Titanium dioxide nanoparticles (TiO2 NPs) were used worldwide for decades, and pregnant women are unable to avoid exposing to them. Studies revealed that TiO2 NPs could kill many kinds of bacteria, but whether they would affect the composition of gut microbiota, especially during pregnancy, was seldom reported. And, what adverse effects may be brought to pregnant females was also unknown. In this study, we established the prenatal exposure model of rats to explore the effects of TiO2 NPs on gut microbiota. We observed an increasing trend, but not a significant change of alpha-diversity among control and exposure groups at gestation day (GD) 10 and GD 17 during normal pregnancy process. Each different time point had unique gut microbiota operational taxonomic units (OTUs) characteristics. The abundance of Ellin6075 decreased at GD 10 and GD 17, Clostridiales increased at GD 10, and Dehalobacteriaceae decreased at GD 17 after TiO2 NPs exposure. Further phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt) prediction indicated that the type 2 diabetes mellitus related genes were enhanced, and taurine metabolism was weakened at the second-trimester. Further study showed that the rats’ fasting blood glucose levels significantly increased at GD 10 (P < 0.05) and GD 17 (P < 0.01) after exposure. Our study pointed out that TiO2 NPs induced the alteration of gut microbiota during pregnancy and increased the fasting blood glucose of pregnant rats, which might increase the potential risk of gestational diabetes of pregnant women.

Background: Concerns have been raised regarding the effects of perfluoroalkyl substance (PFAS) exposure on cardiovascular diseases (CVD), but clear evidence linking PFAS exposure to CVD is lacking, and the mechanism remains unclear. Objectives: To study the association between PFASs and CVD in U.S. population, and to reveal the mechanism of PFASs’ effects on CVD. Methods: To assess the relationships between individual blood serum PFAS levels and the risk of total CVD or its subtypes, multivariable logistic regression analysis and partial least squares discriminant analysis (PLS-DA) were conducted on all participants or subgroups among 3391 adults from the National Health and Nutrition Examination Survey (NHANES). The SuperPred and GeneCards databases were utilized to identify potential targets related to PFAS and CVD, respectively. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of intersection genes were performed using Metascape. Protein interaction networks were generated, and core targets were identified with STRING. Molecular docking was achieved using Autodock Vina 1.1.2. Results: There was a positive association between Me-PFOSA-AcOH and CVD (OR = 1.28, p = 0.022), especially coronary heart disease (CHD) (OR = 1.47, p = 0.007) and heart attack (OR = 1.58, p < 0.001) after adjusting for all potential covariates. Me-PFOSA-AcOH contributed the most to distinguishing between individuals in terms of CVD and non-CVD. Significant moderating effects for Me-PFOSA-AcOH were observed in the subgroup analysis stratified by sex, ethnicity, education level, PIR, BMI, smoking status, physical activity, and hypertension (p < 0.05). The potential intersection targets were mainly enriched in CVD-related pathways, including the inflammatory response, neuroactive ligand–receptor interaction, MAPK signaling pathway, and arachidonic acid metabolism. TLR4 was identified as the core target for the effects of Me-PFOSA-AcOH on CVD. Molecular docking results revealed that the binding energy of Me-PFOSA-AcOH to the TLR4-MD-2 complex was −7.2 kcal/mol, suggesting that Me-PFOSA-AcOH binds well to the TLR4-MD-2 complex. Conclusions: Me-PFOSA-AcOH exposure was significantly associated with CVD. Network toxicology and molecular docking uncovered novel molecular targets, such as TLR4, and identified the inflammatory and metabolic mechanisms underlying Me-PFOSA-AcOH-induced CVD.

Titanium dioxide nanoparticles (TiO₂ NPs) are used extensively in our daily lives, and their toxic effects on the placenta have been reported. Animal studies indicated that placental development is impaired after maternal exposure of TiO₂ NPs, but the underlying mechanisms remain largely unknown. In the present study, we used a human trophoblast-derived cell, HTR8-SVneo, to determine how TiO₂ NPs affected placental functions, and found out potential reversal targets. TEM was employed for TiO₂ NPs morphology observation and uptake assessment. RT-PCR was used to detect the expression of both mRNA and miRNA, and western blotting was used for protein examination. Cell invasion ability was evaluated by Transwell assay, and cytoskeletons were observed by immunofluorescence combined with confocal microscope examination. We found that TiO₂ NPs disrupted cytoskeletons and impaired cell invasion ability. Further investigations showed that TiO₂ NPs increased the expression of a microRNA (miR-96-5p), which targeted and down-regulated the translation of EZR mRNA, a gene that encodes ezrin protein, and affected the cell cytoskeletons and ultimately cell invasion ability. When the expression of miR-96-5p was down-regulated, the expression level of ezrin protein was also reversed, and cell invasion ability was partially restored. Collectively, we determined how miR-96-5p mediates TiO₂ NP-induced placental dysfunction, and provided a potential rescue target for future therapy.

