FOXP2 expression has been associated with the prognosis of some tumors, but the role of FOXP2 in glioblastoma remains unclear. The aim of the present work is to study the role of FOXP2 as a prognostic biomarker in glioblastoma.
 
  This is a retrospective observational case series study in which the expression of FOXP2 has been analyzed both at protein level (immunohistochemistry, n= 62) and at mRNA level (RNAseq, in a cohort of glioblastoma patients from The Cancer Genome Atlas [TCGA] database, n= 148). Other molecular and clinical data have also been included in the study, with special focus on miRNA expression data. Survival analysis using log-rank test and COX-regression have been used. Non-parametric statistical tests were also used to study differences between low and high FOXP2 expression groups.
 
  Patients with a high expression of FOXP2 protein showed a worse prognosis than those patients with low expression in progression-free survival (hazard ratio 1.711; P= 0.034) and overall survival (hazard ratio 1.809; P= 0.014). These associations were still statistically significant in multivariate analysis. No prognostic association was found with FOXP2 RNA expression. Interestingly, 2 miRNAs that target FOXP2 (hsa-miR-181a-2-3p and hsa-miR-20a-3p) showed an interaction effect on overall survival with FOXP2 expression. A low level of these miRNA expression was associated with a significantly worse prognosis in patients with high FOXP2 RNA expression (log-rank test; P < 0.05).
 
  Greater expression of FOXP2 at the protein level is associated with a worse prognosis. This protein expression may be regulated by the expression of specific miRNAs that target FOXP2 mRNA hsa-miR-181a-2-3p and hsa-miR-20a-3p.
 Greater expression of FOXP2 at the protein level is associated with a worse prognosis. This protein expression may be regulated by the expression of specific miRNAs that target FOXP2 mRNA hsa-miR-181a-2-3p and hsa-miR-20a-3p.Epigenetic regulation of gene expression provides a finely tuned response capacity for cells when undergoing environmental changes. However, in the context of human physiology or disease, any cellular imbalance that modulates homeostasis has the potential to trigger molecular changes that result either in physiological adaptation to a new situation or pathological conditions. These effects are partly due to alterations in the functionality of epigenetic regulators, which cause long-term and often heritable changes in cell lineages. As such, free radicals resulting from unbalanced/extended oxidative stress have been proved to act as modulators of epigenetic agents, resulting in alterations of the epigenetic landscape. In the present review we will focus on the particular effect that oxidative stress and free radicals produce in histone post-translational modifications that contribute to altering the histone code and, consequently, gene expression. The pathological consequences of the changes in this epigenetic layer of regulation of gene expression are thoroughly evidenced by data gathered in many physiological adaptive processes and in human diseases that range from age-related neurodegenerative pathologies to cancer, and that include respiratory syndromes, infertility, and systemic inflammatory conditions like sepsis.
  The goal of this study was to examine the association between aspects of the psychosocial work environment and prevalence of musculoskeletal disorders (MSDs) and associated functional consequences among pediatric healthcare providers.
 
  The psychosocial work demands make pediatric care providers susceptible to MSDs and subsequent functional consequences, but research on this at-risk group is lacking.
 
  Randomly selected pediatric registered nurses, behavioral health specialists, and patient care assistants (N=569) completed a survey assessing psychosocial factors, MSDs, and functional consequences (e.g., missing work). Logistic regression was used to assess associations between psychosocial factors and outcomes.
 
  The analysis yielded moderate-to-strong, significant associations between psychosocial environment factors and MSDs and their functional consequences. The odds of MSDs increased nearly three-fold in the highest quartile of the psychosocial summary score vs. the lowest (OR 2.7, 95% CI 1.6-4.5). The highest quartiles of the psychosocial environment measures were significantly associated with functional consequences of MSDs.
 
  Results confirm knowledge about the association between the psychosocial environment and MSDs and demonstrates the association also exists among pediatric providers. Our study highlights the importance of studying the functional consequences of MSDs, which characterize the impact of MSD burden at work and elsewhere.
 Results confirm knowledge about the association between the psychosocial environment and MSDs and demonstrates the association also exists among pediatric providers. Our study highlights the importance of studying the functional consequences of MSDs, which characterize the impact of MSD burden at work and elsewhere.Incomplete polymerization or biodegradation of dental resin materials results in the release of resin monomers such as triethylene glycol dimethacrylate (TEGDMA), causing severe injury of dental pulp cells. To date, there has been no efficient treatment option for this complication, in part due to the lack of understanding of the mechanism underlying these phenomena. Here, for the first time, we found that notoginsenoside R1 (NR1), a bioactive ingredient extracted from Panax notoginseng, exerted an obvious protective effect on TEGDMA-induced mitochondrial apoptosis in the preodontoblast mDPC6T cell line. In terms of the mechanism of action, NR1 enhanced the level of phosphorylated Akt (protein kinase B), resulting in the activation of a transcriptional factor, nuclear factor erythroid 2-related factor 2 (Nrf2), and eventually upregulating cellular ability to resist TEGDMA-related toxicity. Inhibiting the Akt/Nrf2 pathway by pharmaceutical inhibitors significantly decreased NR1-mediated cellular antioxidant properties and aggravated mitochondrial oxidative damage in TEGDMA-treated cells. Interestingly, NR1 also promoted mitophagy, which was identified as the potential downstream of the Akt/Nrf2 pathway. Blocking the Akt/Nrf2 pathway inhibited mitophagy and abolished the protection of NR1 on cells exposed to TEGDMA.  https://www.selleckchem.com/products/rituximab.html  In conclusion, these findings reveal that the activation of Akt/Nrf2 pathway-mediated mitophagy by NR1 might be a promising approach for preventing resin monomer-induced dental pulp injury.