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Supplementary Figure S1,Figure S2,Figure S3,Table S1，Table S2，Table S3，and Table S4.

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.

Coronavirus disease 2019 (COVID-19) outbreaks in the past were mostly caused by overseas transmission, but if control measures are not appropriately applied, domestic transmission could also cause large-scale local epidemics.This report covers all information of epidemic investigation processes, epidemiological characteristics and exposure history, transmission chains, sequencing results as well as public health measures taken for the COVID-19 cluster epidemic caused by the Delta variant in a cosmetic hospital in Yantai City in August 2021.The information provided in this report, including active case finding, community management, and mass testing, may assist public health professionals in dealing with local COVID-19 epidemics caused by domestic transmission.

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.

Epidemiological studies have associated ambient fine particulate matter (PM2.5) exposure with lung cancer, in which epithelial-mesenchymal transition (EMT) is an initial process. Thus, it is important to identify the key molecule or pathway involved in the PM2.5 induced EMT. Human bronchial epithelial (HBE) cells were exposed to PM2.5 (100 or 500 μg/ml) for 30 passages and analyzed by metabolomics to identify the alteration of metabolites related to PM2.5 exposure. The expression levels of EMT markers were evaluated by qRT-PCR and Western blot assays in HBE cells and murine lung tissues. Reduced epithelial markers, increased mesenchymal markers expression levels and increased capacity of metastasis were observed in PM2.5-exposed HBE cells. Metabolomics analysis suggested upregulation of citrate acid with fold change (FC) of 2.89 or 4.18 in 100 or 500 μg/ml PM2.5 treated HBE cells. For both of the in vitro and in vivo study, the up-regulation of ATP citrate lyase (ACLY) was confirmed following PM2.5 exposure. Importantly, ACLY knockdown in HBE cells reversed EMT, migration and invasion capacities in HBE cells induced by PM2.5. Taken together, our data suggest that inhibition of ACLY demonstrates a protection against PM2.5-induced EMT, providing a concern on the molecular mechanisms of PM2.5-associated pulmonary disorders.

In the case of fire, explosive spalling often occurs in cementitious composites due to dense microstructure and high pore-pressure. Polymer fibers were proved to be effective in mitigating such behavior. However, deterioration of these fiber-reinforced cementitious composites inevitably occurs, which is vital for the prediction of structural performance and prevention of catastrophic disaster. This paper concentrates on the behavior and mechanism of the deterioration of polyvinyl alcohol fiber-reinforced engineered cementitious composite (PVA-ECC) after exposure to elevated temperatures. Surface change, cracking, and spalling behavior of the cubic specimens were observed at room temperature, and after exposure to 200 &deg, C, 400 &deg, C, 600 &deg, C, 800 &deg, C, and 1200 &deg, C. Losses in specimen weight and compressive strength were evaluated. Test results indicated that explosive spalling behavior was effectively prevented with 2.0 vol% polyvinyl alcohol fiber although the strength monotonically decreased with heating temperature. X-ray diffraction curves showed that the calcium hydroxide initially decomposed in the range of 400&ndash, 600 &deg, C, and finished beyond 600 &deg, C, while calcium silicate hydrate began at around 400 &deg, C and completely decomposed at approximately 800 &deg, C. Micrographs implied a reduction in fiber diameter at 200 &deg, C, exhibiting apparent needle-like channels beyond 400 &deg, C. When the temperature was increased to 600 &deg, C and above, the dents were gradually filled with newly produced substance due to the synergistic effect of thermal expansion, volume expansion of chemical reactions, and pore structure coarsening

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.

The single nucleotide polymorphism (SNP), -397G > T (rs13278062) polymorphism, in the promoter of Death Receptor 4 (DR4) had been reported to be associated with a significantly increased risk for bladder cancer. However, the association of this SNP with the risk of colorectal cancer has not been reported. In this study, we performed a case-control study in 1,078 colorectal cancer patients and 1,175 matched healthy controls to evaluate the association of the potential functional genetic variants in DR4 with risk and survival of colorectal cancer. PCR-TaqMan were used to genotype the rs13278062, rs1000294 and rs2235126 polymorphisms. We found that subjects carrying the rs13278062 GT/TT genotypes had a significantly lower risk and increased survival time when compared to the GG genotype. We also constructed the rs13278062 GT/TT genotype in SW480 and SW620 cells (rs13278062 is GG in both cell lines) with the CRISPR/Cas9 system. Flow cytometry experiments showed that the rs13278062 TT genotype promoted apoptosis in colorectal cancer cells. In vitro and in vivo experiments established that the rs13278062 G to T mutation inhibited carcinogenesis and metastasis of colorectal cancer. Chromatin immunoprecipitation (ChIP) assays revealed that the rs13278062 G > T polymorphism altered the binding affinity of the transcription factors Sp1/NF1 to the rs13278062 mutation region. Immunohistochemistry, western blot, and qPCR corroborated that the rs13278062 GT/TT genotypes increased the expression of DR4 protein in colorectal cancer tissues and cells. In conclusion, these findings indicate that DR4 mediated progression, invasion, metastasis and survival of colorectal cancer via the Sp1/NF1 switch axis on genomics locus.

