ABSTRACT
Deep learning models have been widely used during the last decade due to their outstanding learning and abstraction capacities. However, one of the main challenges any scientist has to face using deep learning models is to establish the network's architecture. Due to this difficulty, data scientists usually build over complex models and, as a result, most of them result computationally intensive and impose a large memory footprint, generating huge costs, contributing to climate change and hindering their use in computational-limited devices. In this paper, we propose a novel dense feed-forward neural network constructing method based on pruning and transfer learning. Its performance has been thoroughly assessed in classification and regression problems. Without any accuracy loss, our approach can compress the number of parameters by more than 70%. Even further, choosing the pruning parameter carefully, most of the refined models outperform original ones. Furthermore, we have verified that our method not only identifies a better network architecture but also facilitates knowledge transfer between the original and refined models. The results obtained show that our constructing method not only helps in the design of more efficient models but also more effective ones.
Subject(s)
Climate Change , Neural Networks, Computer , Concept Formation , KnowledgeABSTRACT
Titanium dioxide as a food additive (E171) has been demonstrated to facilitate growth of chemically induced colorectal tumours in vivo and induce transcriptomic changes suggestive of an immune system impairment and cancer development. The present study aimed to investigate the molecular mechanisms behind the tumour stimulatory effects of E171 in combination with azoxymethane (AOM)/dextran sodium sulphate (DSS) and compare these results to a recent study performed under the same conditions with E171 only. BALB/c mice underwent exposure to 5 mg/kgbw/day of E171 by gavage for 2, 7, 14, and 21 days. Whole genome mRNA microarray analyses on the distal colon were performed. The results show that E171 induced a downregulation of genes involved in the innate and adaptive immune system, suggesting impairment of this system. In addition, over time, signalling genes involved in colorectal cancer and other types of cancers were modulated. In relation to cancer development, effects potentially associated with oxidative stress were observed through modulation of genes related to antioxidant production. E171 affected genes involved in biotransformation of xenobiotics which can form reactive intermediates resulting in toxicological effects. These transcriptomics data reflect the early biological responses induced by E171 which precede tumour formation in an AOM/DSS mouse model.
Subject(s)
Azoxymethane/toxicity , Colonic Neoplasms/genetics , Transcriptome/genetics , Animals , Antioxidants/metabolism , Dextran Sulfate/toxicity , Female , Male , Mice , Mice, Inbred BALB C , Oxidative Stress/drug effects , RNA, Messenger/genetics , Xenobiotics/metabolismABSTRACT
We investigated gene expression responses in BALB/c mice exposed by gavage to 5 mg/kg bw/day of E171 for 2, 7, 14 and 21 days. Food additive E171 (titanium dioxide) has been shown to induce oxidative stress and DNA damage in vitro as well as facilitating growth of colorectal tumours in vivo. Full genome expression changes of the colon of mice were investigated by using Agilent SurePrint G3 mouse Gene exp 60kv2 microarrays slides. The data presented in this DiB include all differentially expressed for each time point with EntrezGeneID, gene symbols, gene names and Log2FC as well as genes included in pathways after over-representation analysis in ConsensusPathDataBase. The functions of these genes in relation to the colon were described in our associated article (Proquin et al., 2017 in press) [1]. Raw and normalized gene expression data are available through NCBI GEO (GEO accession: GSE92563).
ABSTRACT
Dietary factors that may influence the risks of colorectal cancer, including specific supplements, are under investigation. Previous studies showed the capacity of food additive titanium dioxide (E171) to induce DNA damage in vitro and facilitate growth of colorectal tumours in vivo. This study aimed to investigate the molecular mechanisms behind these effects after E171 exposure. BALB/c mice were exposed by gavage to 5 mg/kgbw/day of E171 for 2, 7, 14, and 21 days. Transcriptome changes were studied by whole genome mRNA microarray analysis on the mice's distal colons. In addition, histopathological changes as well as a proliferation marker were analysed. The results showed significant gene expression changes in the olfactory/GPCR receptor family, oxidative stress, the immune system and of cancer related genes. Transcriptome analysis also identified genes that thus far have not been included in known biological pathways and can induce functional changes by interacting with other genes involved in different biological pathways. Histopathological analysis showed alteration and disruption in the normal structure of crypts inducing a hyperplastic epithelium. At cell proliferation level, no consistent increase over time was observed. These results may offer a mechanistic framework for the enhanced tumour growth after ingestion of E171 in BALB/c mice.
