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Journal articles on the topic 'FANTOM5'

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Author: Grafiati

Published: 11 March 2023

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1

Abugessaisa, Imad, Jordan A. Ramilowski, Marina Lizio, Jesicca Severin, Akira Hasegawa, Jayson Harshbarger, Atsushi Kondo, et al. "FANTOM enters 20th year: expansion of transcriptomic atlases and functional annotation of non-coding RNAs." Nucleic Acids Research 49, no. D1 (November 19, 2020): D892—D898. http://dx.doi.org/10.1093/nar/gkaa1054.

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Abstract The Functional ANnoTation Of the Mammalian genome (FANTOM) Consortium has continued to provide extensive resources in the pursuit of understanding the transcriptome, and transcriptional regulation, of mammalian genomes for the last 20 years. To share these resources with the research community, the FANTOM web-interfaces and databases are being regularly updated, enhanced and expanded with new data types. In recent years, the FANTOM Consortium's efforts have been mainly focused on creating new non-coding RNA datasets and resources. The existing FANTOM5 human and mouse miRNA atlas was supplemented with rat, dog, and chicken datasets. The sixth (latest) edition of the FANTOM project was launched to assess the function of human long non-coding RNAs (lncRNAs). From its creation until 2020, FANTOM6 has contributed to the research community a large dataset generated from the knock-down of 285 lncRNAs in human dermal fibroblasts; this is followed with extensive expression profiling and cellular phenotyping. Other updates to the FANTOM resource includes the reprocessing of the miRNA and promoter atlases of human, mouse and chicken with the latest reference genome assemblies. To facilitate the use and accessibility of all above resources we further enhanced FANTOM data viewers and web interfaces. The updated FANTOM web resource is publicly available at https://fantom.gsc.riken.jp/.

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2

Mojarad, Musa, Fariba Sarhangnia, Amin Rezaeipanah, Hamin Parvin, and Samad Nejatian. "Modeling Hereditary Disease Behavior Using an Innovative Similarity Criterion and Ensemble Clustering." Current Bioinformatics 16, no. 5 (August 11, 2021): 749–64. http://dx.doi.org/10.2174/1574893616999210128175715.

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Background: Today, there are various theories about the causes of hereditary diseases, but doctors believe that both genetic and environmental factors play an essential role in the incidence and spread of these diseases. Objective: In order to identify genes that are cause the disease, inter-cell or inter-tissue communications must be determined. The inter-cells or inter-tissues interaction could be illustrated by applying the gene expression. The disorders that have led to widespread changes could be identified by investigating gene expression information. Methods: In this paper, identifying inter-cell and inter-tissue communications for various diseases has been accomplished utilizing an innovative similarity criterion of the graph topological structure characteristics and an extended clustering ensemble. The proposed method is performed in two stages: first, several clustering models have been combined to detect initial inter-cell or inter-tissue communications and produce better results than singular algorithms. Second, the cell-to-cell or tissue-totissue similarity in each cluster is identified through a similarity criterion based on the graph topological structure. Results: The evaluation of the proposed method has been carried out, benefiting the UCI and FANTOM5 datasets. The results of experiments over FANTOM5 dataset report that the Silhouette coefficient equals 0.901 in 18 clusters for cells and equal to 0.762 in 13 clusters for tissues. Conclusion: The maximum inter-cells or inter-tissues similarity in each cluster can be exploited to detect the relationships between diseases.

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Chang, Yu-Ling, Krishna Sriram, Zhenping Wang, Satomi Igawa, Chia-Chi Wu, Paul Insel, and Anna Di Nardo. "Dermal Fibroblasts Control Mast Cell reactivity to commensal bacteria." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 122.15. http://dx.doi.org/10.4049/jimmunol.202.supp.122.15.

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Abstract Background Our data suggests, and current literature supports, that when mast cells (MCs) leave the blood and interact with dermal fibroblasts (DFs), they assume a bacterial tolerant phenotype in order to prevent unnecessary inflammation during the encounter with the beneficial commensal microbiome. We hypothesize that the mechanisms that induce the MC tolerant phenotype in human skin is due to dermal fibroblasts interactions. Methods We mimicked the “in vivo” setting by conditioning human cord blood MC (hMC) with human dermal fibroblast (hDF) and, then exposed them to commensal bacteria supernatant. Human MC transcriptome data from the RNA-seq FANTOM5 data collection on MCs freshly isolated from human skin (FANTOM5 study Motakis_et_al_2013) was used to investigate the innate immune phenotype of MCs in the skin. We determined the genes that make hDFs unique by comparing their gene expression profiles with lung and cardiac fibroblasts using RNA-seq analysis and challenged hMCs with the products of these genes. Results We have discovered that hDF conditioned with hMCs, show a decreased expression of interleukins upon commensal stimulation; specifically, multiple cytokines/chemokine such as pro-inflammatory cytokine GM-SCF, IL-8, MCP-1 and anti-inflammatory cytokines IL-10, IL-13 are down-regulated by at least 95% and these cytokines can be controlled by the product of hDF unique genes. Conclusion The human dermal MC reactivity is controlled by hDF’s unique genes that play an important role in regulating the hMC NF-Kb pathway.

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Abugessaisa, Imad, Hisashi Shimoji, Serkan Sahin, Atsushi Kondo, Jayson Harshbarger, Marina Lizio, Yoshihide Hayashizaki, et al. "FANTOM5 transcriptome catalog of cellular states based on Semantic MediaWiki." Database 2016 (2016): baw105. http://dx.doi.org/10.1093/database/baw105.

