia and have great clinical application prospects. The clinical value of ncRNAs needs to be tested by further multicentre, comprehensive and prospective studies, and the test criteria should be established.

Effects of ER-resident and secreted AGR2 on cell proliferation, migration, invasion, and survival in PANC-1 pancreatic cancer cells.

BACKGROUND: Anterior gradient-2 (AGR2) is a proto-oncogene involved in tumorigenesis and cancer progression. AGR2, predominantly localized in the endoplasmic reticulum (ER), is also a secreted protein detected in the extracellular compartment in multiple cancers. However, the biological functions of intracellular and extracellular AGR2 remain to be elucidated. METHODS: Based on the biochemical structure of AGR2 protein, PANC-1 pancreatic cancer cells stably expressing ER-resident or secreted AGR2 were generated by a lentivirus-mediated stable overexpression system. The capacities of cell proliferation, migration, invasion and survival were assessed in PANC-1 stable cells. Moreover, EGFR expression and activation were determined to explore the possible mechanism of AGR2 roles in pancreatic cancer tumorigenesis. RESULTS: It was discovered that secreted AGR2, but not ER-resident AGR2, promotes cell proliferation, migration and invasion of PANC-1 cells. Moreover, the data indicated that both the ER-resident and the secreted AGR2 enhance the survival capacity of PANC-1 cells after tunicamycin-induced ER stress and gemcitabine treatment. However, EGFR expression and activation were not found to be involved in AGR2-dependent oncogenic phenotypes in PANC-1 cells. CONCLUSIONS: Secreted AGR2 is predominantly involved in cell proliferation, migration and invasion in PANC-1 pancreatic cancer cells. Both secreted and ER-resident AGR2 contribute to the survival of PANC-1 cells under the challenging conditions. These findings provide insight into how different localizations of AGR2 have contributed to pancreatic cancer growth, metastasis, and drug sensitivity.

Lnc-RNA LINC01279 induces endometriosis via targeting of HOXA10.

AIM: To explore the regulatory role and molecular mechanism of lncRNA-LINC01279 in endometriosis (EMs). METHODS: Between September 2018 and July 2019, 20 EMs patients and 20 healthy subjects were recruited to detect the expression of lncRNA-LINC01279 in EMs and in normal endometrium via qRT-PCR. Autograft was used to establish EMs models on Spraque-Dawley (SD) rats, which was followed by taking volume measurements of EMs endometrium and observing pathological changes in the morphology of EMs via hematoxylin and eosin (H&E) staining. The qRT-PCR technique was further carried out to determine mRNA expression of lncRNA-LINC01279 and HOXA10 in the serum of EMs rats and LINC01279 shRNA-transfected rats, while the protein expression of HOXA10 was determined using a Western blot. RESULTS: EMs patients presented with upregulation of lncRNA-LINC01279 and downregulation of HOXA10 (p < 0.01 or 0.001). Online predictions further revealed that lncRNA-LINC01279 regulated the expression of HOXA10 via miRNA-135b. In EMs models, it was observed that there were a significantly enlarged endometrium and poor pathological morphology, significant upregulation of lncRNA-LINC01279, and downregulation of miR-135b and HOXA10 in serum (p < 0.05, 0.01 or 0.001). In the lncRNA-LINC01279 shRNA group, EMs rats, following treatment, had a sharp decrease in the volume of EMs endometrium, and an improvement in pathological morphology, while lncRNA-LINC01279 was downregulated, with upregulation of miR-135b and HOXA10 (p < 0.05, 0.01 or 0.001). CONCLUSION: LncRNA-LINC01279, by the mechanism of targeting miR-135b, has the potential to downregulate the expression of HOXA10, and therefore, can promote the development and progression of EMs.

Increased miRNA-518b inhibits trophoblast migration and angiogenesis by targeting EGR1 in early embryonic arrest†.