Air pollution is becoming an increased burden to the world. Previous studies have confirmed its effects on adverse birth outcomes, but few associated with premature small for gestational age (SGA). We report a retrospective cohort study conducted in Changzhou city to evaluate the association between air pollutants (PM2.5, SO2 and NO2) and premature SGA during pregnancy. A total of 46,224 births were collected from January, 2013 to December, 2016, in Changzhou Maternity and Child Health Care Hospital, finally 2709 preterm births were admitted for study. Corresponding air monitoring data were collected from Changzhou Environmental Protection Agency. Generalized estimating equations were used to examine the association between these air pollutants and premature SGA controlling for individual covariates in single- and multi-pollutant models. We found that, in the third trimester, every 10 μg/m3 increments in PM2.5 concentration were associated with premature SGA (OR = 1.18, 95% CI: 1.03–2.83; OR = 1.37, 95% CI: 1.03–3.58) in two- and three-pollutants models. In the whole gestation, a 10 μg/m3 increment in PM2.5 concentration in two- and three-pollutant models were related to premature SGA (OR = 1.53, 95% CI: 1.38–2.47; OR = 1.73, 95% CI: 1.18–2.57). The OR (95% CI) of premature SGA were increasing across quintiles of PM2.5, SO2, NO2 concentrations during the whole gestation period adjusting for confounders (P for trend < 0.001). These results indicated that pregnant women exposed to PM2.5, combined with other pollutants in the third trimester have a higher risk to deliver premature SGA babies, providing further evidence linking PM2.5 and pregnancy outcomes.

Background: White lesions of the vulva are a common vulvar disease of unclear etiology. Although a variety of treatments have been used to treat the disease in clinical practice, there is currently a lack of effective radical therapies. This study aimed to compare the feasibility and effectiveness of fractional ultrapulsed CO₂ laser with that of high-intensity focused ultrasound in the treatment of white lesions of the vulva. Methods: A total of 60 patients with pruritus vulvae who were treated at the Center for Diagnosis and Treatment of Cervical Diseases in our hospital between December, 2017, and December 2018 were enrolled in this study. The possibility of malignant lesions of the vulva was ruled out by histopathological diagnosis following colposcopic biopsy. The patients were randomly divided into two groups: a laser treatment group (group L, n=30) and a focused ultrasound treatment group (group U, n=30). The patients were monitored for changes in signs and symptoms during and after treatment, and the treatment outcomes of the two groups were compared. Results: The local symptoms of pruritus were alleviated by both the fractional ultrapulsed CO₂ laser and high-intensity focused ultrasound. The patients in group L had no significant adverse reactions during the operation and needed no special postoperative treatment. The total effective rate in group L was 96.7%. In group U, five patients felt mild burning during the operation, painful blisters arose on the skin of the ablated area, and long-lasting local edema was observed. Seven patients had subcutaneous nodules. The total effective rate in group U was 90.0%. Conclusions: Fractional ultrapulsed CO₂ laser is a minimally invasive, effective, and safe treatment for white lesions of the vulva. It causes few complications and does not affect the daily and working life of patients. Therefore, it should be widely applied in clinical practice.

Severe fever with thrombocytopenia syndrome virus (SFTSV) is a tick-borne virus that primarily causes SFTS. Although a common testing route is available, a timely, conventional and accurate method for SFTSV detection is urgently needed. In the present study, we established a platform that combines the recombinase polymerase amplification (RPA) assay with the clustered regularly interspaced short palindromic repeats-CRISPR associated proteins (CRISPR/Cas) 12a technique in one step in one pot. The procedure can be completed within 45 min at a constant temperature without a sophisticated instrument. This method targets the S gene of SFTSV, with a detection limit (LoD) of 11.7 copies per reaction and high specificity, without cross reactivity with other pathogens. Furthermore, across 46 test samples, this method achieved 89.13% consistency with the PCR method (41/46). Together, the reaction system developed in the present study provides not only a novel method for SFTSV detection but also an alternative method for detecting RNA viruses.