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5

良子, 藤川. "FANTOM5データを誰でも活用できる形に." Nature Digest 14, no. 12 (December 2017): 24–27. http://dx.doi.org/10.1038/ndigest.2017.171224.

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6

Kolmykov, Semyon, Ivan Yevshin, Mikhail Kulyashov, Ruslan Sharipov, Yury Kondrakhin, Vsevolod J. Makeev, Ivan V. Kulakovskiy, Alexander Kel, and Fedor Kolpakov. "GTRD: an integrated view of transcription regulation." Nucleic Acids Research 49, no. D1 (November 24, 2020): D104—D111. http://dx.doi.org/10.1093/nar/gkaa1057.

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Abstract The Gene Transcription Regulation Database (GTRD; http://gtrd.biouml.org/) contains uniformly annotated and processed NGS data related to gene transcription regulation: ChIP-seq, ChIP-exo, DNase-seq, MNase-seq, ATAC-seq and RNA-seq. With the latest release, the database has reached a new level of data integration. All cell types (cell lines and tissues) presented in the GTRD were arranged into a dictionary and linked with different ontologies (BRENDA, Cell Ontology, Uberon, Cellosaurus and Experimental Factor Ontology) and with related experiments in specialized databases on transcription regulation (FANTOM5, ENCODE and GTEx). The updated version of the GTRD provides an integrated view of transcription regulation through a dedicated web interface with advanced browsing and search capabilities, an integrated genome browser, and table reports by cell types, transcription factors, and genes of interest.

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7

Sharipov, Ruslan N., Yury V. Kondrakhin, Anna S. Ryabova, Ivan S. Yevshin, and Fedor A. Kolpakov. "Assessment of transcriptional importance of cell line-specific features based on GTRD and FANTOM5 data." PLOS ONE 15, no. 12 (December 21, 2020): e0243332. http://dx.doi.org/10.1371/journal.pone.0243332.

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Creating a complete picture of the regulation of transcription seems to be an urgent task of modern biology. Regulation of transcription is a complex process carried out by transcription factors (TFs) and auxiliary proteins. Over the past decade, ChIP-Seq has become the most common experimental technology studying genome-wide interactions between TFs and DNA. We assessed the transcriptional significance of cell line-specific features using regression analysis of ChIP-Seq datasets from the GTRD database and transcriptional start site (TSS) activities from the FANTOM5 expression atlas. For this purpose, we initially generated a large number of features that were defined as the presence or absence of TFs in different promoter regions around TSSs. Using feature selection and regression analysis, we identified sets of the most important TFs that affect expression activity of TSSs in human cell lines such as HepG2, K562 and HEK293. We demonstrated that some TFs can be classified as repressors and activators depending on their location relative to TSS.

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8

Kyi-Tha-Thu, Chaw, and Toshihiro Takizawa. "Long non-coding RNA expression analysis during mouse testis development using the FANTOM5 data." Journal of Reproductive Immunology 130 (November 2018): 40. http://dx.doi.org/10.1016/j.jri.2018.09.029.

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9

Wang, Junxiao, Shan-Shun Luo, and Toshihiro Takizawa. "In silico analysis of lncRNA expression in the mouse placenta using the FANTOM5 database." Journal of Reproductive Immunology 130 (November 2018): 42. http://dx.doi.org/10.1016/j.jri.2018.09.035.

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10

Santos, Thallis Alves, Aline Ragonezi, Marcio Tokarski, and Bruna Biazotto. "Comissionamento do sistema de planejamento para uso de correção de heterogeneidades: Construção de um fantoma de baixo custo para validação e controle de qualidade em radioterapia." Revista Brasileira de Física Médica 11, no. 3 (November 4, 2018): 13. http://dx.doi.org/10.29384/rbfm.2017.v11.n3.p13.

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A implementação de correções por heterogeneidades no sistema de planejamento de tratamentos radioterápicos melhora a exatidão do cálculo de dose em pacientes submetidos a teleterapia. Estudos mostram que planejamentos sem levar em conta a correção de heterogeneidade podem produzir um subdosagem de até 20% para tumores de pulmão na entrega de dose. Para a validação é necessário adquirir um dos fantomas disponíveis comercialmente. Esses Fantomas permitem a realização dos testes recomendados pelo TRS-430 (Commissioning and Quality Assurance of Computerized Planning Systems for Radiation Treatment of Cancer) e implementação das correções de heterogeneidades. Esse trabalho visa comparar os fantomas disponíveis comercialmente e fazer a análise para construção de um próprio fantoma para validação de forma a cobrir os requisitos necessários

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Aptekmann, Ariel A., Denys Bulavka, Alejandro D. Nadra, and Ignacio E. Sánchez. "Transcription factor specificity limits the number of DNA-binding motifs." PLOS ONE 17, no. 1 (January 28, 2022): e0263307. http://dx.doi.org/10.1371/journal.pone.0263307.

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We study the limits imposed by transcription factor specificity on the maximum number of binding motifs that can coexist in a gene regulatory network, using the SwissRegulon Fantom5 collection of 684 human transcription factor binding sites as a model. We describe transcription factor specificity using regular expressions and find that most human transcription factor binding site motifs are separated in sequence space by one to three motif-discriminating positions. We apply theorems based on the pigeonhole principle to calculate the maximum number of transcription factors that can coexist given this degree of specificity, which is in the order of ten thousand and would fully utilize the space of DNA subsequences. Taking into account an expanded DNA alphabet with modified bases can further raise this limit by several orders of magnitude, at a lower level of sequence space usage. Our results may guide the design of transcription factors at both the molecular and system scale.