Evidence indicates that microRNAs (miRNAs) play essential roles in early embryonic development. The miRNA-518 family is a special biomarker of the placenta, and miRNA-518b is abnormally expressed in placental tissue in preeclampsia. Early growth response protein 1 (EGR1), a zinc finger transcriptional factor, plays an essential role in regulating cell differentiation, angiogenesis, and migration. Moreover, earlier studies have shown that EGR1 protein plays a key role in implantation. However, little is known about the role of miR-518b and EGR1 on early embryonic arrest (EEA) in humans. In our study, increased miR-518b along with decreased EGR1 was found in human villus tissues with EEA. Furthermore, we demonstrated by luciferase assay that miR-518b is a direct regulator of EGR1. After comparing the effect of silencing EGR1, vascular endothelial growth factor (VEGF) individually, and EGR1/VEGF in combination, we found that EGR1 can inhibit migration and angiogenesis of HTR-8 SVneo cells by decreasing the VEGF expression. Hypoxia plays an initial role in early embryonic development, and we found that hypoxia reduces the expression of miR-518b and increases the expression of EGR1 and VEGF to facilitate migration and angiogenesis in a hypoxic model of HTR-8/SVneo cell line. Our findings provide new insights into the role of miR-518b in EEA and implicate the potential application of miR-518b in the diagnosis and development of intervention for EEA.

Malignant transformation of vaginal adenosis to clear cell carcinoma without prenatal diethylstilbestrol exposure: a case report and literature review.

BACKGROUND: We report an extremely rare case of vaginal clear cell carcinoma, which originated from the malignant transformation of vaginal adenosis without prenatal diethylstilbestrol (DES) exposure. CASE PRESENTATION: In this case, the patient was a Chinese woman with a history of two decades of intermittent vaginal pain, sexual intercourse pain and vaginal contact bleeding. On September 1, 2011, when the patient was 39 years old, a vaginal biopsy revealed vaginal adenosis. After intermittent drug and laser treatment, her symptoms did not improve. Four years later, on March 4, 2015, another vaginal biopsy for abnormal vaginal cytology revealed atypical vaginal adenosis. After treatment with sirolimus, her symptoms and abnormal vaginal cytology results persisted, and she underwent laparoscopic hysterectomy with bilateral salpingo-oophorectomy and excision of the vaginal lesions. One year after the hysterectomy, on August 15, 2017, the vaginal cytology results suggested atypical glandular cells, and a biopsy revealed vaginal clear cell carcinoma originating from the atypical vaginal adenosis. A wide local resection of the vaginal lesions was performed, followed by concurrent chemoradiotherapy. Regular follow-up over 16 months showed no evidence of the recurrence of vaginal adenosis or cancer. CONCLUSIONS: Based on the evolution of a series of pathological evidence, we report the fourth case in the world of vaginal clear cell carcinoma originating from vaginal adenosis without prenatal DES exposure. Wide local excision with radiotherapy provided at least 16 months of disease-free survival.

Early missed abortion is associated with villous angiogenesis via the HIF-1α/VEGF signaling pathway.

PURPOSE: To analyze the effects of the hypoxia-inducible factor 1-alpha (HIF-1α)/vascular endothelial growth factor (VEGF) signaling pathway on villous angiogenesis in early missed abortion. METHODS: Immunohistochemical assays were performed to detect the expression of micro-vessel density (MVD), HIF-1α, and VEGF in villous tissue samples from 30 missed abortions and 30 elective abortions in early pregnancy. We further analyzed the correlation between HIF-1α/VEGF and MVD. HTR8/SVneo cells were cultured under hypoxic (1%) or normoxic (20%) conditions, tube formation was investigated, and protein and mRNA level of HIF-1α/VEGF were determined using western blot and qRT-PCR. Finally, HIF-1α was knocked down with siRNA introduced into HTR8/SVneo cell line under hypoxia, and HIF-1α/VEGF expression and HTR8/SVneo tube formation were investigated. RESULTS: The expression of HIF-1α, VEGF, and MVD was lower in the missed abortion than in the elective abortion group. Correlational analysis showed that the expression of HIF-1α and VEGF was positively correlated with MVD in both groups. The levels of HIF-1α/VEGF mRNA and protein in HTR8/SVneo cells were significantly enhanced under hypoxia. HIF-1α knockdown with siRNA inhibited HIF-1α/VEGF mRNA and protein levels of HTR8/SVneo cells induced by hypoxia. Tube formation of HTR8/SVneo cells was significantly enhanced in hypoxic culture and was inhibited by HIF-1α knockdown with siRNA. CONCLUSIONS: Our results reveal a novel role for HIF-1α/VEGF in regulating villous angiogenesis in early pregnancy and suggest that it may be a novel biomarker for missed abortion.

