Bisphenol S exposure induces intestinal inflammation via altering gut microbiome.

Bisphenol S (BPS), a substitute for bisphenol A, is widely used in the manufacture of food packaging materials, raising concern over its toxicity. However, evidence is still lacking on whether gut microbiota involved in BPS induced intestinal inflammation in mammals, as well as its underlying mechanism. Using mouse BPS exposure model, we found intestinal inflammation characterized by shortened colon length, crypt distortion, macrophage accumulation and increased apoptosis.

Hepatic toxicity prediction of bisphenol analogs by machine learning strategy.

Toxicological studies have demonstrated the hepatic toxicity of several bisphenol analogs (BPs), a prevalent type of endocrine disruptor. The development of Adverse Outcome Pathway (AOP) has substantially contributed to the rapid risk assessment for human health. However, the lack of in vitro and in vivo data for the emerging BPs has limited the hazard assessment of these synthetic chemicals.

Multi-omics approach characterizes the role of Bisphenol F in disrupting hepatic lipid metabolism.

Bisphenol F (BPF), a substitute for bisphenol A (BPA), is ubiquitous existed in various environmental media. Exposure to BPF may promote non-alcoholic fatty liver disease (NAFLD), while the potential mechanism is still unknown. In current study, we used in vitro and in vivo model to evaluate its hepatotoxicity and molecular mechanism.

Early-life bisphenol AP exposure impacted neurobehaviors in adulthood through microglial activation in mice.

Bisphenol AP (BPAP), a structural analog of bisphenol A (BPA), has been widely detected in environment and biota. BPAP was reported to interfere with hormone and metabolism, while limited data were available about its effects on neurobehavior, especially exposure to it during early-life time. A mouse model of early-life BPAP exposure was established to evaluate the long-term neurobehaviors in offspring.

Long-Term Degradation Evaluation of the Mismatch of Sensitive Capacitance in MEMS Accelerometers.

During long-term use, MEMS accelerometers will experience degradation, such as bias and scale factor changes. Bias of MEMS capacitive accelerometers usually comes from the mismatch of parasitic capacitance and sensitive capacitance. This paper focuses on the mismatch of sensitive capacitance and analyzes the mechanism of long-term degradation of MEMS accelerometers.

Reliability Evaluation Based on Mathematical Degradation Model for Vacuum Packaged MEMS Sensor.

Vacuum packaging is used extensively in MEMS sensors for improving performance. However, the vacuum in the MEMS chamber gradually degenerates over time, which adversely affects the long-term performance of the MEMS sensor. A mathematical model for vacuum degradation is presented in this article for evaluating the degradation of vacuum packaged MEMS sensors, and a temperature-accelerated test of MEMS gyroscope with different vacuums is performed.

Preimplantation triclosan exposure alters uterine receptivity through affecting tight junction protein†.

Triclosan is a broad-spectrum antibacterial agent and widely exists in environmental media and organisms. Triclosan exposure has been reported to have adverse effects on reproduction including embryo implantation disorder. During the embryo implantation window, it is vital that the endometrium develops into a receptive state under the influence of ovarian hormones.

Calibration Method of Accelerometer Based on Rotation Principle Using Double Turntable Centrifuge.

For linear accelerometers, calibration with a precision centrifuge is a key technology, and the input acceleration imposed on the accelerometer should be accurately obtained in the calibration. However, there are often errors in the installation of sample that make the calibration inaccurate. To solve installation errors and obtain the input acceleration in the calibration of the accelerometer, a calibration method based on the rotation principle using a double turntable centrifuge is proposed in this work.

Prothioconazole induces cell cycle arrest by up-regulation of EIF4EBP1 in extravillous trophoblast cells.

Prothioconazole (PTC) is a new broad-spectrum triazole antibacterial agent that is being widely used in agriculture. PTC has been linked to a number of reproductive outcomes including embryo implantation disorder; however, the exact mechanism underlying this relationship has yet to be determined. Proper trophoblast proliferation and migration is a prerequisite for successful embryo implantation.

Exploration of the developmental toxicity of TCS and PFOS to zebrafish embryos by whole-genome gene expression analyses.

Triclosan (TCS) and perfluorooctane sulfonate (PFOS) are known to have both endocrine disrupting and developmental toxicity effects on zebrafish embryos. Currently, potential molecular mechanisms underlying these toxicological phenomena require further studies. To address this gap in the literature, we used whole transcriptome microarrays to being to address the potential molecular mechanisms underlying developmental toxicity of TCS and PFOS on zebrafish embryos.

Enhancer RNA lnc-CES1-1 inhibits decidual cell migration by interacting with RNA-binding protein FUS and activating PPARγ in URPL.

Unexplained recurrent pregnancy loss (URPL) is a significant reproductive health issue, affecting approximately 5% of pregnancies. Enhancer RNAs (eRNAs) have been reported to play important roles during embryo development and may be related to URPL. To investigate whether and how eRNAs are involved in URPL, we performed RNA sequencing in decidual tissue.

Serum albumin mediates the effect of multiple per- and polyfluoroalkyl substances on serum lipid levels.