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12

Summers, Kim M., and David A. Hume. "Identification of the macrophage-specific promoter signature in FANTOM5 mouse embryo developmental time course data." Journal of Leukocyte Biology 102, no. 4 (July 27, 2017): 1081–92. http://dx.doi.org/10.1189/jlb.1a0417-150rr.

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13

Petre, Zoe. "Fantoma lui Pârvan / Le fantôme de Pârvan." Materiale şi cercetãri arheologice (Serie nouã) 10, no. 1 (2014): 21–28. http://dx.doi.org/10.3406/mcarh.2014.967.

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14

Yu, Nancy Yiu-Lin, Björn M. Hallström, Linn Fagerberg, Fredrik Ponten, Hideya Kawaji, Piero Carninci, Alistair R. R. Forrest, et al. "Complementing tissue characterization by integrating transcriptome profiling from the Human Protein Atlas and from the FANTOM5 consortium." Nucleic Acids Research 43, no. 14 (June 27, 2015): 6787–98. http://dx.doi.org/10.1093/nar/gkv608.

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15

Wang, Hui, Yan Sha, Dan Wang, and Hamed Nazari. "A Gene Expression Clustering Method to Extraction of Cell-to-Cell Biological Communication." Inteligencia Artificial 25, no. 69 (March 11, 2022): 1–12. http://dx.doi.org/10.4114/intartif.vol25iss69pp1-12.

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Graph-based clustering identification is a practical method to detect the communication between nodes in complex networks that has obtained considerable comments. Since identifying different communities in large-scale data is a challenging task, by understanding the communication between the behaviors of the elements in a community (a cluster), the general characteristics of clusters can be predicted. Graph-based clustering methods have played an important role in clustering gene expression data because of their ability to show the relations between the data. In order to be able to identify genes that lead to the development of diseases, the communication between the cells must be established. The communication between different cells can be indicated by the expression of different genes within them. In this study, the problem of cell-to-cell communication is expressed as a graph and the communication are extracted by recognizing the communities. The FANTOM5 dataset is used to simulate and calculate the similarity between cells. After preprocessing and normalizing the data, to convert this data into graphs, the expression of genes in different cells was examined and by considering a threshold and Wilcoxon test, the communication between them were identified through using clustering.

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Dimont, Emmanuel, Oliver Hofmann, Shannan J. Ho Sui, Alistair R. R. Forrest, Hideya Kawaji, and Winston Hide. "CAGExploreR: an R package for the analysis and visualization of promoter dynamics across multiple experiments." Bioinformatics 30, no. 8 (March 26, 2014): 1183–84. http://dx.doi.org/10.1093/bioinformatics/btu125.

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Summary Alternate promoter usage is an important molecular mechanism for generating RNA and protein diversity. Cap Analysis Gene Expression (CAGE) is a powerful approach for revealing the multiplicity of transcription start site (TSS) events across experiments and conditions. An understanding of the dynamics of TSS choice across these conditions requires both sensitive quantification and comparative visualization. We have developed CAGExploreR, an R package to detect and visualize changes in the use of specific TSS in wider promoter regions in the context of changes in overall gene expression when comparing different CAGE samples. These changes provide insight into the modification of transcript isoform generation and regulatory network alterations associated with cell types and conditions. CAGExploreR is based on the FANTOM5 and MPromDb promoter set definitions but can also work with user-supplied regions. The package compares multiple CAGE libraries simultaneously. Supplementary Materials describe methods in detail, and a vignette demonstrates a workflow with a real data example. Availability and implementation: The package is freely available under the MIT license from CRAN (http://cran.r-project.org/web/packages/CAGExploreR). Contact: edimont@mail.harvard.edu Supplementary information: Supplementary data are available at Bioinformatics online.

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WAC-WŁODARCZYK, Andrzej. "Fantomy do testowania systemów obrazowania medycznego w PET na przykładzie fantomu Jaszczaka." PRZEGLĄD ELEKTROTECHNICZNY 1, no. 8 (August 5, 2018): 112–16. http://dx.doi.org/10.15199/48.2018.08.26.

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18

Ning, Boting, Roxana M. Pfefferkorn, Gang Liu, Sherry Zhang, Hanqiao Liu, Christopher Stevenson, Sarah A. Mazzilli, Avrum E. Spira, Marc E. Lenburg, and Jennifer E. Beane. "Abstract 1488: The role of epithelial miR-149 in immune modulation and progression of bronchial premalignant lesions." Cancer Research 82, no. 12_Supplement (June 15, 2022): 1488. http://dx.doi.org/10.1158/1538-7445.am2022-1488.

