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The material of an object can be identified through the analysis of its surface texture. However, it is not easy to determine uneven surface texture via machine vision. The information collected by tactile sensing can well retain the concave and convex features of texture itself, which makes this type of texture recognition relatively simple. In this paper, we design three definitive artificial texture models, and use capacitive flexible tactile perception electronic skin to collect pressure data. We apply constant mass loads on the electronic skin, fully touching the surface to be detected, and then drag the electronic skin to produce relative sliding horizontally which to ensure the stability of the collected data in the vertical direction. Based on the convolutional neural network a classification neural network is constructed. The tactile pressure information is input of the neural network after special processing so that it still retains the spatial and temporal information at the same time. We have completed the detection of the deterministic surface texture of certain objects, and the final accuracy can be achieved more than 90%, which shows that the network has a good recognition ability for the surface texture.

Reproductive epidemiological studies have suggested associations between perinatal exposure to fine particulate matter (PM2.5) and adverse birth outcomes. To explore the effects of early prenatal exposure to PM2.5 on subsequent generations, pregnant mice were exposed to PM2.5 or filtered clean air in whole body dynamic exposure chambers for 14 consecutive days from gestation day (GD) 1.5 to GD15.5. Neurobehavioral tests showed that spontaneous locomotion and exploratory behaviors in the offspring were significantly enhanced in the open field test. Meanwhile, metabolomics analysis suggested activation of dopamine pathway while inhibition of glycine pathway in murine brains. Administration of the DRD4 antagonist, clozapine; or supplementation of glycine receptor agonist, taurine, to mice offspring attenuated the locomotor hyperactivities to levels indistinguishable from controls. These data provide strong evidence that maternal exposure to air pollution might increase the risk for neural disorders in the offspring during critical periods of brain development.

Myeloperoxidase (MPO) promoter SNPs rs2243828 (−764T>C) and rs2333227 (G-463A) program malignant phenotypes by regulating MPO transcriptional activity. In this study, we enrolled a total of 1,175 controls and 1,078 patients with colorectal cancer with comprehensive clinical and survival information to assess whether these SNPs could affect the susceptibility and development of colorectal cancer. The MPO rs2333227 TT genotype significantly increased the risk of colorectal cancer and decreased the overall survival time of patients. Colorectal cancer cells with the rs2333227 TT genotype exhibited enhanced proliferation, migration, and invasion capacity in vitro and in vivo. Mechanistically, we found that MPO SNP rs2333227 C to T mutation altered the binding affinity of the transcription factors AP-2α to the rs2333227 mutation region, sequentially enhancing expression levels of MPO and activating further IL23A–MMP9 axis–mediated oncogenic signaling. Taken together, our findings indicate that MPO SNP rs2333227 serves as a marker of enhanced risk for development of colorectal cancer. Significance: MPO polymorphisms are a guide for high risk and poor prognosis in patients colorectal cancer. Cancer Res; 78(10); 2760–9. ©2018 AACR.

Particulate matter (PM) exposure has been associated with intestinal disorders. Therefore, there is an urgent need to understand the precise molecular mechanism involved and explore potential prevention strategies. In this study, inhaled PM is shown to activate inflammatory pathways in murine colon. In a panel study, it is found that ambient PM levels are significantly associated with elevated number of fecal white blood cells in healthy subjects. Acting as a promoter, PM exposure accelerates chemical carcinogenesis‐induced colonic tumor formation in a murine model. Mechanistically, RNA‐seq assays suggest activation of phosphoinositide 3‐kinase (PI3K)/AKT cascades in chronically PM‐exposed human colon mucosal epithelial cells. Ablation of up‐stream driver fibroblast growth factor receptor 4 (FGFR4) effectively inhibits inflammation and neoplasia in PM‐exposed murine colons. Notably, dietary curcumin supplement is shown to protect against PM‐induced colonic injuries in mice. Collectively, these findings identify that PM exposure accelerates colonic tumorigenesis in a PI3K/AKT‐dependent manner and suggests potential nutrient supplement for prevention.

// Xiaobo Li 1 , Yang lv 2 , Na Gao 1 , Hao Sun 1 , Runze Lu 1 , Hongbao Yang 3 , Chengcheng Zhang 1 , Qingtao Meng 1 , Shenshen Wu 1 , Ai-Qun Li 4 , Yankai Xia 5, * , Rui Chen 1, 6, * 1 Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China 2 Department of Histology and Embryology, Hebei North University, Zhangjiakou, 075000, China 3 Center for Drug Safety Evaluation and Research, China Pharmaceutical University, Nanjing, 211198, China 4 School of Public Health, Medical College, Wuhan University of Science and Technology, Wuhan, 430081, China 5 Key Laboratory of Reproductive Medicine, Institute of Toxicology, Nanjing Medical University, Nanjing 210009, China 6 State Key Laboratory of Bioelectronics, Southeast University, Nanjing, 210096, China * These authors have contributed equally to this work Correspondence to: Rui Chen, e-mail: 101011816@seu.edu.cn Yankai Xia, e-mail: yankaixia@njmu.edu.cn Keywords: PM 2.5 , microRNA, lung cancer, carcinogenesis, actin Received: February 19, 2016 Accepted: April 10, 2016 Published: April 26, 2016 ABSTRACT Recent studies have linked ambient fine particulate matter (PM 2.5 ) to increased lung cancer mortality and morbidity. However, the underlying mechanism causing the adverse effects of PM 2.5 is less clear. In the present study, post-transcriptional profiling was used to explore biological pathways involved in PM 2.5 -induced pulmonary disorders. The carcinogenesis and metastasis of PM 2.5 exposure were evaluated by long-term PM 2.5 exposure tests. We observed dysregulation of actin in A549 cells line and dysplasia in the lungs of mice exposed to PM 2.5 . Both PM 2.5 -exposed cells and animals showed increased Rnd3 expression levels. Moreover, miR-802 mimics rescued actin disorganization in vitro and alveolitis in vivo . Long-term exposure to PM 2.5 promoted carcinogenesis and metastasis of pulmonary cells. Decreased miR-802 expression levels in the serum samples of PM 2.5 -treated mice and individuals from moderately polluted cities were observed. Increased Rnd3 expression levels in lung cancers tissues have been identified by a genome database TCGA, and have been linked to less overall survival probabilities of lung cancer patients. Our findings suggest that dysregulation of actin cytoskeleton and down-regulation of miR-802 expression might be the underlying mechanism involved in the adverse effects of PM 2.5 exposure. In addition, long-term exposure to PM 2.5 demonstrated strong associations with malignant pulmonary disorders.