Perfluoroalkyl and polyfluoroalkyl substances (PFASs) are synthetically manufactured chemicals recognized to be toxic, bioaccumulative, and persistent. Previous studies on PFAS exposure and serum lipid levels have mainly focused on individual PFASs; however, the influence of multiple-PFAS exposure on the serum lipid profile remains unclear. This study was performed to evaluate the combined effects of multiple PFASs on serum lipid levels.

Effects of Microbiota on the Treatment of Obesity with the Natural Product Celastrol in Rats.

Background: Obesity has become one of the most serious issues threatening the health of humankind, and we conducted this study to examine whether and how celastrol protects against obesity.

Methods: We fed male Sprague-Dawley rats a high-fat diet and administered celastrol to obese rats for 3 weeks. By recording body weight (BW) and other measures, we identified the effective dose of celastrol for obesity treatment.

Hypomethylation of PRDM1 is associated with recurrent pregnancy loss.

Recurrent pregnancy loss (RPL) rates have continued to rise during the last few decades, yet the underlying mechanisms remain poorly understood. An emerging area of interest is the mediation of gene expression by DNA methylation during early pregnancy. Here, genome-wide DNA methylation from placental villi was profiled in both RPL patients and controls.

Prenatal low-dose DEHP exposure induces metabolic adaptation and obesity: Role of hepatic thiamine metabolism.

Di-(2-ethylhexyl)-phthalate (DEHP) is a ubiquitous environmental pollutant and is widely used in industrial plastics. However, the long-term health implications of prenatal exposure to DEHP remains unclear. We set out to determine whether prenatal DEHP exposure can induce metabolic syndrome in offspring and investigate the underlying mechanisms.

Correction: Perfluorooctane Sulfonate Disturbs Nanog Expression through miR-490-3p in Mouse Embryonic Stem Cells.

[This corrects the article DOI: 10.1371/journal.pone.

Stereoselective endocrine-disrupting effects of the chiral triazole fungicide prothioconazole and its chiral metabolite.

The wide use of chiral fungicides has generated interest in the stereoselectivity of their ecotoxicological effects. However, there are few studies about the potential endocrine-disrupting effects (EDEs) of chiral fungicides. This study evaluated the hormone receptor activities of the chiral triazole fungicide prothioconazole and its metabolite using reporter gene assays.

Developmental toxicity of triclocarban in zebrafish (Danio rerio) embryos.

Triclocarban (TCC), which is used as an antimicrobial agent in personal care products, has been widely detected in aquatic ecosystems. However, the consequence of TCC exposure on embryo development is still elusive. Here, by using zebrafish embryos, we aimed to understand the developmental defects caused by TCC exposure.

Transcriptome and DNA Methylome Dynamics during Triclosan-Induced Cardiomyocyte Differentiation Toxicity.

Cardiac development is a dynamic process and sensitive to environmental chemicals. Triclosan is widely used as an antibacterial agent and reported to transport across the placenta and affect embryonic development. Here, we used human embryonic stem cell- (hESC-) derived cardiomyocytes (CMs) to determine the effects of TCS exposure on cardiac development.

The enhancer RNA lnc-SLC4A1-1 epigenetically regulates unexplained recurrent pregnancy loss (URPL) by activating CXCL8 and NF-kB pathway.

Background: Enhancer RNAs (eRNAs) are a group of lncRNAs transcribed from enhancers, whose regulatory effects on gene expression are an emerging area of interest. However, the role of eRNAs in regulating trophoblast cells and unexplained recurrent pregnancy loss (URPL) remains elusive.

Methods: We profiled eRNAs in villi from URPL patients and matched controls by RNA-seq.

Neonatal and juvenile exposure to perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS): Advance puberty onset and kisspeptin system disturbance in female rats.

Perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) are widespread and persistent chemicals in the environment, and limited data about their effects on puberty development are available. In order to explore the effects of neonatal and juvenile PFOA/PFOS exposure on puberty maturation, female rats were injected with PFOA or PFOS at 0.1, 1 and 10 mg/kg/day during postnatal day (PND) 1-5 or 26-30.

Integrated analysis of DNA methylome and transcriptome identified CREB5 as a novel risk gene contributing to recurrent pregnancy loss.

Background: Aberrant DNA methylation is considered to be a potential cause of recurrent pregnancy loss (RPL), while potential mechanism has not yet been elucidated.

Methods: In order to uncover the contribution of the perturbation of DNA methylation in RPL, we performed genome-wide DNA methylation analysis combined with genome-wide gene expression in decidua tissue.

Findings: Totally, 539 differentially methylated regions (DMRs) were identified and significantly correlated with gene expressions.

Down-regulated let-7b-5p represses glycolysis metabolism by targeting AURKB in asthenozoospermia.

Glycolysis, through anaerobic respiration, can supply energy for human sperm motility. MicroRNAs (miRNAs) could participate in the glycolytic pathway through regulating target genes. To investigate the potential role of glycolysis-related miRNAs in asthenozoospermia, TaqMan Low Density Array (TLDA) was used to screen potentially functional miRNAs, and seven glycolysis-related miRNAs were isolated to be related to asthenozoospermia.