Invasive prenatal diagnosis of α-thalassemia to control Hb Bart's hydrops fetalis syndrome: 15 years of experience.

PURPOSE: The aim of the present study was to report experiences with invasive prenatal diagnosis of α-thalassemia for the prevention of Hb Bart's hydrops fetalis syndrome in the Guangxi Zhuang Autonomous Region, China. METHODS: Pregnant women and their partners who tested positive for α0-thalassemia or were diagnosed with HbH diseases were counseled and suggested to undergo a prenatal diagnostic procedure for α-thalassemia. Fetal material was obtained by chorionic villus sampling (CVS) between 9 and 13 weeks of gestation, by amniocentesis between 16 and 24 weeks of gestation and by cordocentesis after 24 weeks of gestation. The α0-thalassemia gene types were detected by gap polymerase chain reaction (Gap-PCR). All results were finally confirmed by DNA analysis after delivery or termination of pregnancy. RESULTS: An invasive prenatal α-thalassemia diagnosis was performed in 3155 cases at risk for Hb Bart's hydrops fetalis syndrome at our hospital from 2002 to 2016. CVS was performed in 1559 cases (49.4%), amniocentesis in 1240 cases (39.3%) and cordocentesis in 356 cases (11.3%). In total, 786 fetuses were diagnosed as Hb Bart's hydrops fetalis syndrome. Among these cases, the α-thalassemia genotype was --SEA/--SEA in 784 cases and --SEA/--THAI in 2 cases. All affected pregnancies were terminated in time. CONCLUSIONS: This extensive experience suggests that carrier screening, molecular diagnostics, genetic counselling, and prenatal diagnosis are effective measures to prevent Hb Bart's hydrops fetalis syndrome.

An online secondary path modeling method with regularized step size and self-tuning power scheduling.

This paper investigates the active noise control algorithms and improves them by using online secondary path modeling. The proposed method uses three adaptive filters to track the convergence of the system as well as reduce the target noise. By theoretical analysis, the optimized step size and injected random noise gain are derived. The step size is varied according to the convergence of three adaptive filters and the gain of injected random noise is proportional to the power of modeling error, which makes the method more stable even in the presence of strong perturbation. Compared with previous methods, the proposed method improves the convergence rate and estimation accuracy for both the active control system and the secondary path modeling process with less increase of computational complexity. The simulation results verify the above analysis by controlling three different kinds of noise.

Prenatal Diagnosis and Pregnancy Outcome Analysis of Polyhydramnios.

The aim of the study was to investigate the etiology and pregnancy outcomes in mothers with polyhydramnios through prenatal diagnosis and pregnancy outcome analysis of pregnant women with polyhydramnios. One hundred and thirty women were enrolled. Fifty pregnant women with polyhydramnios were categorized as the case group, and 80 pregnant women with normal amniotic fluid were categorized as the control group. The causes of polyhydramnios and the pregnancy outcomes were analyzed. Two cases had chromosomal abnormalities, seven had severe α-thalassemia, 15 had fetal anomalies, four had maternal-fetal diseases and 22 had unexplained idiopathic polyhydramnios. Significantly, higher occurrences of cesarean section, preterm birth, fetal anomaly, fetal distress, fetal macrosomia and female fetuses occurred in patients with polyhydramnios than in patients without polyhydramnios. Polyhydramnios is associated with a higher occurrence of adverse perinatal outcomes. Intensive monitoring of the maternal-fetal condition and prenatal diagnosis is important in patients with polyhydramnios.

