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In this work, near-infrared light responsive upconversion nanoparticles TiO2/(Ca,Y)F2:Tm,Yb were hydrothermally prepared for tumor control. Moreover, femtosecond laser was adopted to reduce particle size and aggregation of TiO2/(Ca,Y)F2:Tm,Yb, as a strategy to enhance its dispersity. In vitro studies of the biocompatibility and tumor control efficacy of TiO2/(Ca,Y)F2:Tm,Yb were carried out via co-culturing human pancreatic carcinoma cells (CFPAC-1). It was found in the absence of near-infrared light, TiO2/(Ca,Y)F2:Tm,Yb showed no toxicity to CFPAC-1 cells. On contrast, when exposed to near-infrared light, particles exhibited irradiation time, irradiation interval and particle concentration dependent suppression of CFPAC-1 cells proliferation along with portion of S phase cells increase. A nude mouse model with CFPAC-1 cells injection was established and TiO2/(Ca,Y)F2:Tm,Yb was subsequently applied for in vivo tumor control. A 15 days tracking confirmed the antitumor capability of near-infrared light excited TiO2/(Ca,Y)F2:Tm,Yb. Overall, we anticipate that the here-introduced TiO2/(Ca,Y)F2:Tm,Yb can serve as an effective agent for photodynamic antitumor therapy. [ABSTRACT FROM AUTHOR]

p-Alkoxyphenols (AOPs) are a class of ethers that are widely used in industrial and agricultural productions and daily necessities. p-Phenoxyphenol (PhOP) and p-pentyloxyphenol (PeOP) belong to this class and have been reported to be estrogenic in vitro. However, their in vivo estrogenic activities have rarely been of concern. In this study, we performed an immature mouse uterotrophic assay and studied the estrogenic effects of these two compounds in mice. The results revealed that the uterine weights of the animals treated with PhOP significantly increased at doses of 30 and 300 mg kg-1 bw day-1 for 3 days (P < 0.05), while no significant uterotrophic effects were observed in the mice treated with PeOP. Using next-generation transcriptome sequencing (RNA-seq), we also analyzed the gene expression in the uterine tissue of mice treated with PhOP and PeOP. The observed gene regulation patterns of the PhOP- and PeOP-treated specimens were similar to those of the 17β-estradiol (E2)-treated specimens. In particular, some estrogen-responsive genes, such as the Sprr2 gene family, Apoa1, Prap1, and Ahsg, displayed a regulation trend similar to that of E2. In addition, molecule docking analysis revealed that both PhOP and PeOP could be well docked into the active site of hERα, with potential of mean force (PMF) values of − 58.68 and − 52.67 kcal mol-1 for PhOP and PeOP, respectively. The results of this study indicate that PhOP exhibits relatively strong in vivo estrogenic activity, which could be of future concern. [ABSTRACT FROM AUTHOR]

Obesity results from numerous, interacting genetic, behavioral, and physiological factors. Adipogenesis is partially regulated by several adipocyte-selective microRNAs (miRNAs) and transcription factors that regulate proliferation and differentiation of human adipose-derived mesenchymal stem cells (hMSCs-Ad). In this study, we examined the roles of adipocyte-selective miRNAs in the differentiation of hMSCs-Ad to adipocytes. Results showed that the levels of miR-148a, miR-26b, miR-30, and miR-199a increased in differentiating hMSCs-Ad. Among these miRNAs, miR-148a exhibited significant effects on increasing PPRE luciferase activity (it represents PPAR-dependent transcription, a major factor in adipogenesis) than others. Furthermore, miR-148a expression levels increased in adipose tissues from obese people and mice fed high-fat diet. miR-148a acted by suppressing its target gene, Wnt1, an endogenous inhibitor of adipogenesis. Ectopic expression of miR-148a accelerated differentiation and partially rescued Wnt1-mediated inhibition of adipogenesis. Knockdown of miR-148a also inhibited adipogenesis. Analysis of the upstream region of miR-148a locus identified a 3 kb region containing a functional cAMP-response element-binding protein (CREB) required for miR-148a expression in hMSCs-Ad. The results suggest that miR-148a is a biomarker of obesity in human subjects and mouse model, which represents a CREB-modulated miRNA that acts to repress Wnt1, thereby promoting adipocyte differentiation. [ABSTRACT FROM AUTHOR]