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Abstract The molecular events involved in the development of bronchial premalignant lesions (PMLs), and their progression to lung squamous cell carcinoma, are not well understood. Prior work characterized lung PML molecular subtypes by identifying co-expressed gene modules associated with histologic severity and progression/persistence. The proliferative subtype was enriched for PMLs with dysplasia. Genes related to interferon signaling and antigen processing/presentation (Module 9) were decreased in progressive/persistent lesions within this subtype, suggesting early immune suppression is related to PML progression. However, the mechanisms that drive these alterations are unclear. We investigated the role of microRNAs (miRNAs) in regulating gene expression associated with PML outcomes. mRNA and miRNA were extracted and sequenced from longitudinally collected endobronchial biopsies from patients with PMLs (148 samples, 30 patients). miRNAs targeting each gene co-expression module were identified based on target gene enrichment and the degree of negative correlation between the miRNA expression and its targets. Expression association with outcome within the proliferative subtype was tested with a mixed effects model adjusting for batch and patient as random effect. Cell type specificity of miRNA expression was tested based on cell type specific sequencing data from FANTOM5 and cell type marker correlation analysis. Genes regulated by NLRC5 were identified with ChIPseq data from Ludigs et al. Target gene suppression was confirmed by transfecting SW900 cells with miR-149-5p. miR-149-5p level in PML biopsies was examined by miRNA in situ hybridization (miR-ISH). miR-149-5p is identified as potential regulator of Module 9 gene expression and is significantly up-regulated in progressive/persistent PMLs. Its expression is highly enriched in epithelial cells in FANTOM5 and positively correlates with basal cell markers within PMLs. Predicted targets of miR-149-5p are down-regulated in the progressive PMLs in both our and data from Merrick et al. MHC-I and related gene expressions are down-regulated in progressing/persistent PMLs. These genes are regulated by the transcriptional coactivator NLRC5 which is a predicted target gene of miR-149-5p. We find that overexpressing miR-149-5p in SW900 cells decreases the expression levels of both NLRC5 and NLRC5 regulated genes. Additionally, miR-ISH targeting miR-149-5p in proliferative biopsy samples confirm its expression in epithelium compartment and association with outcome. Our data suggest epithelial miR-149-5p might be a key regulator of gene expression contributing to PML progression. We hypothesize that by suppressing NLRC5, miR-149-5p inhibits MHC-I gene expression of epithelial cells, promoting early immune depletion and lesion progression. miR-149-5p might therefore be a therapeutic target for preventing PML progression. Citation Format: Boting Ning, Roxana M. Pfefferkorn, Gang Liu, Sherry Zhang, Hanqiao Liu, Christopher Stevenson, Sarah A. Mazzilli, Avrum E. Spira, Marc E. Lenburg, Jennifer E. Beane. The role of epithelial miR-149 in immune modulation and progression of bronchial premalignant lesions [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1488.

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Li, JiaRui, Lei Chen, Yu-Hang Zhang, XiangYin Kong, Tao Huang, and Yu-Dong Cai. "A Computational Method for Classifying Different Human Tissues with Quantitatively Tissue-Specific Expressed Genes." Genes 9, no. 9 (September 7, 2018): 449. http://dx.doi.org/10.3390/genes9090449.

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Tissue-specific gene expression has long been recognized as a crucial key for understanding tissue development and function. Efforts have been made in the past decade to identify tissue-specific expression profiles, such as the Human Proteome Atlas and FANTOM5. However, these studies mainly focused on “qualitatively tissue-specific expressed genes” which are highly enriched in one or a group of tissues but paid less attention to “quantitatively tissue-specific expressed genes”, which are expressed in all or most tissues but with differential expression levels. In this study, we applied machine learning algorithms to build a computational method for identifying “quantitatively tissue-specific expressed genes” capable of distinguishing 25 human tissues from their expression patterns. Our results uncovered the expression of 432 genes as optimal features for tissue classification, which were obtained with a Matthews Correlation Coefficient (MCC) of more than 0.99 yielded by a support vector machine (SVM). This constructed model was superior to the SVM model using tissue enriched genes and yielded MCC of 0.985 on an independent test dataset, indicating its good generalization ability. These 432 genes were proven to be widely expressed in multiple tissues and a literature review of the top 23 genes found that most of them support their discriminating powers. As a complement to previous studies, our discovery of these quantitatively tissue-specific genes provides insights into the detailed understanding of tissue development and function.

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Hou, Rui, Elena Denisenko, and Alistair R. R. Forrest. "scMatch: a single-cell gene expression profile annotation tool using reference datasets." Bioinformatics 35, no. 22 (April 26, 2019): 4688–95. http://dx.doi.org/10.1093/bioinformatics/btz292.

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Abstract Motivation Single-cell RNA sequencing (scRNA-seq) measures gene expression at the resolution of individual cells. Massively multiplexed single-cell profiling has enabled large-scale transcriptional analyses of thousands of cells in complex tissues. In most cases, the true identity of individual cells is unknown and needs to be inferred from the transcriptomic data. Existing methods typically cluster (group) cells based on similarities of their gene expression profiles and assign the same identity to all cells within each cluster using the averaged expression levels. However, scRNA-seq experiments typically produce low-coverage sequencing data for each cell, which hinders the clustering process. Results We introduce scMatch, which directly annotates single cells by identifying their closest match in large reference datasets. We used this strategy to annotate various single-cell datasets and evaluated the impacts of sequencing depth, similarity metric and reference datasets. We found that scMatch can rapidly and robustly annotate single cells with comparable accuracy to another recent cell annotation tool (SingleR), but that it is quicker and can handle larger reference datasets. We demonstrate how scMatch can handle large customized reference gene expression profiles that combine data from multiple sources, thus empowering researchers to identify cell populations in any complex tissue with the desired precision. Availability and implementation scMatch (Python code) and the FANTOM5 reference dataset are freely available to the research community here https://github.com/forrest-lab/scMatch. Supplementary information Supplementary data are available at Bioinformatics online.