Association study between CYP17 gene polymorphism and endometriosis risk: a meta-analysis.

The cytochrome P450 subfamily 17 (CYP17) gene T > C polymorphism is associated with endometriosis risk. However, studies on the association between the genotyping of MspA1 polymorphism in the 5'-untranslated region of the CYP17 gene and endometriosis risk have reported controversial results. The aim of the present study was to obtain a more precise estimate of the relationship of CYP17 gene polymorphism with endometriosis risk. Relevant articles published up to April 2014 were obtained from Pubmed, Embase, and Cochrane Central electronic databases. Case-control studies about the association between CYP17 gene polymorphisms and endometriosis were selected. Eligible data were extracted by two independent reviewers. The strength of the association between CYP17 and endometriosis was assessed by pooled odds ratios (OR) with 95% confidence intervals (CI). Eligible case-control studies involving 1000 cases and 1167 controls were analyzed from 280 studies. The pooled results showed no association between the CYP17 gene T > C polymorphism and endometriosis risk in the overall population (CC vs TT: OR = 0.92, 95% CI = 0.52-1.61, P = 0.762; TC vs TT: OR = 1.01, 95% CI = 0.72-1.42, P = 0.949; dominant model: OR = 0.94, 95% CI = 0.64-1.39, P = 0.763; recessive model: OR = 0.93, 95% CI = 0.64-1.35, P = 0.712). In the subgroup analysis based on ethnicity, no significant association was found in Asians, Caucasians and mixed population under a recessive model (Asians: OR = 0.76, 95% CI = 0.53-1.07, P = 0.118; Caucasians: OR = 2.47, 95% CI = 0.45-13.66, P = 0.300; mixed population: OR = 1.40, 95% CI = 0.65-3.02, P = 0.712). In conclusion, the meta-analysis suggested that the CYP17 gene polymorphism was not associated with endometriosis risk. Considering the limited sample size and ethnicity included in our meta-analysis, an updated meta-analysis needs to be conducted when larger and more well-designed studies are published.

Maternal IgG Anti-A and Anti-B Titer Levels Screening in Predicting ABO Hemolytic Disease of the Newborn: A Meta-Analysis.

UNLABELLED: Maternal IgG anti-A/B titers have been considered as a susceptible factor to the risk of ABO hemolytic disease in newborn (ABO-HDN). However, the results remain controversial. This meta-analysis aimed to estimate the association between maternal IgG anti-A/B titers and the risk of ABO-HDN. METHODS: Trials on the relationship between maternal IgG anti-A/B titers and the risk of ABO-HDN were collected by searching Embase, PubMed, and Cochrane Central Register of Controlled Trials (CENTRAL) electronic databases. The inclusion criteria were maternal IgG anti-A/B titers screening and the evaluation of clinical outcomes in relation to ABO-HDN. Stata 12.0 was used to analyze the data. RESULTS: A total of 23 trials were eligible for inclusion, of which four trials with 5,246 participants were suitable for this meta-analysis. Meta-analysis results suggested that maternal IgG anti-A/B titers were significantly associated with the risk of ABO-HDN [OR = 2.86, 95% CI = 2.50-3.28; OR = 4.67, 95% CI = 3.92-5.55; OR = 1.61, 95% CI = 1.36-1.91 in titers (128 to 256) vs. titers (64 or lower), titers (512 or higher) vs. titers (64 or lower), and titers (512 or higher) vs. titers (128-256), respectively]. CONCLUSIONS: Our meta-analysis suggests that maternal IgG anti-A/B titers are significantly associated with the risk of ABO-HDN. They contribute to the prediction of risk of ABO-HDN, in addition to the need for invasive treatment for antibody titers ≥512.