Background Inhaled nanoparticles can deposit in the deep lung where they interact with pulmonary cells. Despite numerous studies on pulmonary nanotoxicity, detailed molecular mechanisms of specific nanomaterial-induced lung injury have yet to be identified. Results Using whole-body dynamic inhalation model, we studied the interactions between aluminum oxide nanoparticles (Al2O3 NPs) and the pulmonary system in vivo. We found that seven-day-exposure to Al2O3 NPs resulted in emphysema and small airway remodeling in murine lungs, accompanied by enhanced inflammation and apoptosis. Al2O3 NPs exposure led to suppression of PTPN6 and phosphorylation of STAT3, culminating in increased expression of the apoptotic marker PDCD4. Rescue of PTPN6 expression or application of a STAT3 inhibitor, effectively protected murine lungs from inflammation and apoptosis, as well as, in part, from the induction of chronic obstructive pulmonary disease (COPD)-like effects. Conclusion In summary, our studies show that inhibition of PTPN6 plays a critical role in Al2O3 NPs-induced COPD-like lesions. Electronic supplementary material The online version of this article (10.1186/s12989-017-0234-0) contains supplementary material, which is available to authorized users.

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 , Jihong Hao 3 , Hao Sun 1 , Na Gao 1 , Chengcheng Zhang 1 , Runze Lu 1 , Shizhi Wang 1 , Lihong Yin 1 , Yuepu Pu 1 , Rui Chen 1, 4 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 Clinical Laboratory of The Second Hospital, Hebei Medical University, Shijiazhuang 050000, China 4 State Key Laboratory of Bioelectronics, Southeast University, Nanjing 210096, China Correspondence to: Rui Chen, email: 101011816@seu.edu.cn Keywords: PM 2.5 , metal, autophagy, ribosome, microRNA Received: February 19, 2016 Accepted: May 23, 2016 Published: June 13, 2016 ABSTRACT Metals are vital toxic components of fine particulate matter (PM 2.5 ). Cellular responses to exposure to PM 2.5 or PM metal components remain unknown. Post-transcriptional profiling and subsequent cell- and individual-based assays implied that the metal ion-binding miR-4516/RPL37/autophagy pathway could play a critical role in cellular responses to PM 2.5 and PM metal stresses. miR-4516 was up-regulated in A549 cells exposed to PM 2.5 and in the serum of individuals living in a city with moderate air pollution. The expression levels of the miR-4516 target genes, namely, RPL37 and UBA52, were involved in ribosome function and inhibited by exposure to PM 2.5 and PM metal components. Autophagy in A549 cells was induced by PM 2.5 exposure as a response to decreased RPL37 expression. Moreover, enhanced miR-4516 expression was positively correlated with the augmentation of the internal burden of aluminum and lead in individuals living in a city with moderate air pollution. Hereby, the miR-4516/RPL37/autophagy pathway may represent a novel mechanism that mediates responses to PM metal components.

Epidemiological studies have associated ambient fine particulate matter (PM

Reproductive epidemiological studies have suggested associations between perinatal exposure to fine particulate matter (PM

The single nucleotide polymorphism (SNP), -397G T (rs13278062) polymorphism, in the promoter of Death Receptor 4 (DR4) had been reported to be associated with a significantly increased risk for bladder cancer. However, the association of this SNP with the risk of colorectal cancer has not been reported. In this study, we performed a case-control study in 1,078 colorectal cancer patients and 1,175 matched healthy controls to evaluate the association of the potential functional genetic variants in DR4 with risk and survival of colorectal cancer. PCR-TaqMan were used to genotype the rs13278062, rs1000294 and rs2235126 polymorphisms. We found that subjects carrying the rs13278062 GT/TT genotypes had a significantly lower risk and increased survival time when compared to the GG genotype. We also constructed the rs13278062 GT/TT genotype in SW480 and SW620 cells (rs13278062 is GG in both cell lines) with the CRISPR/Cas9 system. Flow cytometry experiments showed that the rs13278062 TT genotype promoted apoptosis in colorectal cancer cells. In vitro and in vivo experiments established that the rs13278062 G to T mutation inhibited carcinogenesis and metastasis of colorectal cancer. Chromatin immunoprecipitation (ChIP) assays revealed that the rs13278062 G T polymorphism altered the binding affinity of the transcription factors Sp1/NF1 to the rs13278062 mutation region. Immunohistochemistry, western blot, and qPCR corroborated that the rs13278062 GT/TT genotypes increased the expression of DR4 protein in colorectal cancer tissues and cells. In conclusion, these findings indicate that DR4 mediated progression, invasion, metastasis and survival of colorectal cancer via the Sp1/NF1 switch axis on genomics locus.

// 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.

Supporting information. (PDF 615 kb)

Supporting information. (PDF 615 kb)