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Nanoplastics (NPs) are an emerging threat to higher plants in terrestrial ecosystems. However, the molecular of NP-related phytotoxicity remains unclear. In the present study, rice seedlings were exposed to polystyrene (PS, 50 nm) NPs at 0, 50, 100, and 200 mg/L under hydroponic conditions to investigate the induced physiological indices and transcriptional mechanisms. We found that 50, 100, and 200 mg/L PS significantly reduced root (53.05%, 49.61%, and 57.58%, respectively) and shoot (54.63%, 61.56%, and 62.64%, respectively) biomass as compared with the control seedlings. The activities of antioxidant enzymes, including catalase (CAT), peroxidase (POD), superoxide dismutase (SOD), and ascorbate peroxidase (APX), were significantly activated in all PS treatment groups, indicating that PS inhibited plant growth and induced oxidative stress. Transcriptome analyses showed that PS modulated the expression of the genes involved in cell detoxification, active oxygen metabolism, mitogen-activated protein kinase (MAPK), and plant hormone transduction pathways. Our study provides new insights into phytotoxicity by demonstrating the potential underlying toxicity of PS NPs in higher plants. [Display omitted] • PS affects physiological and molecular indices in rice. • ROS signaling may be a key pathway for the adverse responses to PS exposure. • High-concentration PS may affect rice growth via transporter channel proteins. • PS was taken up through the root tip. [ABSTRACT FROM AUTHOR]

Targeting energy metabolism holds the potential to effectively treat a variety of malignant diseases, and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α) is a key regulator of energy metabolism. However, PGC1α′s role in cancer, especially in hepatocellular carcinoma (HCC) remains largely unknown. In the present study, we reported that PGC1α was significantly downregulated in HCC cell lines and specimens. Moreover, reduced expression of PGC1α in tumor cells was correlated with poor prognosis. PGC1α overexpression substantially inhibited cell proliferation and induced apoptosis in vitro and in vivo. On the contrary, the knockdown of PGC1α produced the opposite effect. The mechanism was at least partially due to the upregulation of mitochondrial pyruvate carrier 1 (MPC1) caused by PGC1α, which promoted mitochondrial biogenesis by binding to nuclear respiratory factor 1 (NRF1). Consequently, the production of cellular reactive oxygen species (ROS) caused by mitochondrial oxidation was elevated above a critical threshold for survival. Furthermore, we found that PGC1α could enhance the antitumor activity of sorafenib and doxorubicin in HCC through ROS accumulation-mediated cell death. These results indicate that PGC1α/NRF1-MPC1 axis is involved in HCC progression and could be a promising target for HCC treatment. Image 1 • Low expression of PGC1α and MPC1 was associated with the poor prognosis of HCC. • PGC1α and MPC1 could inhibit HCC cell proliferation and induce apoptosis. • PGC1α/NRF1-MPC1 axis activates mitochondrial biogenesis and drives ROS production. • PGC1α/NRF1-MPC1 axis attenuates HCC progression. • PGC1α could enhance the sensitivity to sorafenib/doxorubicin treatment in HCC. [ABSTRACT FROM AUTHOR]

Abstract Three types of primer layers, including polyurethane (PU), acrylic, and silicone coatings, were developed and deposited on the poly(methylmethacrylate) (PMMA) substrates. Amorphous transparent indium zinc oxide (IZO) films deposited by direct current magnetron sputtering at room temperature on primer-treated and untreated PMMA substrates were investigated ex situ in terms of surface morphology, adhesion, nanoindentation and electrical properties. AFM images show that the microstructure of IZO films was determined by the morphology of the primer layers. IZO films deposited on silicone and acrylic-treated PMMA substrates presented the least surface roughness, which proved that the silicone and acrylic primer layers were more effective to get a dense surface. Nano-scratch tests indicated that the adhesion of IZO films deposited on substrate treated by silicone-based primer layers was superior to that on PU-treated and untreated substrate, which can be attributed to the better mechanical matches of the IZO/primer/PMMA system and the large values of hardness of the silicone primer, which can counterbalance the indentation load and prevent the failure of the films. Highlights • Mechanical properties of IZO films on PMMA substrates pretreated by three kinds of organic primers were studied. • The adhesion properties of coatings on silicone-treated PMMA was superior to that on PU-treated and untreated substrate. • Nanoindentation technique was used to qualitatively assess the nanomechanical changes of coatings and IZO films. [ABSTRACT FROM AUTHOR]

Zinc-doped indium oxide (IZO) film, as an important transparent conductive oxide, has attracted increasing attention in various scientific and engineering areas. In the present work, discharge-voltage and reactive-oxygen controlled IZO films were grown by magnetron sputtering and studied systematically. The microstructure, element distribution and chemical bonding of IZO films were investigated by X-Ray diffraction (XRD), transmission electron microscope (TEM), Energy Dispersive X-Ray Spectroscopy (EDX) and X-ray photoelectron spectroscopy (XPS). The optical and electrical properties of IZO films were studied by controlled oxygen and discharge voltage. The typical microstructure of IZO films with optimal optical and electric properties has been characterized. High discharge voltage and matched oxygen vacancies could promote the low resistivity of IZO films, which could be determined by the electronic concentration and mobility. • IZO films were grown at room temperature by two strategies of oxygen and discharge voltage. •Oxygen supply promotes the decreases of oxygen vacancies and Zn content. •More oxygen promotes IZO film with higher transparency and larger bandgap. •Both high discharge voltage and matched oxygen content bring IZO film the superior carrier concentration and mobility. [ABSTRACT FROM AUTHOR]