The Relationship Between Social Media Use and Negative Emotions Among Chinese Medical College Students: The Mediating Role of Fear of Missing Out and the Moderating Role of Resilience.

Objective: This study aimed to examine the mediating role of fear of missing out (FoMO) and the moderating role of resilience in the association between social media use and negative emotions among medical college students in China during the COVID-19 pandemic. Participants and Methods: A cross-sectional study design was conducted, medical college students from Qiqihar Medical University, China participated in the study. A total of 470 medical college students were recruited voluntarily to complete questionnaires on social media use, FoMO, resilience, and negative emotions. Results: Social media use was positively associated with FoMO and negative emotions among medical students (p < 0.01). The total effect of social media use on negative emotions was significant (ß = 1.101, SE = 0.079, p < 0.001). Social media use had no significant direct effect on negative emotions (ß = 0.168, SE = 0.096, p > 0.05), but it had an indirect effect on negative emotions via mediation of FoMO (ß = 0.933, SE = 0.106, 95% CI: 0.731 to 1.149). Moreover, resilience had a significant moderating effect on the relationship between FoMO and negative emotions (ß = -0.021, SE = 0.005, 95% CI: -0.032 to -0.012). FoMO had a significant positive predictive effect on negative emotions at both levels of resilience (low resilience individuals: ß = 1.079, SE = 0.076, p < 0.001; high resilience individuals: ß = 0.212, SE = 0.094, p < 0.05). Conclusion: Social media use and FoMO may be risk factors for increased negative emotions, and resilience should be considered in prevention and intervention strategies designed to mitigate negative emotions among medical college students.

MiRNA-494 induces trophoblast senescence by targeting SIRT1.

OBJECTIVE: Although the mechanism underlying preeclampsia (PE) has been widely explored, the mechanisms related to senescence have not yet been fully revealed. Therefore, we investigated the role of the miR-494/longevity protein Sirtuin 1 (SIRT1) axis in PE. METHODS: Human placental tissue was obtained from severe preeclampsia (SPE) (n = 20) and gestational age-matched normotensive pregnancies (n = 20), and senescence-associated ß-galactosidase (SAßG) and SIRT1 expression levels were measured. The TargetScan and miRDB databases predicted candidate miRNAs targeting SIRT1, and intersected with differentially expressed miRNAs in the GSE15789 dataset (p < 0.05, |log2FC|≥1.5). Subsequently, we showed that miRNA (miR)-494 expression was significantly elevated in SPE, revealing miR-494 as a candidate SIRT1-binding miRNA. A dual-luciferase assay confirmed the targeting relationship between miR-494 and SIRT1. The senescence phenotype, migration, cell viability, reactive oxygen species (ROS) production levels and inflammatory molecule expression levels were measured after miR-494 expression was altered. We conducted a rescue experiment using SIRT1 plasmids to further demonstrate the regulatory relationship. RESULTS: SIRT1 expression was lower(p < 0.01) and miR-494 expression was higher (p < 0.001) in SPE, and SaßG staining showed premature placental aging in SPE (p < 0.001). Dual-luciferase reporter assays revealed that miR-494 targeted SIRT1. Compared to control cells, HTR-8/SVneo cells with upregulation of miR-494 had remarkably downregulated SIRT1 expression (p < 0.001), more SAßG-positive cells (p < 0.001), cell cycle arrested (p < 0.05), and upregulated P21 and P16 expression (p < 0.01). miR-494 overexpression also decreased HTR-8/SVneo cell migration (p < 0.05) and ATP synthesis (p < 0.001), increased ROS levels (p < 0.001), and upregulated NLRP3 and IL-1ß expression (p < 0.01). SIRT1-overexpressing plasmids partially reversed the effects of miR-494 overexpression in HTR-8/SVneo cells. CONCLUSION: The miR-494/SIRT1 interaction plays a role in the mechanism of premature placental aging in PE patients.