Subject(s)
Food Additives/pharmacology , Titanium/pharmacology , Transcriptome/drug effects , Animals , Female , Gene Expression Regulation/drug effects , Male , Mice , Mice, Inbred BALB C , RNA, Messenger/genetics , RNA, Messenger/metabolismABSTRACT
Colorectal cancer is the fourth worldwide cause of death and even if some dietary habits are consider risk factors, the contribution of food additives including foodgrade titanium dioxide (TiO2), designated as E171, has been poorly investigated. We hypothesized that oral E171 intake could have impact on the enhancement of colorectal tumor formation and we aimed to investigate if E171 administration could enhance tumor formation in a colitis associated cancer (CAC) model. BALB/c male mice were grouped as follows: a) control, b) E171, c) CAC and d) CAC + E171 group (n = 6). E171 used in this study formed agglomerates of 300 nm in water. E171 intragastric administration (5 mg/kg body weight/5 days/10 weeks) was unable to induce tumor formation but dysplastic alterations were observed in the distal colon but enhanced the tumor formation in distal colon (CAC + E171 group) measured by tumor progression markers. Some E171 particles were internalized in colonic cells of the E171 and CAC + E171 groups and both groups showed a decrease in goblet cells in the distal colon. However the CAC + E171 group showed a higher decrease of these cells that act as protection barrier in colon. These results suggest that E171 could worsen pre-existent intestinal diseases.
Subject(s)
Colitis/complications , Colorectal Neoplasms/pathology , Disease Models, Animal , Food Additives/toxicity , Goblet Cells/pathology , Titanium/toxicity , Animals , Cells, Cultured , Colitis/drug therapy , Colorectal Neoplasms/chemically induced , Goblet Cells/drug effects , Male , Mice , Mice, Inbred BALB CABSTRACT
Current evidence of engineered nanomaterials' (ENM) toxicity has led to a latent concern about hazards for both humans and the environment. For this reason, some efforts have been made to suggest frameworks or other guidance to regulate ENM handling; however, the real exposure risk to humans has not been well established. The aims of this work were to analyze the difficulties in establishing regulations for ENM and to discuss some considerations that may be helpful for policy makers involved in the regulation of ENM. Difficulties in establishing regulations are based on the novel properties of ENM associated with cytotoxic effects, the insufficiency of standardized methods to test those effects and the lack of epidemiological evidence of ENM toxicity, especially in occupational settings. Nevertheless, we offer some suggestions for establishing regulations, which include frameworks oriented towards protecting personnel exposed to ENM without decreasing production. In addition, we propose an ENM data sheet to offer available information of ENM. Finally, ethical aspects should also be considered in developing ENM regulations because every person who is working around or consuming ENM has the right to be informed about the potential risk.
Subject(s)
Legislation as Topic/trends , Nanostructures , Cell Survival/drug effects , Environmental Exposure/adverse effects , Environmental Exposure/legislation & jurisprudence , Epidemiologic Research Design , Humans , Occupational Exposure/adverse effects , Occupational Exposure/legislation & jurisprudence , Occupational Exposure/prevention & control , Public Policy , Risk , Risk AssessmentABSTRACT
Extirpación de liquido de la cavidad pleural a traves de punción transparietal con el objetivo de analizar y llegar a resultado etiológivo con fines terapeuticos
Subject(s)
PleuraABSTRACT
Proyecto de grado orientado a incrementar la producción de ají en la Provincia Luis Calvo, considerando una evaluación del comportamiento fenológico y agronómico, la adaptación y la rentabilidad del cultivo en sus siete nuevas variedades