Zinc oxide nanoparticles induces cell death and consequently leading to incomplete neural tube closure through oxidative stress during embryogenesis.

The implementation of Zinc oxide nanoparticles (ZnO NPs) raises concerns regarding their potential toxic effects on human health. Although more and more researches have confirmed the toxic effects of ZnO NPs, limited attention has been given to their impact on the early embryonic nervous system. This study aimed to explore the impact of exposure to ZnO NPs on early neurogenesis and explore its underlying mechanisms. We conducted experiments here to confirm the hypothesis that exposure to ZnO NPs causes neural tube defects in early embryonic development. We first used mouse and chicken embryos to confirm that ZnO NPs and the Zn2+ they release are able to penetrate the placental barrier, influence fetal growth and result in incomplete neural tube closure. Using SH-SY5Y cells, we determined that ZnO NPs-induced incomplete neural tube closure was caused by activation of various cell death modes, including ferroptosis, apoptosis and autophagy. Moreover, dissolved Zn2+ played a role in triggering widespread cell death. ZnO NPs were accumulated within mitochondria after entering cells, damaging mitochondrial function and resulting in the over production of reactive oxygen species, ultimately inducing cellular oxidative stress. The N-acetylcysteine (NAC) exhibits significant efficacy in mitigating cellular oxidative stress, thereby alleviating the cytotoxicity and neurotoxicity brought about by ZnO NPs. These findings indicated that the exposure of ZnO NPs in early embryonic development can induce cell death through oxidative stress, resulting in a reduced number of cells involved in early neural tube closure and ultimately resulting in incomplete neural tube closure during embryo development. The findings of this study could raise public awareness regarding the potential risks associated with the exposure and use of ZnO NPs in early pregnancy.

The impact of metabolic surgery on natural conception rates in women with infertility, obesity and polycystic ovary syndrome: a retrospective study.

BACKGROUND: Women with obesity and polycystic ovary syndrome (OPOS) are at high risk for infertility. However, the reproductive effects of metabolic surgery on women with infertility and OPOS have not been fully elucidated. OBJECTIVES: We investigated the natural conception rates after metabolic surgery, and the variables associated with infertility in women with OPOS. SETTING: Shanghai Sixth People's Hospital, Shanghai, China. METHODS: This study included 72 women with infertility and OPOS who underwent metabolic surgery and were followed up for 4 years after surgery. Finally, 54 patients completed the study. Reproductive outcomes were assessed, along with changes in anthropometric parameters and metabolic indices before and 1 year after surgery (prepregnancy). Logistic regression analysis was used to identify variables influencing natural conception and delivery outcomes. RESULTS: After metabolic surgery, 35 patients (64.8%) became pregnant naturally, while 16 were still unable to conceive naturally. Preoperative body mass index (BMI) tended to be lower in the natural conception group than in the no natural conception group (38.9 ± 6.9 versus 43.6 ± 11.0 kg/m2, P = .070) and there were no significant differences in weight loss between the 2 groups after surgery. Logistic regression analysis showed that the BMI 1 year after surgery (prepregnancy) was an independent predictor of natural conception, and receiver operating characteristic analysis showed that a BMI of 27.0 kg/m2 was the optimal cutoff for predicting successful natural conception after surgery. CONCLUSIONS: Metabolic surgery can improve fertility in women with OPOS. Patients with a BMI < 27.0 kg/m2 1 year after surgery (prepregnancy) are more likely to become pregnant naturally and give birth.

Mesenchymal stem cells paracrine proteins from three-dimensional dynamic culture system promoted wound healing in third-degree burn models.

Recovery of skin function remains a significant clinical challenge for deep burns owing to the severe scar formation and poor appendage regeneration, and stem cell therapy has shown great potential for injured tissue regeneration. Here, a cell-free therapy system for deep burn skin was explored using mesenchymal stem cell paracrine proteins (MSC-PP) and polyethylene glycol (PEG) temperature-sensitive hydrogels. A three-dimensional (3D) dynamic culture system for MSCs' large-scale expansion was established using a porous gelatin microcarrier crosslinked with hyaluronic acid (PGM-HA), and the purified MSC-PP from culture supernatant was characterized by mass spectrometric analysis. The results showed the 3D dynamic culture system regulated MSCs cell cycle, reduced apoptosis, and decreased lactic acid content, and the MSC-PP produced in 3D group can promote cell proliferation, migration, and adhesion. The MSC-PP + PEG system maintained stable release in 28 days of observation in vitro. The in vivo therapeutic efficacy was investigated in the rabbit's third-degree burn model, and saline, PEG, MSC-PP, and MSC-PP + PEG treatments groups were set. The in vivo results showed that the MSC-PP + PEG group significantly improved wound healing, inhibited scar formation, and facilitated skin appendage regeneration. In conclusion, the MSC-PP + PEG sustained-release system provides a potentially effective treatment for deep burn skin healing.