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Alves, Juliane, Luciana Batista Nogueira, Críssia Carem Paiva Fontainha Fontainha, and Tarcísio Passos Ribeiro Campos. "Doses Absorvidas em Órgãos Internos em Fantoma Feminino de Tórax em Radiologia Diagnóstica." Revista Brasileira de Física Médica 14 (December 21, 2020): 517. http://dx.doi.org/10.29384/rbfm.2020.v14.19849001517.

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Os exames radiológicos por imagens no qual os pacientes são submetidos tem aumentado de forma considerável, tornando crescente a exposição às radiações ionizantes. Muito se conhece da dose na entrada na pele em diversas técnicas radiológicas, entretanto não se discriminam as doses em órgãos sensíveis do corpo. Neste trabalho foi proposto mensurar doses absorvidas em órgãos internos de um fantoma feminino de tórax, através de exposições de raios X diagnóstico. Para o estudo foi utilizado dois equipamentos de raios X e um fantoma de tórax do grupo de pesquisa Núcleo de Radiações Ionizantes NRI/UFMG. Como dosímetros foram utilizados filmes radiocrômicos XRQA2, que foram posicionados dentro do fantoma de tórax, localizados no coração, pulmão direito e esquerdo, mama e pele. Foram realizadas duas exposições, em posicionamento antero-posterior (AP) e lateral de tórax. Após as exposições, os filmes radiocrômicos foram digitalizados e mapas de suas intensidades em RGB (red, green e blue) foram gerados. Os dados dos filmes irradiados foram convertidos em densidade ótica e posteriormente em dose, de acordo com a curva de calibração construída. Valores médios de dose e seus desvios padrões foram gerados para análise e para avaliação das doses absorvidas nos tecidos equivalentes (TE) de órgãos internos. Após análise, foi observado que as doses médias encontradas nos TE de órgãos internos estão correlacionadas aos níveis de referência em radiodiagnósticos (NRDs) (MINISTÉRIO DA SAÚDE ,1998) preconizados pela dose de entrada na pele em pacientes adultos e com dados na literatura. O estudo demonstra a possibilidade de monitorar as doses absorvidas em órgãos internos utilizando fantomas antropomórficos e antropométricos, estabelecendo assim novas metodologias de otimização para minimizar danos biológicos e clínicos induzidos pela exposição à radiação no radiodiagnóstico.

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Gong, Siming, Yingjuan Duan, Changwu Wu, Georg Osterhoff, Nikolas Schopow, and Sonja Kallendrusch. "A Human Pan-Cancer System Analysis of Procollagen-Lysine, 2-Oxoglutarate 5-Dioxygenase 3 (PLOD3)." International Journal of Molecular Sciences 22, no. 18 (September 14, 2021): 9903. http://dx.doi.org/10.3390/ijms22189903.

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The overexpression of the enzymes involved in the degradation of procollagen lysine is correlated with various tumor entities. Procollagen-lysine, 2-oxoglutarate 5-dioxygenase 3 (PLOD3) expression was found to be correlated to the progression and migration of cancer cells in gastric, lung and prostate cancer. Here, we analyzed the gene expression, protein expression, and the clinical parameters of survival across 33 cancers based on the Clinical Proteomic Tumor Analysis Consortium (CPTAC), function annotation of the mammalian genome 5 (FANTOM5), Gene Expression Omnibus (GEO), Genotype-Tissue Expression (GTEx), Human Protein Atlas (HPA) and The Cancer Genome Atlas (TCGA) databases. Genetic alteration, immune infiltration and relevant cellular pathways were analyzed in detail. PLOD3 expression negatively correlated with survival periods and the infiltration level of CD8+ T cells, but positively correlated to the infiltration of cancer associated fibroblasts in diverse cancers. Immunohistochemistry in colon carcinomas, glioblastomas, and soft tissue sarcomas further confirm PLOD 3 expression in human cancer tissue. Moreover, amplification and mutation accounted for the largest proportion in esophageal adenocarcinoma and uterine corpus endometrial carcinoma, respectively; the copy number alteration of PLOD3 appeared in all cancers from TCGA; and molecular mechanisms further proved the effect of PLOD3 on tumorigenesis. In particular, PLOD3 expression appears to have a tumor immunological effect, and is related to multiple immune cells. Furthermore, it is also associated with tumor mutation burden and microsatellite instability in various tumors. PLOD3 acts as an inducer of various cancers, and it could be a potential biomarker for prognosis and targeted treatment.

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Vacca, Annalaura, Masayoshi Itoh, Hideya Kawaji, Erik Arner, Timo Lassmann, Carsten O. Daub, Piero Carninci, et al. "Conserved temporal ordering of promoter activation implicates common mechanisms governing the immediate early response across cell types and stimuli." Open Biology 8, no. 8 (August 2018): 180011. http://dx.doi.org/10.1098/rsob.180011.

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The promoters of immediate early genes (IEGs) are rapidly activated in response to an external stimulus. These genes, also known as primary response genes, have been identified in a range of cell types, under diverse extracellular signals and using varying experimental protocols. Whereas genomic dissection on a case-by-case basis has not resulted in a comprehensive catalogue of IEGs, a rigorous meta-analysis of eight genome-wide FANTOM5 CAGE (cap analysis of gene expression) time course datasets reveals successive waves of promoter activation in IEGs, recapitulating known relationships between cell types and stimuli: we obtain a set of 57 (42 protein-coding) candidate IEGs possessing promoters that consistently drive a rapid but transient increase in expression over time. These genes show significant enrichment for known IEGs reported previously, pathways associated with the immediate early response, and include a number of non-coding RNAs with roles in proliferation and differentiation. Surprisingly, we also find strong conservation of the ordering of activation for these genes, such that 77 pairwise promoter activation orderings are conserved. Using the leverage of comprehensive CAGE time series data across cell types, we also document the extensive alternative promoter usage by such genes, which is likely to have been a barrier to their discovery until now. The common activation ordering of the core set of early-responding genes we identify may indicate conserved underlying regulatory mechanisms. By contrast, the considerably larger number of transiently activated genes that are specific to each cell type and stimulus illustrates the breadth of the primary response.

