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Diets are key determinants of nutrition and health and play a significant role in the environment. In this article, we aim to (i) describe dietary transitions and health in China and the consequent environmental challenges; (ii) identify differences between current Chinese diets and healthy reference diets; (iii) conduct a systematic review assessing the health impacts of four reference diets on the Chinese population, and (iv) simulate changes in greenhouse gas emissions under different diet scenarios. The results show differences between the Chinese diets and reference diets, with the current Chinese diet including mainly grains (especially refined rice), excessive meat consumption, and insufficient consumption of fruit and milk. If all Chinese consumers adopt one of the healthy reference diets all the time, the incidence of diet‐related chronic disease and mortality would be significantly reduced. Such dietary shifts would also reduce greenhouse gas emissions by 146–202 million tons (18–25 percent) compared with the projected emissions level in 2030. [ABSTRACT FROM AUTHOR]

Temporal event sequence alignment has been used in many domains to visualize nuanced changes and interactions over time. Existing approaches align one or two sentinel events. Overview tasks require examining all alignments of interest using interaction and time or juxtaposition of many visualizations. Furthermore, any event attribute overviews are not closely tied to sequence visualizations. We present Sequence Braiding, a novel overview visualization for temporal event sequences and attributes using a layered directed acyclic network. Sequence Braiding visually aligns many temporal events and attribute groups simultaneously and supports arbitrary ordering, absence, and duplication of events. In a controlled experiment we compare Sequence Braiding and IDMVis on user task completion time, correctness, error, and confidence. Our results provide good evidence that users of Sequence Braiding can understand high-level patterns and trends faster and with similar error. A full version of this paper with all appendices; the evaluation stimuli, data, and analysis code; and source code are available at $\text{osf.io}/\mathrm{mq}2\mathrm{wt}$ . [ABSTRACT FROM AUTHOR]

Proliferation and metastasis are significantly malignant characteristics of human lung cancer, but the underlying molecular mechanisms are poorly understood. Chromobox 4 (CBX4), a member of the Polycomb group (PcG) family of epigenetic regulatory factors, enhances cellular proliferation and promotes cancer cell migration. However, the effect of CBX4 in the progression of lung cancer is not fully understood. We found that CBX4 is highly expressed in lung tumours compared with adjacent normal tissues. Overexpression of CBX4 significantly promotes cell proliferation and migration in human lung cancer cell lines. The knockdown of CBX4 obviously suppresses the cell growth and migration of human lung cancer cells in vitro. Also, the proliferation and metastasis in vivo are blocked by CBX4 knockdown. Furthermore, CBX4 knockdown effectively arrests cell cycle at the G0/G1 phase through suppressing the expression of CDK2 and Cyclin E and decreases the formation of filopodia through suppressing MMP2, MMP9 and CXCR4. Additionally, CBX4 promotes proliferation and metastasis via regulating the expression of BMI‐1 which is a significant regulator of proliferation and migration in lung cancer cells. Taken together, these data suggest that CBX4 is not only a novel prognostic marker but also may be a potential therapeutic target in lung cancer. [ABSTRACT FROM AUTHOR]

Aim: To confirm Cu2-xSe nanoparticles (NPs) could inhibit autophagic degradation and based on this property to develop a novel therapeutic strategy for cancer treatment. Materials & methods: Transmission electronic microscopy and confocal laser-scanning microscope were used to observe the accumulation of autophagosome. Western blot was used to investigate the expression of autophagy-associated proteins. Chemotherapeutic drug oxaliplatin was cotreatment with Cu2-xSe in vivo and in vitro to study therapeutic efficacy of autophagy caused by Cu2-xSe NPs. Results & conclusion: Cu2-xSe NPs significantly induce autophagosome accumulation in hepatocellular carcinoma cells, and they mainly inhibit the late-stage autophagy degradation through reducing lysosomal cathepsin activity. Moreover, Cu2-xSe NPs enhance the anticancer activity of oxaliplatin in vivo and in vitro through blocking autophagosome degradation. [ABSTRACT FROM AUTHOR]

The anti-infection ability and skin regeneration are important aspects on the progress of wound healing, which needs an ideal wound dressing that not only resists bacteria but also promotes skin regeneration. In this study, zinc oxide/silver/polyvinylpyrrolidone/polycaprolactone (ZnO/Ag/PVP/PCL) nanofibres were prepared through electrospinning. Firstly, zinc oxide nanoparticles (ZnONPs) and silver nanoparticle (AgNPs) were synthesized respectively. Secondly, the two nanoparticles were mixed with polyvinylpyrrolidone (PVP) and polycaprolactone (PCL) to obtain the nanofibres. The results of scanning electron microscopy (SEM) showed that ZnONPs and AgNPs were 40.07 ± 9.70 nm and 37.46 ± 12.02 nm, respectively. After electrospinning, the nanofibres were 368.22 ± 123.96 nm in diameter. Infrared spectroscopy revealed that ZnONPs/AgNPs bimetallic nanomaterials were physically embedded in the nanofibres. The antibacterial effects against Staphylococcus aureus and Escherichia coli of ZnO/Ag/PVP/PCL nanofibres were significantly better than these of the single metal material-loaded nanofibres. More importantly, the combination of ZnO and Ag reduced the cytotoxicity of ZnO/Ag/PVP/PCL bimetallic nanofibres toward fibroblasts. These findings demonstrated that ZnO/Ag/PVP/PCL bimetallic nanofibres should be of greater interest than the single metal nanomaterial-loaded nanofibres in inhibiting growth of bacteria. [ABSTRACT FROM AUTHOR]

Abstract: IR‐783 is a kind of heptamethine cyanine dye that exhibits imaging, cancer targeting and anticancer properties. A previous study reported that its imaging and targeting properties were related to mitochondria. However, the molecular mechanism behind the anticancer activity of IR‐783 has not been well demonstrated. In this study, we showed that IR‐783 inhibits cell viability and induces mitochondrial apoptosis in human breast cancer cells. Exposure of MDA‐MB‐231 cells to IR‐783 resulted in the loss of mitochondrial membrane potential (MMP), adenosine triphosphate (ATP) depletion, mitochondrial permeability transition pore (mPTP) opening and cytochrome c (Cyto C) release. Furthermore, we found that IR‐783 induced dynamin‐related protein 1 (Drp1) translocation from the cytosol to the mitochondria, increased the expression of mitochondrial fission proteins mitochondrial fission factor (MFF) and fission‐1 (Fis1), and decreased the expression of mitochondrial fusion proteins mitofusin1 (Mfn1) and optic atrophy 1 (OPA1). Moreover, knockdown of Drp1 markedly blocked IR‐783‐mediated mitochondrial fission, loss of MMP, ATP depletion, mPTP opening and apoptosis. Our in vivo study confirmed that IR‐783 markedly inhibited tumour growth and induced apoptosis in an MDA‐MB‐231 xenograft model in association with the mitochondrial translocation of Drp1. Taken together, these findings suggest that IR‐783 induces apoptosis in human breast cancer cells by increasing Drp1‐mediated mitochondrial fission. Our study uncovered the molecular mechanism of the anti‐breast cancer effects of IR‐783 and provided novel perspectives for the application of IR‐783 in the treatment of breast cancer. [ABSTRACT FROM AUTHOR]