Recent evidence consolidates the deleterious impact of environmental exposure on testicular damage. Environmental exposures can instigate testicular toxicity, causing damage to the Sertoli-Sertoli cell-mediated blood-testis barrier (BTB) integrity, alterations in hormone levels orchestrated by aberrant Leydig cells, and disruption of spermatogenesis. Despite diverse study designs and methodologies, a consensus is emerging on how environmental factors induce oxidative stress by elevating ROS levels, affecting autophagy through pathways such as the ROS-mediated mTOR signaling pathway, ultimately culminating in testicular damage. This review synthesizes existing literature on how environmental exposures, including metals, air pollutants, industrial contaminants, and pesticides, disturb testicular homeostasis via autophagy-mediated oxidative stress, highlighting recent significant advancements. It also explores interventions like antioxidant support and autophagy regulation to alleviate testicular damage. These findings underscore the importance of elucidating the mechanisms of autophagy influenced by environmental exposures in disrupting the equilibrium of oxidative stress, identifying potential drug targets, and establishing a groundwork for enhancing future treatments and clinical management of testicular injuries.

Backgrounds: Uterine corpus endometrial carcinoma (UCEC) is one of the greatest threats on the female reproductive system. The aim of this study is to explore the inflammation-related LncRNA (IRLs) signature predicting the clinical outcomes and response of UCEC patients to immunotherapy and chemotherapy. Methods: Consensus clustering analysis was employed to determine inflammation-related subtype. Cox regression methods were used to unearth potential prognostic IRLs and set up a risk model. The prognostic value of the prognostic model was calculated by the Kaplan-Meier method, receiver operating characteristic (ROC) curves, and univariate and multivariate analyses. Differential abundance of immune cell infiltration, expression levels of immunomodulators, the status of tumor mutation burden (TMB), the response to immune checkpoint inhibitors (ICIs), drug sensitivity, and functional enrichment in different risk groups were also explored. Finally, we used quantitative real-time PCR (qRT-PCR) to confirm the expression patterns of model IRLs in clinical specimens. Results: All UCEC cases were divided into two clusters (C1 = 454) and (C2 = 57) which had significant differences in prognosis and immune status. Five hub IRLs were selected to develop an IRL prognostic signature (IRLPS) which had value in forecasting the clinical outcome of UCEC patients. Biological processes related to tumor and immune response were screened. Function enrichment algorithm showed tumor signaling pathways (ERBB signaling, TGF-β signaling, and Wnt signaling) were remarkably activated in high-risk group scores. In addition, the high-risk group had a higher infiltration level of M2 macrophages and lower TMB value, suggesting patients with high risk were prone to a immunosuppressive status. Furthermore, we determined several potential molecular drugs for UCEC. Conclusion: We successfully identified a novel molecular subtype and inflammation-related prognostic model for UCEC. Our constructed risk signature can be employed to assess the survival of UCEC patients and offer a valuable reference for clinical treatment regimens.

In present work, silica pillared montmorillonite material (C-SiO₂-OMT) was prepared via the sol–gel method, and the influence of the powder on thermal stability and flammability performance of polypropylene (PP) composites was investigated. Characterization of C-SiO₂-OMT, elucidated with X-ray diffraction, transmission electron microscopy, and N₂ adsorption–desorption, suggested that the powder had a mesoporous lamellar structure with high specific surface area and mesoporous volume. The formation of porous structure of C-SiO₂-OMT was more conducive than organically modified montmorillonite (OMT) to slowing the volatilization of pyrolytic products generated during thermal degradation process, which led to PP/C-SiO₂-OMT microcomposite show better thermal stability than PP/OMT nanocomposite at high temperature range. Flammability properties of these polymer materials evaluated by microscale combustion calorimetry, and cone calorimetry showed a contrary tendency, but C-SiO₂-OMT holds high promise to reduce the smoke yield. Copyright © 2013 John Wiley & Sons, Ltd.

Lipid metabolism is important in various cancers. However, the association between lipid metabolism and uterine corpus endometrial carcinoma (UCEC) is still unclear. In this study, we collected clinicopathologic parameters and the expression of lipid metabolism-related genes (LMRGs) from the Cancer Genome Atlas (TCGA). A lipid metabolism-related risk model was built and verified. The risk score was developed based on 11 selected LMRGs. The expression of 11 LMRGs was confirmed by qRT-PCR in clinical samples. We found that the model was an independent prediction factor of UCEC in terms of multivariate analysis. The overall survival (OS) of low-risk group was higher than that in the high-risk group. GSEA revealed that MAPK signaling pathway, ERBB signaling pathway, ECM receptor interaction, WNT pathway, and TGF-β signaling pathway were enriched in the high-risk group. Low-risk group was characterized by high tumor mutation burden (TMB) and showed sensitive response to immunotherapy and chemotherapy. In brief, we built a lipid metabolism gene expression-based risk signature which can reflect the prognosis of UCEC patients and their response to chemotherapeutics and immune therapy.

Placental trophoblast dysfunction is one of the main causes of missed abortion (MA). The expression and regulation of specific molecules play crucial roles in this complex process. Among these, human deoxycytidine triphosphate pyrophosphatase 1 (DCTPP1), a key enzyme, not only participates in nucleotide metabolism but also plays an indispensable role in maintaining genomic stability. To delve deeper into the mechanism of DCTPP1 in placental trophoblast cell function, we used an immortalized human first-trimester extravillous trophoblast cell line (HTR8/SVneo) as an experimental model for functional studies. A decrease in DCTPP1 expression leads to an increase in oxidative stress and decreased cell viability ultimately leading to apoptosis. Further analysis revealed an interaction between DCTPP1 and the AU-rich element RNA-binding protein 1 (AUF1). A decrease of AUF1 induced oxidative stress imbalance, leading to apoptosis in HTR8/SVneo cells. These findings highlight DCTPP1 as a potential biomarker and an effective drug target for the treatment or prevention of MA.