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Fong, Sarah L., and John A. Capra. "Modeling the Evolutionary Architectures of Transcribed Human Enhancer Sequences Reveals Distinct Origins, Functions, and Associations with Human Trait Variation." Molecular Biology and Evolution 38, no. 9 (May 10, 2021): 3681–96. http://dx.doi.org/10.1093/molbev/msab138.

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Abstract Despite the importance of gene regulatory enhancers in human biology and evolution, we lack a comprehensive model of enhancer evolution and function. This substantially limits our understanding of the genetic basis of species divergence and our ability to interpret the effects of noncoding variants on human traits. To explore enhancer sequence evolution and its relationship to regulatory function, we traced the evolutionary origins of transcribed human enhancer sequences with activity across diverse tissues and cellular contexts from the FANTOM5 consortium. The transcribed enhancers are enriched for sequences of a single evolutionary age (“simple” evolutionary architectures) compared with enhancers that are composites of sequences of multiple evolutionary ages (“complex” evolutionary architectures), likely indicating constraint against genomic rearrangements. Complex enhancers are older, more pleiotropic, and more active across species than simple enhancers. Genetic variants within complex enhancers are also less likely to associate with human traits and biochemical activity. Transposable-element-derived sequences (TEDS) have made diverse contributions to enhancers of both architectures; the majority of TEDS are found in enhancers with simple architectures, while a minority have remodeled older sequences to create complex architectures. Finally, we compare the evolutionary architectures of transcribed enhancers with histone-mark-defined enhancers. Our results reveal that most human transcribed enhancers are ancient sequences of a single age, and thus the evolution of most human enhancers was not driven by increases in evolutionary complexity over time. Our analyses further suggest that considering enhancer evolutionary histories provides context that can aid interpretation of the effects of variants on enhancer function. Based on these results, we propose a framework for analyzing enhancer evolutionary architecture.

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Aguiar, Jennifer A., Benjamin J.-M. Tremblay, Michael J. Mansfield, Owen Woody, Briallen Lobb, Arinjay Banerjee, Abiram Chandiramohan, et al. "Gene expression and in situ protein profiling of candidate SARS-CoV-2 receptors in human airway epithelial cells and lung tissue." European Respiratory Journal 56, no. 3 (July 16, 2020): 2001123. http://dx.doi.org/10.1183/13993003.01123-2020.

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In December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged, causing the coronavirus disease 2019 (COVID-19) pandemic. SARS-CoV, the agent responsible for the 2003 SARS outbreak, utilises angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) host molecules for viral entry. ACE2 and TMPRSS2 have recently been implicated in SARS-CoV-2 viral infection. Additional host molecules including ADAM17, cathepsin L, CD147 and GRP78 may also function as receptors for SARS-CoV-2.To determine the expression and in situ localisation of candidate SARS-CoV-2 receptors in the respiratory mucosa, we analysed gene expression datasets from airway epithelial cells of 515 healthy subjects, gene promoter activity analysis using the FANTOM5 dataset containing 120 distinct sample types, single cell RNA sequencing (scRNAseq) of 10 healthy subjects, proteomic datasets, immunoblots on multiple airway epithelial cell types, and immunohistochemistry on 98 human lung samples.We demonstrate absent to low ACE2 promoter activity in a variety of lung epithelial cell samples and low ACE2 gene expression in both microarray and scRNAseq datasets of epithelial cell populations. Consistent with gene expression, rare ACE2 protein expression was observed in the airway epithelium and alveoli of human lung, confirmed with proteomics. We present confirmatory evidence for the presence of TMPRSS2, CD147 and GRP78 protein in vitro in airway epithelial cells and confirm broad in situ protein expression of CD147 and GRP78 in the respiratory mucosa.Collectively, our data suggest the presence of a mechanism dynamically regulating ACE2 expression in human lung, perhaps in periods of SARS-CoV-2 infection, and also suggest that alternative receptors for SARS-CoV-2 exist to facilitate initial host cell infection.

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Cao, Peng, Fan Li, Yajie Xiao, Shan Hu, Kangle Kong, Peng Han, Jiaqi Yue, et al. "Identification and Validation of 7-lncRNA Signature of Epigenetic Disorders by Comprehensive Epigenetic Analysis." Disease Markers 2022 (February 21, 2022): 1–14. http://dx.doi.org/10.1155/2022/5118444.

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The survival rate of patients with lung adenocarcinoma (LUAD) is low. This study analyzed the correlation between the expression of long noncoding RNA (lncRNA) and epigenetic alterations along with the investigation of the prognostic value of these outcomes for LUAD. Differentially expressed lncRNAs were identified based on multiomic data and positively related genes using DESeq2 in R, differentially histone-modifying genes specific to LUAD based on histone modification data, gene enhancers from information collected from the FANTOM5 (Function Annotation Of The Mammalian Genome-5) (fantom.gsc.riken.jp/5) human enhancer database, gene promoters using the ChIPseeker and the human lincRNAs Transcripts database in R, and differentially methylated regions (DMRs) using Bumphunter in R. Overall survival was estimated by Kaplan-Meier, comparisons were performed among groups using log-rank tests to derive differences between sample subclasses, and epigenetic lncRNAs (epi-lncRNAs) potentially relevant to LUAD prognosis were identified. A total of seven dysregulated epi-lncRNAs in LUAD were identified by comparing histone modifications and alterations in histone methylation regions on lncRNA promoter and enhancer elements, including H3K4me2, H3K27me3, H3K4me1, H3K9me3, H4K20me1, H3K9ac, H3K79me2, H3K27ac, H3K4me3, and H3K36me3. Furthermore, 69 LUAD-specific dysregulated epi-lncRNAs were identified. Moreover, lncRNAs-based prognostic analysis of LUAD samples was performed and explored that seven of these lncRNAs, including A2M-AS1, AL161431.1, DDX11-AS1, FAM83A-AS1, MHENCR, MNX1-AS1, and NKILA (7-EpiLncRNA), showed the potential to serve as markers for LUAD prognosis. Additionally, patients having a high 7-EpiLncRNA score showed a generally more unfavorable prognosis compared with those which scored lower. Seven lncRNAs were identified as markers of prognosis in patients with LUAD. The outcomes of this research will help us understand epigenetically aberrant regulation of lncRNA expression in LUAD in a better way and have implications for research advances in the regulatory role of lncRNAs in LUAD.

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Gueler Dalvi, Giovanni, and Pedro Bertemes Filho. "Detecção de Fraturas Ósseas em Fantomas por Espectroscopia de Impedância." Revista Brasileira de Física Médica 15 (July 14, 2021): 614. http://dx.doi.org/10.29384/rbfm.2021.v15.19849001614.

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A maioria das técnicas de diagnóstico por imagem para detecção de fraturas ósseas utiliza equipamentos que emitem radiação, que pode ser prejudicial à saúde humana, mesmo em pequenas doses. Sem dúvida, estudos são necessários e novas técnicas que busquem a redução dessas exposições ao raio-x. O objetivo deste artigo é desenvolver um fantoma biológico 3D e investigar a sensibilidade de detecção de ossos, inteiro e fraturado, por meio da espectroscopia de impedância elétrica. Além disso, são investigados os efeitos das diferentes posições dos eletrodos na sensibilidade da técnica de medição. As medições foram realizadas por um espectroscópio de impedância comercial da Zurich Instruments (modelo HF2IS) na faixa de frequência de 1 kHz a 1 MHz. Quatro eletrodos circulares (modelo MELCTEC) foram usados para conectar o fantoma ao HF2IS. O HF2IS foi inicialmente calibrado medindo um resistor de 100 Ω e 1% de precisão. Vetores de calibração de magnitude e fase foram calculados e então usados para ajustar os dados dos fantomas com e sem osso. Os resultados mostraram que os valores de módulo e fase para o simulador puro e com osso fraturado são bem próximos enquanto para o osso inteiro apresentam notável variação, principalmente em frequências acima de 100 kHz. Observou-se que a distância entre os eletrodos causa um pequeno efeito no módulo de impedância, enquanto as mudanças de fase são mais significativas em alta frequência. Também foi observado que a fase de impedância é mais sensível à geometria do eletrodo com e sem ossos fraturados. Esta pode ser uma ferramenta útil para detecção sem imagem de fraturas de ossos humanos como uma abordagem de baixo custo, não invasiva e não prejudicial à saúde humana.

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Setiawati, Evi, Ridwan Eko Susanto, and Fajar Arianto. "Penentuan Faktor Koreksi Dosis Radiasi Sinar-X Linac 6 MV Pada Ketidakhomogenan Jaringan Tubuh dengan MCNPX." Jurnal Ilmiah Aplikasi Isotop dan Radiasi 18, no. 1 (December 26, 2022): 17. http://dx.doi.org/10.17146/jair.2022.18.1.6586.

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Salah satu metode untuk menghitung dosis radiasi yang dihasilkan oleh linac adalah dengan menggunakan program simulasi MCNPX. Tujuan penelitian ini adalah untuk menentukan karakteristik kurva Percentage Depth Dose (PDD) untuk berkas sinar-x 6 MV dan faktor koreksi dari distribusi dosis akibat adanya ketidakhomogenan jaringan tubuh. Penelitian ini menggunakan fantom jenis ORNL-MIRD phantom (1996 version) yang telah dimodifikasi. Fantom dibedakan menjadi fantom homogen yaitu dengan komposisi air dan jaringan lunak dan fantom nonhomogen dengan komposisi jaringan lunak yang didalamnya terdapat organ paru-paru pada kedalaman 5-14 cm dan jaringan lunak yang didalamnya terdapat organ tulang belakang pada kedalaman 5-10 cm. Luas lapangan penyinaran radiasi 10 x 10 cm2 dengan arah penyinaran radiasi Anterior-Posterior (AP) serta Posterior-Anterior (PA) dengan SSD 100 cm. Dalam penelitian ini didapatkan karakteristik kurva PDD yang sama antara fantom dengan komposisi air dan fantom dengan komposisi jaringan lunak yaitu dosis maksimum berada pada kedalaman 1,5-2,0 cm. Pada fantom nonhomogen yaitu jaringan lunak yang terdapat organ paru-paru mengalami peningkatan dosis dengan deviasi tertinggi sebesar 49,748 % dan keberadaan organ tulang belakang mengalami penurunan dosis dengan deviasi tertinggi sebesar 31,044 %. Rentang faktor koreksi akibat adanya organ paru-paru adalah 0,701-1,663 sedangkan akibat adanya organ tulang belakang adalah 0,586-0,983.

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Yani, Sitti. "Analisis Kurva Dose Volume Histogram (DVH) pada Teknik 3D Konformal dengan Metode Monte Carlo." POSITRON 11, no. 1 (October 15, 2021): 19. http://dx.doi.org/10.26418/positron.v11i1.44052.

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Pemilihan sudut penyinaran yang tepat dalam terapi 3D konformal beberapa jenis kanker sangat menentukan keberhasilan pengobatan. Oleh karena itu, tujuan penelitian ini adalah untuk menganalisis dose volume histogram (DVH) teknik 3D konformal dengan konfigurasi sudut penyinaran yang berbeda pada fantom inhomogenitas dengan metode Monte Carlo (MC). EGSnrc-DOSXYZnrc MC digunakan untuk menyimulasikan teknik 3D konformal pada fantom inhomogenitas. Fantom inhomogenitas terdiri atas material air dan paru-paru dimana material paru-paru berada di dalam fantom air pada kedalaman 2 cm dari permukaan fantom air. Fantom ini diradiasi dengan sumber radiasi monoenergetik 10 MeV dengan sudut penyinaran 0 – 360o. Data distribusi dosis yang diperoleh diolah untuk memperoleh data DVH. Analisis DVH juga dilakukan dengan mengkombinasikan beberapa sudut penyinaran dan pembobotan. Hasil yang diperoleh menunjukkan bahwa distribusi dosis hasil simulasi beragam terhadap sudut penyinaran. Dari kurva DVH diperoleh bahwa sudut penyinaran pada 0o, 20o, 40o, 320o, dan 340o dengan pembobotan memberikan kurva DVH target yang paling baik dibandingkan dengan set-up sudut penyinaran lainnya. Pembobotan dapat mereduksi dosis pada resiko organ dan meningkatkan dosis pada target.

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30

Stenson, Ben J. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 107, no. 5 (August 18, 2022): 457. http://dx.doi.org/10.1136/archdischild-2022-324737.

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Stenson, B. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 86, no. 2 (March 1, 2002): 72F—a—72. http://dx.doi.org/10.1136/fn.86.2.f72-a.

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Ward-Platt, M. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 86, no. 3 (May 1, 2002): 142F —a—142. http://dx.doi.org/10.1136/fn.86.3.f142-a.

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Stenson, B. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 87, no. 1 (July 1, 2002): 2F —a—2. http://dx.doi.org/10.1136/fn.87.1.f2-a.

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Platt, M. W. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 87, no. 2 (September 1, 2002): 1F—1. http://dx.doi.org/10.1136/fn.87.2.f1.

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Stenson, B. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 87, no. 3 (November 1, 2002): 235F—235. http://dx.doi.org/10.1136/fn.87.3.f235.

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Platt, M. W. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 88, no. 1 (January 1, 2003): 2F —a—2. http://dx.doi.org/10.1136/fn.88.1.f2-a.

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Stenson, B. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 88, no. 2 (March 1, 2003): 80F —a—80. http://dx.doi.org/10.1136/fn.88.2.f80-a.

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Platt, M. W. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 88, no. 3 (May 1, 2003): 166F —a—166. http://dx.doi.org/10.1136/fn.88.3.f166-a.

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Platt, M. W. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 88, no. 4 (July 1, 2003): 260F —a—260. http://dx.doi.org/10.1136/fn.88.4.f260-a.

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Ward Platt, M. "FANTOMS." Archives of Disease in Childhood - Fetal and Neonatal Edition 88, no. 5 (September 1, 2003): 354F —a—354. http://dx.doi.org/10.1136/fn.88.5.f354-a.

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Stenson, B. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 88, no. 6 (November 1, 2003): 448F —a—448. http://dx.doi.org/10.1136/fn.88.6.f448-a.

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Ward Platt, M. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 89, no. 1 (January 1, 2004): 1F—1. http://dx.doi.org/10.1136/fn.89.1.f1.

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Stark, A. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 89, no. 2 (March 1, 2004): 96F —a—96. http://dx.doi.org/10.1136/fn.89.2.f96-a.

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Platt, M. W. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 94, no. 6 (October 21, 2009): F391. http://dx.doi.org/10.1136/fnn.2009.174714.

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Stenson, B. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 94, no. 5 (August 21, 2009): F313. http://dx.doi.org/10.1136/adc.2009.170647.

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Stenson, B. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 95, no. 1 (December 17, 2009): F1. http://dx.doi.org/10.1136/adc.2009.179952.

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Stenson, B. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 95, no. 3 (May 1, 2010): F153. http://dx.doi.org/10.1136/adc.2009.189506.

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Platt, M. W. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 95, no. 2 (March 1, 2010): F79. http://dx.doi.org/10.1136/adc.2010.185983.

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Platt, M. W. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 95, no. 4 (June 24, 2010): F231. http://dx.doi.org/10.1136/adc.2010.194191.

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Platt, M. W. "Fantoms." Archives of Disease in Childhood - Fetal and Neonatal Edition 95, no. 5 (August 17, 2010): F309. http://dx.doi.org/10.1136/adc.2010.199125.

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